Anaplastology: The art and science of restoring a malformed or absent part of the human body through artificial means. An anaplastologist makes prosthetic devices. From the Greek ana, again, + plastos, formed. See also: Prosthesis.
Friday, July 24, 2009
Thursday, July 23, 2009
Definition of Analytic specificity
Analytic specificity: How well an assay detects only a specific substance and does not detect closely related substances.
Definition of Analogous
Analogous: In anatomy, similar in appearance or function but otherwise different. Two structures may be analogous if they serve the same purpose but differ evolutionary in origin as, for example, human and insect legs. As compared to homologous.
Definition of ANA
ANA: Antinuclear antibody, an unusual
antibody directed against structures within the nucleus of the
cell. ANAs are found in patients whose immune system is predisposed to cause inflammation against their own body tissues. Antibodies that are directed against one's own tissues are referred to as autoantibodies. The propensity for the immune system to
work against its own body is referred to as autoimmunity. ANAs
indicate the possible presence of autoimmunity.
The fluorescent antinuclear antibody test (FANA) was designed by George Friou, M.D. in 1957. It is done on a blood sample. The antibodies in the serum of the blood are exposed in the laboratory to cells and then one determines whether or not antibodies are present that react with various parts of the nucleus of the cell. It is a sensitive screening test used to detect autoimmune diseases.
Autoimmune diseases are conditions characterized by a
disorder of the immune system featured by the abnormal production of
antibodies (autoantibodies) directed against the tissues of the
body. Autoimmune diseases are typically feature inflammation of
various tissues of the body. ANAs are found in patients with a
number of autoimmune diseases, such as systemic lupus erythematosus,
Sjogren syndrome, rheumatoid arthritis, polymyositis, scleroderma,
Hashimoto thyroiditis, juvenile diabetes mellitus, Addison
disease, vitiligo, pernicious anemia, glomerulonephritis, and
pulmonary fibrosis. ANAs can also be found in patients with chronic
infections and cancer. Many medications including procainamide (PROCAN SR), hydralazine, and dilantin can stimulate the production of ANAs.
ANAs present different patterns depending on the
staining of the cell nucleus in the laboratory: homogeneous, or
diffuse; speckled; nucleolar; and peripheral or rim. While these
patterns are not specific for any one illness, certain illnesses can
more frequently be associated with one pattern or another. For
example, the nucleolar pattern is more commonly seen in the disease
scleroderma. The speckled pattern is seen in many conditions and in
persons who do not have any autoimmune disease.
ANAs are present in approximately 5% of the normal population, usually in low titers (low levels). These persons have no disease. Titers of lower than 1:80 are less likely to be significant. Even higher titers are insignificant with aging over age 60 years. Ultimately, the ANA result must be interpreted in the specific context of the symptoms and other test results for the patient. It may or may not be significant in an individual.
antibody directed against structures within the nucleus of the
cell. ANAs are found in patients whose immune system is predisposed to cause inflammation against their own body tissues. Antibodies that are directed against one's own tissues are referred to as autoantibodies. The propensity for the immune system to
work against its own body is referred to as autoimmunity. ANAs
indicate the possible presence of autoimmunity.
The fluorescent antinuclear antibody test (FANA) was designed by George Friou, M.D. in 1957. It is done on a blood sample. The antibodies in the serum of the blood are exposed in the laboratory to cells and then one determines whether or not antibodies are present that react with various parts of the nucleus of the cell. It is a sensitive screening test used to detect autoimmune diseases.
Autoimmune diseases are conditions characterized by a
disorder of the immune system featured by the abnormal production of
antibodies (autoantibodies) directed against the tissues of the
body. Autoimmune diseases are typically feature inflammation of
various tissues of the body. ANAs are found in patients with a
number of autoimmune diseases, such as systemic lupus erythematosus,
Sjogren syndrome, rheumatoid arthritis, polymyositis, scleroderma,
Hashimoto thyroiditis, juvenile diabetes mellitus, Addison
disease, vitiligo, pernicious anemia, glomerulonephritis, and
pulmonary fibrosis. ANAs can also be found in patients with chronic
infections and cancer. Many medications including procainamide (PROCAN SR), hydralazine, and dilantin can stimulate the production of ANAs.
ANAs present different patterns depending on the
staining of the cell nucleus in the laboratory: homogeneous, or
diffuse; speckled; nucleolar; and peripheral or rim. While these
patterns are not specific for any one illness, certain illnesses can
more frequently be associated with one pattern or another. For
example, the nucleolar pattern is more commonly seen in the disease
scleroderma. The speckled pattern is seen in many conditions and in
persons who do not have any autoimmune disease.
ANAs are present in approximately 5% of the normal population, usually in low titers (low levels). These persons have no disease. Titers of lower than 1:80 are less likely to be significant. Even higher titers are insignificant with aging over age 60 years. Ultimately, the ANA result must be interpreted in the specific context of the symptoms and other test results for the patient. It may or may not be significant in an individual.
Definition of Amyotrophic lateral sclerosis 8
Amyotrophic lateral sclerosis 8: ALS8. A form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal dominant manner due to mutation in a gene on chromosome 20ptel.
Wednesday, July 22, 2009
Definition of Amyotrophic lateral sclerosis 7
Amyotrophic lateral sclerosis 7: ALS7. A form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal dominant manner due to mutation in a gene on chromosome 20ptel.
Definition of Amyotrophic lateral sclerosis 6
Amyotrophic lateral sclerosis 6: ALS6. A form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal dominant manner due to mutation in a gene on chromosome 16q12.
Definition of Amyotrophic lateral sclerosis 5
Amyotrophic lateral sclerosis 5: ALS5. A form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal recessive manner due to mutation in a gene on chromosome 15q15.1-q21.1.
Definition of Amyotrophic lateral sclerosis 4
Amyotrophic lateral sclerosis 4: ALS4. A juvenile-onset form of amyotrophic lateral sclerosis (ALS) with no bulbar involvement, inherited in an autosomal dominant manner and caused by mutation in a gene on chromosome 9q34.
Definition of Amyotrophic lateral sclerosis 3
Amyotrophic lateral sclerosis 3: ALS3. An adult-onset form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal dominant manner and caused by mutation in a gene on chromosome 18q21.
Definition of Amyotrophic lateral sclerosis 2
Amyotrophic lateral sclerosis 2: ALS2. A juvenile-onset form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal recessive manner and caused by mutation in the gene encoding alsin on chromosome 2q33.
Definition of Amyotrophic lateral sclerosis 1
Amyotrophic lateral sclerosis 1: ALS1. A form of amyotrophic lateral sclerosis (ALS) inherited in an autosomal dominant manner and caused by mutation in the superoxide dismutase-1 gene (SOD1) on chromosome 21q22.1. About 15 to 20% of familial ALS is type 1 (ALS1). Sporadic cases of ALS are sometimes due to new mutation in the SOD1 gene.
Amyotrophic lateral sclerosis (ALS): A classic motor neuron
disease. Motor neuron diseases are progressive chronic diseases of
the nerves that come from the spinal cord responsible for supplying
electrical stimulation to the muscles. This stimulation is
necessary for the movement of body parts.
LOU GEHRIG'S DISEASE: Amyotrophic lateral sclerosis is quite a mouthful. The
disease is therefore usually referred to simply as ALS. In North
America it is sometimes called "Lou Gehrig's disease" after the great
durable baseball player who had it. The movie, "Pride of the
Yankees", tells the his life story. As a New York Yankee, Gehrig was named the American League's most valuable player 4 times (in 1927, 1931, 1934 and 1936). In 14 seasons Gehrig did not miss a single game for a total of 2,130 games. Gehrig was born in 1903, and he died in 1941 at the age of 38.
EPIDEMIOLOGY: ALS strikes in mid-life, most often in the
fifth through seventh decades of life. Men are about one-and-a-half
times more
likely to have the disease as women. It affects about 20,000
Americans with 5,000 new cases occurring in the United States each
year.
THE DISEASE PROCESS: ALS occurs when specific nerve cells
in the brain and spinal
cord that control voluntary movement gradually degenerate. The loss
of these motor neurons causes the muscles under their control to
weaken and waste away, leading to paralysis. The cause of this
disease process is still unknown.
SIGNS AND SYMPTOMS: ALS manifests itself in different ways,
depending on which muscles weaken first. Symptoms may include
tripping and falling, loss of motor control in hands and arms,
difficulty speaking, swallowing and/or breathing, persistent fatigue,
and twitching and cramping, sometimes quite severely.
TREATMENT: There is no cure for ALS; nor is there a proven
therapy that will prevent or reverse the course of the disorder. The
Food and Drug Administration (FDA) approved riluzole, the first drug
that has been shown to prolong the survival of ALS patients. Patients
may also
receive supportive treatments that address some of their symptoms.
PROGNOSIS (OUTLOOK): ALS is progressive and fatal. The
usual causes of death of patients with motor neuron diseases are not
directly related to the disease, but result from simultaneous
additional illnesses which ultimately occur because of weakness of
the body. These illnesses are often infections.
DURATION OF DISEASE: ALS usually leads to death within 5
years of the time the diagnosis of ALS is made; the range is from 2
to 7 years.
disease. Motor neuron diseases are progressive chronic diseases of
the nerves that come from the spinal cord responsible for supplying
electrical stimulation to the muscles. This stimulation is
necessary for the movement of body parts.
LOU GEHRIG'S DISEASE: Amyotrophic lateral sclerosis is quite a mouthful. The
disease is therefore usually referred to simply as ALS. In North
America it is sometimes called "Lou Gehrig's disease" after the great
durable baseball player who had it. The movie, "Pride of the
Yankees", tells the his life story. As a New York Yankee, Gehrig was named the American League's most valuable player 4 times (in 1927, 1931, 1934 and 1936). In 14 seasons Gehrig did not miss a single game for a total of 2,130 games. Gehrig was born in 1903, and he died in 1941 at the age of 38.
EPIDEMIOLOGY: ALS strikes in mid-life, most often in the
fifth through seventh decades of life. Men are about one-and-a-half
times more
likely to have the disease as women. It affects about 20,000
Americans with 5,000 new cases occurring in the United States each
year.
THE DISEASE PROCESS: ALS occurs when specific nerve cells
in the brain and spinal
cord that control voluntary movement gradually degenerate. The loss
of these motor neurons causes the muscles under their control to
weaken and waste away, leading to paralysis. The cause of this
disease process is still unknown.
SIGNS AND SYMPTOMS: ALS manifests itself in different ways,
depending on which muscles weaken first. Symptoms may include
tripping and falling, loss of motor control in hands and arms,
difficulty speaking, swallowing and/or breathing, persistent fatigue,
and twitching and cramping, sometimes quite severely.
TREATMENT: There is no cure for ALS; nor is there a proven
therapy that will prevent or reverse the course of the disorder. The
Food and Drug Administration (FDA) approved riluzole, the first drug
that has been shown to prolong the survival of ALS patients. Patients
may also
receive supportive treatments that address some of their symptoms.
PROGNOSIS (OUTLOOK): ALS is progressive and fatal. The
usual causes of death of patients with motor neuron diseases are not
directly related to the disease, but result from simultaneous
additional illnesses which ultimately occur because of weakness of
the body. These illnesses are often infections.
DURATION OF DISEASE: ALS usually leads to death within 5
years of the time the diagnosis of ALS is made; the range is from 2
to 7 years.
Definition of Amusia
Amusia: The inability to recognize musical tones or to reproduce them. Amusia can be congenital (present at birth) or be acquired sometime later in life (as from brain damage).
Amusia is composed of a- + -musia and literally means the lack of music. Also commonly called tone deafness.
Amusia is composed of a- + -musia and literally means the lack of music. Also commonly called tone deafness.
Definition of Amsler grid
Amsler grid: While conducting an eye examination, the
eye care professional may ask the patient to look at an Amsler grid.
This grid is a pattern that resembles a checkerboard. The patient
covers one eye and stares at a black dot in the center of the grid.
While staring at the dot, the patient may notice that the straight
lines in the pattern appear wavy.
This kind of wavy pattern on viewing the Amsler grid is abnormal.
It can be an important warning sign of what is called wet age-related
macular degeneration. The macula is an area in the retina of the
eye that is responsible for central (straight-ahead) vision. It
deteriorates most often after age 60 resulting in age-related macular
degeneration (AMD). An early sign of the dangerous "wet" type of
AMD is the wavy appearance of the lines on the Amsler grid. The early
diagnosis of wet AMD is critical since laser surgery is urgently
needed to preserve sight.
The Amsler grids shown here are reduced in size; eye care
specialists have full-size grids in their office and for the patient
to use at home.
eye care professional may ask the patient to look at an Amsler grid.
This grid is a pattern that resembles a checkerboard. The patient
covers one eye and stares at a black dot in the center of the grid.
While staring at the dot, the patient may notice that the straight
lines in the pattern appear wavy.
This kind of wavy pattern on viewing the Amsler grid is abnormal.
It can be an important warning sign of what is called wet age-related
macular degeneration. The macula is an area in the retina of the
eye that is responsible for central (straight-ahead) vision. It
deteriorates most often after age 60 resulting in age-related macular
degeneration (AMD). An early sign of the dangerous "wet" type of
AMD is the wavy appearance of the lines on the Amsler grid. The early
diagnosis of wet AMD is critical since laser surgery is urgently
needed to preserve sight.
The Amsler grids shown here are reduced in size; eye care
specialists have full-size grids in their office and for the patient
to use at home.
Tuesday, July 21, 2009
Definition of Amplification, DNA
Amplification, DNA: The production of multiple copies of a sequence of DNA. Repeated copying of a piece of DNA.
DNA amplification plays a role in cancer cells. A tumor cell amplifies, or copies, DNA segments as a result of cell signals and sometimes environmental events.
Amplification can occur in vivo (in the living individual) or in vitro (literally "in glass", or in a plastic vessel in the laboratory).
DNA amplification plays a role in cancer cells. A tumor cell amplifies, or copies, DNA segments as a result of cell signals and sometimes environmental events.
Amplification can occur in vivo (in the living individual) or in vitro (literally "in glass", or in a plastic vessel in the laboratory).
Definition of Amplification
Amplification: Making multiple copies of a gene or of any sequence of DNA. Repeated copying of a piece of DNA.
In amplification there is an increase in the number of copies of any particular piece of DNA. Gene amplification plays a role in cancer cells. A tumor cell amplifies, or copies, DNA segments as a result of cell signals and sometimes environmental events.
Amplification can occur in vivo (in the living individual) or in vitro (literally "in glass", or in a plastic vessel in the laboratory).
In amplification there is an increase in the number of copies of any particular piece of DNA. Gene amplification plays a role in cancer cells. A tumor cell amplifies, or copies, DNA segments as a result of cell signals and sometimes environmental events.
Amplification can occur in vivo (in the living individual) or in vitro (literally "in glass", or in a plastic vessel in the laboratory).
Definition of Amphetamine
Amphetamine: A drug with a stimulant effect on the central nervous system that can be both physically and psychologically addictive when overused. This drug has been much abused recreationally. The street term "speed" refers to stimulant drugs such as amphetamine.
Monday, July 20, 2009
Definition of Amnesia
Amnesia: Lack of memory. Amnesia after trauma can be antegrade or retrograde, depending upon whether the lack of memory relates to events occurring after or before the trauma. Amnesia is as compared to hypermnesia and hypomnesia. From a- + the Greek mneme, memory. See also: Antegrade amnesia ; and Retrograde amnesia.
Definition of Ammonia
Ammonia: A colorless gas with a very sharp odor. Made both by humans and by nature, ammonia dissolves easily in water and evaporates quickly. Liquid ammonia is found in many household cleaners. Ammonia is irritating to the skin, eyes, nose, throat, and lungs. Exposure to high concentrations in the air can severely burn the skin, eyes, throat, or lungs. In extreme cases, blindness, lung damage, or death can occur. Breathing lower concentrations causes coughing and nose and throat irritation. Swallowing ammonia may burn the mouth, throat, and stomach.
The amount of ammonia produced by humans every year is almost equal to that produced by nature every year. Ammonia is produced naturally in soil by bacteria, decaying plants and animals, and animal wastes. Ammonia is essential for many biological processes. Most of the ammonia produced in chemical factories is used to make fertilizers. The remaining is used in textiles, plastics, explosives, pulp and paper production, food and beverages, household cleaning products, refrigerants, and other products. It is also used in smelling salts.
The amount of ammonia produced by humans every year is almost equal to that produced by nature every year. Ammonia is produced naturally in soil by bacteria, decaying plants and animals, and animal wastes. Ammonia is essential for many biological processes. Most of the ammonia produced in chemical factories is used to make fertilizers. The remaining is used in textiles, plastics, explosives, pulp and paper production, food and beverages, household cleaning products, refrigerants, and other products. It is also used in smelling salts.
Definition of Amini, Fariborz
Amini, Fariborz: Iranian-born American psychiatrist (1930-2004), at the University of California, San Francisco (UCSF), known for using science to study the phenomenon of love. In his work, Amini explained "how lingering but forgotten impressions, like a smell or sound associated with a person or a positive experience, become embedded in the mind's memory banks, where neurons constantly fire and forge connections. Over time these links are reinforced through repeated exposure, leading to affectional bonds." This thesis was set forth in "A General Theory of Love" (2000) which Amini published in 2000 with his UCSF colleagues Thomas Lewis and Richard Lannon. He was also called Fari Amini.
Saturday, July 18, 2009
Definition of Ambulatory
Ambulatory: Able to ambulate, to walk about, not bed-ridden or
hospitalized.
hospitalized.
Definition of Ambulance
Ambulance: Although you are undoubtedly familiar with
the sound of the siren and the sight of the flashing lights of the ambulance, you may not
necessarily know that the ambulance began as a walking hospital. The word
"ambulance" indeed started off as a walking hospital, "un hopital
ambulant" in French, meaning literally "a walking hospital." The
"hopital ambulant" was devised during the campaigns of Napoleon to bring
medical aid directly to his troops in the field. The original "hopital
ambulant" was a mobile unit designed to carry dressings and drugs to the wounded and
evacuate the injured from the line of battle. The British, knowing a good idea when they
saw it, came up with their own version of the "hopital ambulant." But they
economized by dropping the "hopital" and corrupted "ambulant" to
"ambulance." The French, of course, have for many years railed against the
incursions of Anglo-Saxon words into the pure precincts of the French language.
Nonetheless, they rejected their own "hopital ambulant" and embraced the
English "ambulance." So, in France today you can no longer see a hospital
walking but "ambulances" are very much in evidence.
the sound of the siren and the sight of the flashing lights of the ambulance, you may not
necessarily know that the ambulance began as a walking hospital. The word
"ambulance" indeed started off as a walking hospital, "un hopital
ambulant" in French, meaning literally "a walking hospital." The
"hopital ambulant" was devised during the campaigns of Napoleon to bring
medical aid directly to his troops in the field. The original "hopital
ambulant" was a mobile unit designed to carry dressings and drugs to the wounded and
evacuate the injured from the line of battle. The British, knowing a good idea when they
saw it, came up with their own version of the "hopital ambulant." But they
economized by dropping the "hopital" and corrupted "ambulant" to
"ambulance." The French, of course, have for many years railed against the
incursions of Anglo-Saxon words into the pure precincts of the French language.
Nonetheless, they rejected their own "hopital ambulant" and embraced the
English "ambulance." So, in France today you can no longer see a hospital
walking but "ambulances" are very much in evidence.
Definition of Amblyopia, nocturnal
Amblyopia, nocturnal: Amblyopia refers to blindness so nocturnal amblyopia is, literally, night blindness. Listed in medical dictionaries under "Nyctalopia" from the Greek nyct (night) + aloas (obscure or blind) + opsis (vision), the condition
involves impaired vision in dim light and in the dark due
to impaired function of specific vision cells (namely, the rods)
in the retina.
Night blindness, a classic finding in vitamin A deficiency, was discovered by the English physician William Heberden (1710-1801). (Heberden also described other medical disorders of importance including angina
(chest pain that is often severe and crushing, due to an
inadequate supply of oxygen to the heart muscle) and Heberden's
nodes, bumps around the small joints due to osteoarthritis.)
Night blindness (nyctalopia) is also called day sight and
nyctanopia.
involves impaired vision in dim light and in the dark due
to impaired function of specific vision cells (namely, the rods)
in the retina.
Night blindness, a classic finding in vitamin A deficiency, was discovered by the English physician William Heberden (1710-1801). (Heberden also described other medical disorders of importance including angina
(chest pain that is often severe and crushing, due to an
inadequate supply of oxygen to the heart muscle) and Heberden's
nodes, bumps around the small joints due to osteoarthritis.)
Night blindness (nyctalopia) is also called day sight and
nyctanopia.
Amblyopia: Partial or complete loss of vision in one eye caused by conditions that affect the normal development of vision. These conditions include strabismus, in which the eyes are crossed inward (esotropia) or turned outward (exotropia) and anisometropia, in which there is a major difference in refractive error between the two eyes from nearsightedness, farsightedness, or astigmatism. Less common causes of amblyopia include ptosis (drooping) of one eyelid, disease of the cornea (preventing light from entering the eye), congenital cataract, and injury to the eye of a young child.
In amblyopia, the brain favors one eye over the other. The other eye is ignored. It is not adequately stimulated and the visual brain cells do not mature normally. Amblyopia is the most common cause of monocular blindness, partial or complete blindness in one eye. Amblyopia affects 2 to 3% of children in the US.
Treatment of strabismus may involve surgical correction of the eye muscle imbalance. In the case of severe refractive error, it should be corrected by glasses, contact lenses or, if appropriate, lasix. Wearing an eye patch over the stronger eye is a hallowed treatment for amblyopia. Another option is atropine eye drops to blur the vision temporarily in the stronger eye. Weekend atropine provides an improvement in visual acuity of a magnitude similar to that provided by daily atropine in treating moderate amblyopia.
The term "amblyopia" is sometimes incorrectly used interchangeably with lazy eye. "Amblyopia" is made up of ambly- from the Greek "amblys" meaning blunt, dull, faint, or dim and -opia from the Greek "ops" meaning eye, and refers to vision, so amblyopia is literally dim vision.
See also: Anisometropia: Nocturnal amblyopia; Strabismus.
In amblyopia, the brain favors one eye over the other. The other eye is ignored. It is not adequately stimulated and the visual brain cells do not mature normally. Amblyopia is the most common cause of monocular blindness, partial or complete blindness in one eye. Amblyopia affects 2 to 3% of children in the US.
Treatment of strabismus may involve surgical correction of the eye muscle imbalance. In the case of severe refractive error, it should be corrected by glasses, contact lenses or, if appropriate, lasix. Wearing an eye patch over the stronger eye is a hallowed treatment for amblyopia. Another option is atropine eye drops to blur the vision temporarily in the stronger eye. Weekend atropine provides an improvement in visual acuity of a magnitude similar to that provided by daily atropine in treating moderate amblyopia.
The term "amblyopia" is sometimes incorrectly used interchangeably with lazy eye. "Amblyopia" is made up of ambly- from the Greek "amblys" meaning blunt, dull, faint, or dim and -opia from the Greek "ops" meaning eye, and refers to vision, so amblyopia is literally dim vision.
See also: Anisometropia: Nocturnal amblyopia; Strabismus.
Definition of Ambient
Ambient: Surrounding, present on all sides; encompassing. As, the ambient noise is deafening, or the ambient light is blinding. From the Latin "ambire" meaning "to go around."
Definition of Amaurotic familial idiocy
Amaurotic familial idiocy:
An outdated term for Tay-Sachs disease (TSD) which is concisely defined by OMIM (Online Mendelian Inheritance in Man) as "an autosomal recessive, progressive neurodegenerative disorder, which in the classic infantile form, is usually fatal by age 2 or 3 years, results from deficiency of the enzyme hexosaminidase A. " "Autosomal" points to the gene for TSD residing on a nonsex (autosomal) chromosome (namely, chromosome15q23-q24). "Recessive" indicates a person with 2 copies of the gene has TSD whereas someone with 1 copy is a carrier in normal health. TSD worsens, with time, as the central nervous system progressively deteriorates. The "classic" ("textbook") type of TSD has its insidious onset in infancy. The child with TSD usually develops normally for the first few months of life. An exaggerated startle reaction may first be noted. Head control is lost by 6-8 months of age. The infant cannot roll over or sit up. Spasticity and rigidity develop. Excessive drooling and convulsions become evident. Blindness and head enlargement set in by the second year. "Fatal by age 2 or 3 years" today would be modified to "fatal by age 5." After age 2, total constant nursing care is needed. Death is due usually to cachexia (wasting away) or aspiration pneumonia initiated by food going down "the wrong way" into the lungs. TSD is due to deficiency of an enzyme (a protein needed to catalyze a specific chemical reaction within the body). Lack of the enzyme which results in failure to process a lipid (a fat) which accumulates and is deposited in the brain and other tissues, to their detriment. The enzyme is called hexosaminidase-A (hex-A) and the lipid that is deposited is called GM2-ganglioside TSD is a model of a fatal metabolic disease that occurs primarily within a well-defined subpopulation. It is one of several genetic diseases found more often in persons of Jewish origin. (Other Jewish genetic diseases include Gaucher disease, Niemann-Pick disease, Bloom syndrome, and factor XI deficiency). The frequency of TSD is much higher in Ashkenazi Jews (of European origin) than in other groups of Jews. (In the U.S., 95% of Jews are Ashkenazi and are at risk for TSD). TSD occurs more rarely, in non-Jews. Knowledge of the biochemical basis TSD has permitted screening programs for carrier detection and prenatal diagnosis of TSD. There are forms of TSD with somewhat more hex-A and hence later onset, termed juvenile TSD and adult TSH. Alternative names for TSD itself are type 1 GM2-gangliosidosis, B variant GM2-gangliosidosis, hexosaminidase A deficiency, hex-A deficiency. TSD is named for the English physician Waren Tay (1843-1927) and the New York neurologist Bernard (Barney) Sachs (1858-1944). Tay in 1881 studied an infant with progressive neurological impairment and described "symmetrical changes in the yellow spot in each eye", the "cherry-red spots" characteristic of TSD. Sachs saw a child In 1887 and the child's sister in 1898 with the cherry-red spots and "arrested cerebral development" and in 1910 he demonstrated the presence of accumulated lipid in the brain and retina.
An outdated term for Tay-Sachs disease (TSD) which is concisely defined by OMIM (Online Mendelian Inheritance in Man) as "an autosomal recessive, progressive neurodegenerative disorder, which in the classic infantile form, is usually fatal by age 2 or 3 years, results from deficiency of the enzyme hexosaminidase A. " "Autosomal" points to the gene for TSD residing on a nonsex (autosomal) chromosome (namely, chromosome15q23-q24). "Recessive" indicates a person with 2 copies of the gene has TSD whereas someone with 1 copy is a carrier in normal health. TSD worsens, with time, as the central nervous system progressively deteriorates. The "classic" ("textbook") type of TSD has its insidious onset in infancy. The child with TSD usually develops normally for the first few months of life. An exaggerated startle reaction may first be noted. Head control is lost by 6-8 months of age. The infant cannot roll over or sit up. Spasticity and rigidity develop. Excessive drooling and convulsions become evident. Blindness and head enlargement set in by the second year. "Fatal by age 2 or 3 years" today would be modified to "fatal by age 5." After age 2, total constant nursing care is needed. Death is due usually to cachexia (wasting away) or aspiration pneumonia initiated by food going down "the wrong way" into the lungs. TSD is due to deficiency of an enzyme (a protein needed to catalyze a specific chemical reaction within the body). Lack of the enzyme which results in failure to process a lipid (a fat) which accumulates and is deposited in the brain and other tissues, to their detriment. The enzyme is called hexosaminidase-A (hex-A) and the lipid that is deposited is called GM2-ganglioside TSD is a model of a fatal metabolic disease that occurs primarily within a well-defined subpopulation. It is one of several genetic diseases found more often in persons of Jewish origin. (Other Jewish genetic diseases include Gaucher disease, Niemann-Pick disease, Bloom syndrome, and factor XI deficiency). The frequency of TSD is much higher in Ashkenazi Jews (of European origin) than in other groups of Jews. (In the U.S., 95% of Jews are Ashkenazi and are at risk for TSD). TSD occurs more rarely, in non-Jews. Knowledge of the biochemical basis TSD has permitted screening programs for carrier detection and prenatal diagnosis of TSD. There are forms of TSD with somewhat more hex-A and hence later onset, termed juvenile TSD and adult TSH. Alternative names for TSD itself are type 1 GM2-gangliosidosis, B variant GM2-gangliosidosis, hexosaminidase A deficiency, hex-A deficiency. TSD is named for the English physician Waren Tay (1843-1927) and the New York neurologist Bernard (Barney) Sachs (1858-1944). Tay in 1881 studied an infant with progressive neurological impairment and described "symmetrical changes in the yellow spot in each eye", the "cherry-red spots" characteristic of TSD. Sachs saw a child In 1887 and the child's sister in 1898 with the cherry-red spots and "arrested cerebral development" and in 1910 he demonstrated the presence of accumulated lipid in the brain and retina.
Definition of AMA
AMA: The American Medical Association. The AMA's
mission statement proclaims:
"We are the Voice of the American Medical Profession.
"We are the partnership of physicians and their professional
associations dedicated to promoting the art and science of medicine
and the betterment of public health.
"We serve the physicians and their patients by establishing
and promoting ethical, educational, and clinical standards for the
medical profession and by advocating for the highest principle of
all--the integrity of the physician/patient relationship."
mission statement proclaims:
"We are the Voice of the American Medical Profession.
"We are the partnership of physicians and their professional
associations dedicated to promoting the art and science of medicine
and the betterment of public health.
"We serve the physicians and their patients by establishing
and promoting ethical, educational, and clinical standards for the
medical profession and by advocating for the highest principle of
all--the integrity of the physician/patient relationship."
Alzheimer's disease: A progressive neurologic disease of the
brain that leads to the irreversible loss of neurons and dementia. The clinical hallmarks of Alzheimer's disease are progressive impairment in memory, judgment, decision making, orientation to physical surroundings, and language. A working diagnosis of Alzheimer disease is usually made on the basis of the neurologic examination. A definitive diagnosis can be made only at autopsy. On a cellular level, Alzheimer's disease is characterized by unusual helical protein filaments in nerve cells (neurons) of the brain. These odd twisted filaments are called neurofibrillary tangles. On a functional level, there is degeneration of the cortical regions, especially the frontal and temporal lobes, of the brain.
Alzheimer's disease is the most common of all neurodegenerative diseases. It accounts for about two-thirds of cases of dementia
with vascular causes and other neurodegenerative diseases making up most of the
rest.
The average time of survival from the initial diagnosis of Alzheimer's disease was found (in a study reported in 2004) to be 4.2 years for men and 5.7 years for women. Men had poorer survival across all age groups compared with women and survival was decreased in all age groups compared with the life expectancy of the US population.
The German psychiatrist and pathologist Alois Alzheimer (1864-1915) first described this form of presenile dementia in 1907. (German psychiatrist Emil Kraepelin named the disease in his honor.) For more information, see: Alzheimer's disease. See also: Alzheimer's disease, early-onset familial.
brain that leads to the irreversible loss of neurons and dementia. The clinical hallmarks of Alzheimer's disease are progressive impairment in memory, judgment, decision making, orientation to physical surroundings, and language. A working diagnosis of Alzheimer disease is usually made on the basis of the neurologic examination. A definitive diagnosis can be made only at autopsy. On a cellular level, Alzheimer's disease is characterized by unusual helical protein filaments in nerve cells (neurons) of the brain. These odd twisted filaments are called neurofibrillary tangles. On a functional level, there is degeneration of the cortical regions, especially the frontal and temporal lobes, of the brain.
Alzheimer's disease is the most common of all neurodegenerative diseases. It accounts for about two-thirds of cases of dementia
with vascular causes and other neurodegenerative diseases making up most of the
rest.
The average time of survival from the initial diagnosis of Alzheimer's disease was found (in a study reported in 2004) to be 4.2 years for men and 5.7 years for women. Men had poorer survival across all age groups compared with women and survival was decreased in all age groups compared with the life expectancy of the US population.
The German psychiatrist and pathologist Alois Alzheimer (1864-1915) first described this form of presenile dementia in 1907. (German psychiatrist Emil Kraepelin named the disease in his honor.) For more information, see: Alzheimer's disease. See also: Alzheimer's disease, early-onset familial.
Definition of Alzheimer disease, early-onset familial
Alzheimer disease, early-onset familial: Alzheimer disease that runs in families and strikes at an unusually early age (with its onset under the age of 60). About 7% of early-onset cases of Alzheimer's are familial and are inherited in an autosomal dominant manner with high penetrance.
Mutations in three different genes -- the amyloid precursor protein (APP) gene and the presenilin 1 and 2 (PSEN1 and PSEN2) genes -- have been discovered in families with early-onset familial Alzheimer's disease. Taken together, these mutations only account for about 20-50% of familial Alzheimer's, indicating that other genes remain to be found in this disorder.
The APP gene encodes the beta-amyloid protein which accumulates abnormally in the brain in Alzheimer's disease. The protein products of the PSEN1 and PSEN2 genes interact with proteins are involved in signalling processes within and between cells.
Although familial Alzheimer's disease is responsible for a small minority of cases of Alzheimer's disease, it is important, not only for the families with it, but also for what we can learn about all of Alzheimer's disease from it.
Mutations in three different genes -- the amyloid precursor protein (APP) gene and the presenilin 1 and 2 (PSEN1 and PSEN2) genes -- have been discovered in families with early-onset familial Alzheimer's disease. Taken together, these mutations only account for about 20-50% of familial Alzheimer's, indicating that other genes remain to be found in this disorder.
The APP gene encodes the beta-amyloid protein which accumulates abnormally in the brain in Alzheimer's disease. The protein products of the PSEN1 and PSEN2 genes interact with proteins are involved in signalling processes within and between cells.
Although familial Alzheimer's disease is responsible for a small minority of cases of Alzheimer's disease, it is important, not only for the families with it, but also for what we can learn about all of Alzheimer's disease from it.
Friday, July 17, 2009
Definition of Alveolar
Alveolar: Pertaining to the alveoli, the tiny air sacs in the lungs. The exchange of oxygen and carbon dioxide takes place in the alveoli which look like cells in a honeycomb.
The word comes from the Latin diminutive of "alveus" meaning a cavity or hollow = a little cavity or hollow.
The word comes from the Latin diminutive of "alveus" meaning a cavity or hollow = a little cavity or hollow.
Altretamine: Brand name: Hexalen. An oral drug used to treat ovarian cancer that has persisted or has recurred following treatment with other anti-cancer drugs. It was approved for this use by the FDA in 1990. Altretamine also has been used for treating lung cancer, although this is an off-label use.
Definition of Altitude, high
Altitude, high: Altitude sickness occurs at high altitude. So what is high altitude?
Altitude is defined on the following scale:
High altitude: 8,000 - 12,000 feet (2,438 - 3,658 meters);
Very high altitude: 12,000 - 18,000 feet (3,658 - 5,487 meters); and
Extremely high altitude: 18,000+ feet (5,500+ meters).
Most people can go up to 8,000 feet (2,438 meters) with minimal effects. If you have been at that altitude before and had no problems, you can probably return to that altitude without problems if (and only if) you are properly acclimatized.
If you have not been to high altitude before, caution is strongly recommended. No specific factors such as age, sex, or physical condition are known to correlate with the susceptibility to altitude sickness. Some people are simply more susceptible than others. There is no telling, so caution is the better part of wisdom.
Altitude is defined on the following scale:
High altitude: 8,000 - 12,000 feet (2,438 - 3,658 meters);
Very high altitude: 12,000 - 18,000 feet (3,658 - 5,487 meters); and
Extremely high altitude: 18,000+ feet (5,500+ meters).
Most people can go up to 8,000 feet (2,438 meters) with minimal effects. If you have been at that altitude before and had no problems, you can probably return to that altitude without problems if (and only if) you are properly acclimatized.
If you have not been to high altitude before, caution is strongly recommended. No specific factors such as age, sex, or physical condition are known to correlate with the susceptibility to altitude sickness. Some people are simply more susceptible than others. There is no telling, so caution is the better part of wisdom.
Definition of Altitude sickness
Altitude sickness: Altitude sickness (or altitude illness) is a disorder caused by being at high altitude. It more commonly occurs above 8,000 feet (2,440 meters).
The cause of altitude illness is a matter of oxygen physiology. At sea level the concentration of oxygen is about 21% and the barometric pressure averages 760 mmHg. As altitude increases, the concentration remains the same but the number of oxygen molecules per breath is reduced. At 12,000 feet (3,658 meters) the barometric pressure is only 483 mmHg, so there are roughly 40% fewer oxygen molecules per breath. In order to oxygenate the body effectively, your breathing rate (even while at rest) has to increase. This extra ventilation increases the oxygen content in the blood, but not to sea level concentrations. Since the amount of oxygen required for activity is the same, the body must adjust to having less oxygen. In addition, high altitude and lower air pressure cause fluid to leak from the capillaries which can cause fluid build-up in both the lungs and the brain. Continuing to higher altitudes without proper acclimatization can lead to potentially serious, even life-threatening illnesses.
The prevention of altitude illnesses falls into two categories, proper acclimatization and preventive medications. A few basic guidelines for proper acclimatization are:
If possible, don't fly or drive to high altitude. Start below 10,000 feet (3,048 meters) and walk up.
If you do fly or drive, do not over-exert yourself or move higher for the first 24 hours.
If you go above 10,000 feet (3,048 meters), only increase your altitude by 1,000 feet (305 meters) per day and for every 3,000 feet (915 meters) of elevation gained, take a rest day.
"Climb High and sleep low." This is the maxim used by climbers. You can climb more than 1,000 feet (305 meters) in a day as long as you come back down and sleep at a lower altitude.
If you begin to show symptoms of moderate altitude illness, don't go higher until symptoms decrease ("Don't go up until symptoms go down").
If symptoms increase, go down, down, down!
Keep in mind that different people will acclimatize at different rates. Make sure all of your party is properly acclimatized before going higher.
Stay properly hydrated. Acclimatization is often accompanied by fluid loss, so you need to drink lots of fluids to remain properly hydrated (at least 3-4 quarts per day). Urine output should be copious and clear.
Take it easy; don't over-exert yourself when you first get up to altitude. Light activity during the day is better than sleeping because respiration decreases during sleep, exacerbating the symptoms.
Avoid tobacco and alcohol and other depressant drugs including, barbiturates, tranquilizers, and sleeping pills. These depressants further decrease the respiratory drive during sleep resulting in a worsening of the symptoms.
Eat a high carbohydrate diet (more than 70% of your calories from carbohydrates) while at altitude.
The acclimatization process is inhibited by dehydration, over-exertion, and alcohol and other depressant drugs.
Preventive medications for altitudes illness are two drugs: one called DIAMOX (acetazolamide) and the other called dexamethasone (a steroid).
DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation. This is especially helpful at night when respiratory drive is decreased. Since it takes a while for DIAMOX to have an effect, it is advisable to start taking it 24 hours before you go to altitude and continue for at least 5 days at higher altitude.
Dexamethasone (a steroid) is likewise a prescription drug. It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). Like DIAMOX, it should be used with caution and only on the advice of a physician because of possible serious side effects. It may be combined with DIAMOX. No other medications have been proven valuable for preventing AMS. (Based in part on the Princeton University Outdoor Action "Guide to High Altitude: Acclimatization and Illnesses" by Rick Curtis).
This entry does not deal with acute mountain sickness (AMS) or, in any detail, with acclimatization. For information on these topics, please see the respective entries to Acute mountain sickness (AMS) and to Acclimatization.
The cause of altitude illness is a matter of oxygen physiology. At sea level the concentration of oxygen is about 21% and the barometric pressure averages 760 mmHg. As altitude increases, the concentration remains the same but the number of oxygen molecules per breath is reduced. At 12,000 feet (3,658 meters) the barometric pressure is only 483 mmHg, so there are roughly 40% fewer oxygen molecules per breath. In order to oxygenate the body effectively, your breathing rate (even while at rest) has to increase. This extra ventilation increases the oxygen content in the blood, but not to sea level concentrations. Since the amount of oxygen required for activity is the same, the body must adjust to having less oxygen. In addition, high altitude and lower air pressure cause fluid to leak from the capillaries which can cause fluid build-up in both the lungs and the brain. Continuing to higher altitudes without proper acclimatization can lead to potentially serious, even life-threatening illnesses.
The prevention of altitude illnesses falls into two categories, proper acclimatization and preventive medications. A few basic guidelines for proper acclimatization are:
If possible, don't fly or drive to high altitude. Start below 10,000 feet (3,048 meters) and walk up.
If you do fly or drive, do not over-exert yourself or move higher for the first 24 hours.
If you go above 10,000 feet (3,048 meters), only increase your altitude by 1,000 feet (305 meters) per day and for every 3,000 feet (915 meters) of elevation gained, take a rest day.
"Climb High and sleep low." This is the maxim used by climbers. You can climb more than 1,000 feet (305 meters) in a day as long as you come back down and sleep at a lower altitude.
If you begin to show symptoms of moderate altitude illness, don't go higher until symptoms decrease ("Don't go up until symptoms go down").
If symptoms increase, go down, down, down!
Keep in mind that different people will acclimatize at different rates. Make sure all of your party is properly acclimatized before going higher.
Stay properly hydrated. Acclimatization is often accompanied by fluid loss, so you need to drink lots of fluids to remain properly hydrated (at least 3-4 quarts per day). Urine output should be copious and clear.
Take it easy; don't over-exert yourself when you first get up to altitude. Light activity during the day is better than sleeping because respiration decreases during sleep, exacerbating the symptoms.
Avoid tobacco and alcohol and other depressant drugs including, barbiturates, tranquilizers, and sleeping pills. These depressants further decrease the respiratory drive during sleep resulting in a worsening of the symptoms.
Eat a high carbohydrate diet (more than 70% of your calories from carbohydrates) while at altitude.
The acclimatization process is inhibited by dehydration, over-exertion, and alcohol and other depressant drugs.
Preventive medications for altitudes illness are two drugs: one called DIAMOX (acetazolamide) and the other called dexamethasone (a steroid).
DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation. This is especially helpful at night when respiratory drive is decreased. Since it takes a while for DIAMOX to have an effect, it is advisable to start taking it 24 hours before you go to altitude and continue for at least 5 days at higher altitude.
Dexamethasone (a steroid) is likewise a prescription drug. It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). Like DIAMOX, it should be used with caution and only on the advice of a physician because of possible serious side effects. It may be combined with DIAMOX. No other medications have been proven valuable for preventing AMS. (Based in part on the Princeton University Outdoor Action "Guide to High Altitude: Acclimatization and Illnesses" by Rick Curtis).
This entry does not deal with acute mountain sickness (AMS) or, in any detail, with acclimatization. For information on these topics, please see the respective entries to Acute mountain sickness (AMS) and to Acclimatization.
Definition of Altitude illness
Altitude illness: Altitude illness (or altitude sickness) is a disorder caused by being at high altitude. It commonly occurs above 8,000 feet (2,440 meters).
The cause of altitude illness is a matter of oxygen physiology. At sea level the concentration of oxygen is about 21% and the barometric pressure averages 760 mmHg. As altitude increases, the concentration remains the same but the number of oxygen molecules per breath is reduced. At 12,000 feet (3,658 meters) the barometric pressure is only 483 mmHg, so there are roughly 40% fewer oxygen molecules per breath. In order to oxygenate the body effectively, your breathing rate (even while at rest) has to increase. This extra ventilation increases the oxygen content in the blood, but not to sea level concentrations. Since the amount of oxygen required for activity is the same, the body must adjust to having less oxygen. In addition, high altitude and lower air pressure cause fluid to leak from the capillaries which can cause fluid build-up in both the lungs and the brain. Continuing to higher altitudes without proper acclimatization can lead to potentially serious, even life-threatening illnesses.
The prevention of altitude illnesses falls into two categories, proper acclimatization and preventive medications. A few basic guidelines for proper acclimatization are:
If possible, don't fly or drive to high altitude. Start below 10,000 feet (3,048 meters) and walk up.
If you do fly or drive, do not over-exert yourself or move higher for the first 24 hours.
If you go above 10,000 feet (3,048 meters), only increase your altitude by 1,000 feet (305 meters) per day and for every 3,000 feet (915 meters) of elevation gained, take a rest day.
"Climb High and sleep low." This is the maxim used by climbers. You can climb more than 1,000 feet (305 meters) in a day as long as you come back down and sleep at a lower altitude.
If you begin to show symptoms of moderate altitude illness, don't go higher until symptoms decrease ("Don't go up until symptoms go down").
If symptoms increase, go down, down, down!
Keep in mind that different people will acclimatize at different rates. Make sure all of your party is properly acclimatized before going higher.
Stay properly hydrated. Acclimatization is often accompanied by fluid loss, so you need to drink lots of fluids to remain properly hydrated (at least 3-4 quarts per day). Urine output should be copious and clear.
Take it easy; don't over-exert yourself when you first get up to altitude. Light activity during the day is better than sleeping because respiration decreases during sleep, exacerbating the symptoms.
Avoid tobacco and alcohol and other depressant drugs including, barbiturates, tranquilizers, and sleeping pills. These depressants further decrease the respiratory drive during sleep resulting in a worsening of the symptoms.
Eat a high carbohydrate diet (more than 70% of your calories from carbohydrates) while at altitude.
The acclimatization process is inhibited by dehydration, over-exertion, and alcohol and other depressant drugs.
Preventive medications for altitudes illness are two drugs: one called DIAMOX (acetazolamide) and the other called dexamethasone (a steroid).
DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation. This is especially helpful at night when respiratory drive is decreased. Since it takes a while for DIAMOX to have an effect, it is advisable to start taking it 24 hours before you go to altitude and continue for at least 5 days at higher altitude.
Dexamethasone (a steroid) is likewise a prescription drug. It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). Like DIAMOX, it should be used with caution and only on the advice of a physician because of possible serious side effects. It may be combined with DIAMOX. No other medications have been proven valuable for preventing AMS. (Based in part on the Princeton University Outdoor Action "Guide to High Altitude: Acclimatization and Illnesses" by Rick Curtis).
This entry does not deal with acute mountain sickness (AMS) or, in any detail, with acclimatization. For information on these topics, please see the respective entries to Acute mountain sickness (AMS) and to Acclimatization.
The cause of altitude illness is a matter of oxygen physiology. At sea level the concentration of oxygen is about 21% and the barometric pressure averages 760 mmHg. As altitude increases, the concentration remains the same but the number of oxygen molecules per breath is reduced. At 12,000 feet (3,658 meters) the barometric pressure is only 483 mmHg, so there are roughly 40% fewer oxygen molecules per breath. In order to oxygenate the body effectively, your breathing rate (even while at rest) has to increase. This extra ventilation increases the oxygen content in the blood, but not to sea level concentrations. Since the amount of oxygen required for activity is the same, the body must adjust to having less oxygen. In addition, high altitude and lower air pressure cause fluid to leak from the capillaries which can cause fluid build-up in both the lungs and the brain. Continuing to higher altitudes without proper acclimatization can lead to potentially serious, even life-threatening illnesses.
The prevention of altitude illnesses falls into two categories, proper acclimatization and preventive medications. A few basic guidelines for proper acclimatization are:
If possible, don't fly or drive to high altitude. Start below 10,000 feet (3,048 meters) and walk up.
If you do fly or drive, do not over-exert yourself or move higher for the first 24 hours.
If you go above 10,000 feet (3,048 meters), only increase your altitude by 1,000 feet (305 meters) per day and for every 3,000 feet (915 meters) of elevation gained, take a rest day.
"Climb High and sleep low." This is the maxim used by climbers. You can climb more than 1,000 feet (305 meters) in a day as long as you come back down and sleep at a lower altitude.
If you begin to show symptoms of moderate altitude illness, don't go higher until symptoms decrease ("Don't go up until symptoms go down").
If symptoms increase, go down, down, down!
Keep in mind that different people will acclimatize at different rates. Make sure all of your party is properly acclimatized before going higher.
Stay properly hydrated. Acclimatization is often accompanied by fluid loss, so you need to drink lots of fluids to remain properly hydrated (at least 3-4 quarts per day). Urine output should be copious and clear.
Take it easy; don't over-exert yourself when you first get up to altitude. Light activity during the day is better than sleeping because respiration decreases during sleep, exacerbating the symptoms.
Avoid tobacco and alcohol and other depressant drugs including, barbiturates, tranquilizers, and sleeping pills. These depressants further decrease the respiratory drive during sleep resulting in a worsening of the symptoms.
Eat a high carbohydrate diet (more than 70% of your calories from carbohydrates) while at altitude.
The acclimatization process is inhibited by dehydration, over-exertion, and alcohol and other depressant drugs.
Preventive medications for altitudes illness are two drugs: one called DIAMOX (acetazolamide) and the other called dexamethasone (a steroid).
DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation. This is especially helpful at night when respiratory drive is decreased. Since it takes a while for DIAMOX to have an effect, it is advisable to start taking it 24 hours before you go to altitude and continue for at least 5 days at higher altitude.
Dexamethasone (a steroid) is likewise a prescription drug. It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). Like DIAMOX, it should be used with caution and only on the advice of a physician because of possible serious side effects. It may be combined with DIAMOX. No other medications have been proven valuable for preventing AMS. (Based in part on the Princeton University Outdoor Action "Guide to High Altitude: Acclimatization and Illnesses" by Rick Curtis).
This entry does not deal with acute mountain sickness (AMS) or, in any detail, with acclimatization. For information on these topics, please see the respective entries to Acute mountain sickness (AMS) and to Acclimatization.
Definition of Alternative Medicine, National Center for Compleme
Alternative Medicine, National Center for Complementary &: See: National Center for Complementary & Alternative Medicine.
Alternative medicine: Healing arts not taught in traditional Western medical schools that promote options to conventional medicine that is taught in these schools.. An example of an alternative therapy is using a special diet to treat cancer instead of undergoing surgery, radiation, or chemotherapy that has been recommended by a Western physician. Complementary medicine is different from alternative medicine. Whereas complementary medicine is used together with conventional medicine, alternative medicine is used in place of conventional medicine. See also complementary medicine, conventional medicine.
Definition of Alternative medical system
Alternative medical system: A system of alternative medicine built upon a complete system of theory and practice. Often, such systems have evolved apart from and earlier than the conventional medical approach used in the US or Europe. Alternative medical systems may have evolved in Western or non-Western cultures. Examples of alternative medical systems that have developed in Western cultures include homeopathic medicine and naturopathic medicine. Examples of systems that have developed in non-Western cultures include traditional Chinese medicine and Ayurveda.
Definition of Alternating hemiplegia syndrome
Alternating hemiplegia syndrome: See: Alternating hemiplegia of childhood.
Thursday, July 16, 2009
Definition of ALS
ALS: Amyotrophic lateral sclerosis. ALS has two meanings. One meaning of ALS refers to several adult diseases characterized by progressive degeneration of motor neurons. (In the UK, the term "motor neuron disease" is used for these disorders.) The second meaning of ALS refers to a specific form of motor neuron disease in which there are both upper and lower motor neuron signs. Motor neuron diseases such as ALS are progressive chronic diseases of the nerves that come from the spinal cord and supply electrical
stimulation to the muscles. This stimulation is necessary for the movement of body parts.
Amyotrophic lateral sclerosis is quite a mouthful. The disease is therefore usually referred to simply as ALS or in North America as Lou Gehrig's disease after the great baseball player who died of it.
ALS strikes in mid-life, most often in the fifth through seventh decades of life. Men are about one-and-a-half
times more likely to have the disease as women.
ALS occurs when specific nerve cells in the brain and spinal
cord that control voluntary movement gradually degenerate. The loss
of these motor neurons causes the muscles under their control to
weaken and waste away, leading to paralysis.
ALS manifests itself in different ways, depending on which muscles weaken first. Symptoms may include
tripping and falling, loss of motor control in hands and arms,
difficulty speaking, swallowing and/or breathing, persistent fatigue,
and twitching and cramping, sometimes quite severely.
There is no cure for ALS; nor is there a proven therapy that will prevent or reverse the course of the disorder. The
Food and Drug Administration (FDA) approved riluzole, the first drug
that has been shown to prolong the survival of ALS patients. Patients
may also receive supportive treatments that address some symptoms.
ALS is progressive and fatal. The
usual causes of death of patients with motor neuron diseases are not
directly related to the disease, but result from simultaneous
additional illnesses which ultimately occur because of weakness of
the body. These illnesses are often infections. ALS usually leads to death within 5 years of the time the diagnosis of ALS is made; the range is from 2 to 7 years.
stimulation to the muscles. This stimulation is necessary for the movement of body parts.
Amyotrophic lateral sclerosis is quite a mouthful. The disease is therefore usually referred to simply as ALS or in North America as Lou Gehrig's disease after the great baseball player who died of it.
ALS strikes in mid-life, most often in the fifth through seventh decades of life. Men are about one-and-a-half
times more likely to have the disease as women.
ALS occurs when specific nerve cells in the brain and spinal
cord that control voluntary movement gradually degenerate. The loss
of these motor neurons causes the muscles under their control to
weaken and waste away, leading to paralysis.
ALS manifests itself in different ways, depending on which muscles weaken first. Symptoms may include
tripping and falling, loss of motor control in hands and arms,
difficulty speaking, swallowing and/or breathing, persistent fatigue,
and twitching and cramping, sometimes quite severely.
There is no cure for ALS; nor is there a proven therapy that will prevent or reverse the course of the disorder. The
Food and Drug Administration (FDA) approved riluzole, the first drug
that has been shown to prolong the survival of ALS patients. Patients
may also receive supportive treatments that address some symptoms.
ALS is progressive and fatal. The
usual causes of death of patients with motor neuron diseases are not
directly related to the disease, but result from simultaneous
additional illnesses which ultimately occur because of weakness of
the body. These illnesses are often infections. ALS usually leads to death within 5 years of the time the diagnosis of ALS is made; the range is from 2 to 7 years.
Definition of Alport syndrome
Alport syndrome: An hereditary condition characterized by kidney disease, sensorineural (nerve) deafness and sometimes eye defects.
The classic disorder as described by Alport in 1927 is nephritis (inflammation of the kidney), often progressing to renal failure, and sensorineural (nerve) hearing loss affecting both sexes in successive generations. The kidney disease becomes evident as recurrent microscopic or gross hematuria (blood in the urine) as early as childhood, and usually earlier in males than in females. Progression to renal failure is gradual and usually occurs in males by the fifth decade.
The sensorineural (nerve) hearing loss in Alport syndrome primarily affects high tones and occurs in 30 to 50% of relatives with renal disease. The severity of the auditory and renal features do not correlate in a given individual with Alport syndrome.
Alport syndrome is not one disease. It has diverse genetic causes; there are X-linked and autosomal dominant and recessive forms of Alport syndrome. There are also diverse clinical types of Alport syndrome including, for example, juvenile-onset Alport syndrome with deafness, adult-onset Alport syndrome with deafness, and adult Alport syndrome without deafness.
The X-linked disorder that has come to be known as Alport syndrome is characterized by hematuria (blood in the urine), progressive renal failure, and sensorineural (nerve) hearing loss and is frequently associated with both eye abnormalities (such as lens and retinal anomalies) as well as the identification of mutations in the gene encoding what is called the basement membrane specific type IV collagen alpha-5 chain (COL4A5), an X-linked gene. This syndrome was proven to be an X-linked dominant disorder.
The classic disorder as described by Alport in 1927 is nephritis (inflammation of the kidney), often progressing to renal failure, and sensorineural (nerve) hearing loss affecting both sexes in successive generations. The kidney disease becomes evident as recurrent microscopic or gross hematuria (blood in the urine) as early as childhood, and usually earlier in males than in females. Progression to renal failure is gradual and usually occurs in males by the fifth decade.
The sensorineural (nerve) hearing loss in Alport syndrome primarily affects high tones and occurs in 30 to 50% of relatives with renal disease. The severity of the auditory and renal features do not correlate in a given individual with Alport syndrome.
Alport syndrome is not one disease. It has diverse genetic causes; there are X-linked and autosomal dominant and recessive forms of Alport syndrome. There are also diverse clinical types of Alport syndrome including, for example, juvenile-onset Alport syndrome with deafness, adult-onset Alport syndrome with deafness, and adult Alport syndrome without deafness.
The X-linked disorder that has come to be known as Alport syndrome is characterized by hematuria (blood in the urine), progressive renal failure, and sensorineural (nerve) hearing loss and is frequently associated with both eye abnormalities (such as lens and retinal anomalies) as well as the identification of mutations in the gene encoding what is called the basement membrane specific type IV collagen alpha-5 chain (COL4A5), an X-linked gene. This syndrome was proven to be an X-linked dominant disorder.
Definition of Alpha-synuclein
Alpha-synuclein: One in a family of structurally related proteins that are prominently expressed in the central nervous system. Aggregated alpha-synuclein proteins form brain lesions that are hallmarks of some neurodegenerative diseases (synucleinopathies). The gene for alpha-synuclein, which is called SNCA, is on chromosome 4q21. One form of hereditary Parkinson disease is due to mutations in SNCA. Another form of hereditary Parkinson disease is due to a triplication of SNCA. See also: Parkinson disease gene.
Definition of Alpha-glucosidase inhibitor
Alpha-glucosidase inhibitor: A class of oral medications for type 2 diabetes that decrease the absorption of carbohydrates from the intestine, resulting in a slower and lower rise in blood glucose throughout the day, especially right after meals. Before carbohydrates are absorbed from food, they must be broken down into smaller sugar particles like glucose by enzymes in the small intestine. One of the enzymes involved in breaking down carbohydrates is called alpha glucosidase. By inhibiting this enzyme, carbohydrates are not broken down as efficiently and glucose absorption is delayed. The alpha-glucosidase inhibitors include Precose (acarbose) and
Glyset (miglitol).
Glyset (miglitol).
Definition of Alpha-ethltryptamine
Alpha-ethltryptamine: An illicit hallucinogenic drug related to tryptamine. Street names for alpha-ethyltryptamine include:
Alpha-ET; ET; Love pearls; Trip (also refers to LSD).
Many agents in the class of tryptamines are hallucinogenic substances that exist naturally in some plants, fungi, and animals, but also can be produced synthetically. These hallucinogens have been placed in Schedule I of the CSA (Controlled Substances Act) and include psilocybin, psilocyn, bufotenine, alpha-ethyltryptamine, diethyltryptamine, and dimethyltryptamine. There are also numerous types of tryptamines available, including AMT (alpha-methyltryptamine) and Foxy (5-MeO-DIPT), that are not listed under the CSA.
Alpha-ET; ET; Love pearls; Trip (also refers to LSD).
Many agents in the class of tryptamines are hallucinogenic substances that exist naturally in some plants, fungi, and animals, but also can be produced synthetically. These hallucinogens have been placed in Schedule I of the CSA (Controlled Substances Act) and include psilocybin, psilocyn, bufotenine, alpha-ethyltryptamine, diethyltryptamine, and dimethyltryptamine. There are also numerous types of tryptamines available, including AMT (alpha-methyltryptamine) and Foxy (5-MeO-DIPT), that are not listed under the CSA.
Wednesday, July 15, 2009
Alpha thalassemia: A blood disorder, thalassemia is not one disease but rather a group of disorders that have a single feature in common: they all have a genetic defect in the production of hemoglobin, the protein that enables red blood cells to carry oxygen.
All forms of hemoglobin are made up of two
molecules: heme and globin. Globin is made up of 4
polypeptide chains. In normal adult hemoglobin (Hb A), the
predominant type of hemoglobin after the first year of life, 2 of the globin polypeptide chains are identical to one another and are designated the alpha chains. The other 2 chains are also identical to one another but differ from the alpha chains and are termed the beta chains. In fetal hemoglobin (Hb F), the predominant hemoglobin during
fetal development, there are 2 alpha chains and 2 different chains called gamma chains.
The problem in the thalassemias is with globin
production. The thalassemias are classified according to the type of globin polypeptide chain that is underproduced. The alpha chain is involved in alpha thalassemia (and the beta chain is affected in the more familiar beta thalassemia).
In alpha thalassemia, the heterozygous state (with a single gene for alpha thalassemia) is innocuous or harmless. There are no symptoms or at most mild anemia, because there is another gene still able to make alpha chains.
However, the homozygous state (with both genes for alpha thalassemia) is lethal before birth because no alpha chains can be made and without alpha chains, there can be no Hb F or Hb A and without Hb F or Hb A, the inevitable result is an unsuccessful pregnancy.
All forms of hemoglobin are made up of two
molecules: heme and globin. Globin is made up of 4
polypeptide chains. In normal adult hemoglobin (Hb A), the
predominant type of hemoglobin after the first year of life, 2 of the globin polypeptide chains are identical to one another and are designated the alpha chains. The other 2 chains are also identical to one another but differ from the alpha chains and are termed the beta chains. In fetal hemoglobin (Hb F), the predominant hemoglobin during
fetal development, there are 2 alpha chains and 2 different chains called gamma chains.
The problem in the thalassemias is with globin
production. The thalassemias are classified according to the type of globin polypeptide chain that is underproduced. The alpha chain is involved in alpha thalassemia (and the beta chain is affected in the more familiar beta thalassemia).
In alpha thalassemia, the heterozygous state (with a single gene for alpha thalassemia) is innocuous or harmless. There are no symptoms or at most mild anemia, because there is another gene still able to make alpha chains.
However, the homozygous state (with both genes for alpha thalassemia) is lethal before birth because no alpha chains can be made and without alpha chains, there can be no Hb F or Hb A and without Hb F or Hb A, the inevitable result is an unsuccessful pregnancy.
Definition of Alpha interferon
Alpha interferon: A protein produced by the body in response to an infection. There are 3 major classes of interferon -- alpha, beta, and gamma.
Definition of Alpha helix
Alpha helix: The coiled structure of many proteins consisting of a single chain of amino acids stabilized by hydrogen bonds. The alpha helix was first proposed by Linus Pauling and Robert Corey in a brilliant series of paper in the early 1950s. It is also known as the Pauling-Corey helix. See also: Pauling, Linus.
Definition of Alpha blocker
Alpha blocker: A drug that blocks receptors in arteries and smooth muscle. This action relaxes the blood vessels and leads to an increase in blood flow and a lower pressure for the control of hypertension. The action in the urinary tract enhances urinary flow in prostatic hypertrophy (enlarged prostate). The alpha blockers include doxazosin (Cardura), prazosin (Minipress), and The alpha blockers include doxazosin (Cardura), prazosin (Minipress), and terazosin (Hytrin).
Definition of Alpers disease
Alpers disease: A progressive disease of the nervous system characterized by spasticity (tightness), myoclonus and dementia and by liver problems with jaundice and cirrhosis. This disorder, first described by Alpers in 1931 as "Diffuse progressive degeneration of gray matter of cerebrum", usually begins early in life with convulsions. A continuous seizure (status epilepticus) is often the final event.
Alpers disease is due to more than one cause. Some cases are inherited as autosomal recessive traits with both parents appearing normal but carrying one Alpers gene and each of their children, boys and girls alike, standing a 1 in 4 risk of receiving both of the parental Alpers genes and of suffering from this dread disease.
Other cases of Alpers disease are disorders of oxidative phosphorylation, including mitochondrial DNA depletion syndromes. (Phosphorylation is the addition of phosphate to an organic compound, such as the addition of phosphate to ADP [adenosine diphosphate] to form ATP [adenosine triphosphate] or the addition of phosphate to glucose to produce glucose monophosphate, through the action of enzymes known as phosphotransferases or kinases.)
Alpers disease is also called Alpers progressive infantile poliodystrophy, progressive infantile poliodystrophy, diffuse degeneration of cerebral gray matter with hepatic cirrhosis, and Alpers diffuse degeneration of cerebral gray matter with hepatic cirrhosis.
Alpers disease is due to more than one cause. Some cases are inherited as autosomal recessive traits with both parents appearing normal but carrying one Alpers gene and each of their children, boys and girls alike, standing a 1 in 4 risk of receiving both of the parental Alpers genes and of suffering from this dread disease.
Other cases of Alpers disease are disorders of oxidative phosphorylation, including mitochondrial DNA depletion syndromes. (Phosphorylation is the addition of phosphate to an organic compound, such as the addition of phosphate to ADP [adenosine diphosphate] to form ATP [adenosine triphosphate] or the addition of phosphate to glucose to produce glucose monophosphate, through the action of enzymes known as phosphotransferases or kinases.)
Alpers disease is also called Alpers progressive infantile poliodystrophy, progressive infantile poliodystrophy, diffuse degeneration of cerebral gray matter with hepatic cirrhosis, and Alpers diffuse degeneration of cerebral gray matter with hepatic cirrhosis.
Definition of Alopecia, traumatic
Alopecia, traumatic: Hair loss caused by injury to the scalp.
Traumatic alopecia is usually caused by grooming methods that attempt to straighten the natural kinkiness of hair in order to make the hair more manageable. It is a result of stress traction injury from tight rollers and braiding as well as overheating the hair shafts. Vigorous combing and chemical bleaches and styling products can additionally irritate the scalp to cause further hair loss.
Traumatic alopecia commonly occurs on both sides of the scalp and the broken-off hairs are frequently visible.
Traumatic alopecia is treated by discontinuing the styling practices causing the hair and scalp injury. Partial or complete regrowth of hair can follow, but permanent loss of hair can occur when the roots of the hairs are severely damaged.
To minimize risk of injury to scalp, if a person decides to continue or resume styling, it is best to use looser and larger wrapping and braids to reduce tension on the scalp and hair. Chemicals should only be applied to the hair and not the scalp directly. The hair should be unbraided at least every two weeks.
Traumatic alopecia in the United States is a common form of hair loss in African-American women.
Traumatic alopecia is usually caused by grooming methods that attempt to straighten the natural kinkiness of hair in order to make the hair more manageable. It is a result of stress traction injury from tight rollers and braiding as well as overheating the hair shafts. Vigorous combing and chemical bleaches and styling products can additionally irritate the scalp to cause further hair loss.
Traumatic alopecia commonly occurs on both sides of the scalp and the broken-off hairs are frequently visible.
Traumatic alopecia is treated by discontinuing the styling practices causing the hair and scalp injury. Partial or complete regrowth of hair can follow, but permanent loss of hair can occur when the roots of the hairs are severely damaged.
To minimize risk of injury to scalp, if a person decides to continue or resume styling, it is best to use looser and larger wrapping and braids to reduce tension on the scalp and hair. Chemicals should only be applied to the hair and not the scalp directly. The hair should be unbraided at least every two weeks.
Traumatic alopecia in the United States is a common form of hair loss in African-American women.
Definition of Alopecia capitis totalis
Alopecia capitis totalis: Loss of all of the scalp hair. Alopecia means baldness and capitis refers to the head. Alopecia capitis totalis is thus total baldness of the scalp with normal hair elsewhere on the body.
Aside from alopecia capitis totalis, other forms of alopecia include:
Alopecia universalis: Loss of all of the hair, not only on the scalp, but also on the entire body.
Alopecia areata: Patchy areas of baldness.
Hair loss as a result of chemotherapy, the resultant hair loss usually being temporary.
Hair loss as a result of radiation therapy administered to the head, the hair loss usually being permanent, due to irreversible damage to the hair follicles.
Bald pate: Common male-pattern baldness localized to the front and top of the head, due to genetic (hereditary) factors.
Aside from alopecia capitis totalis, other forms of alopecia include:
Alopecia universalis: Loss of all of the hair, not only on the scalp, but also on the entire body.
Alopecia areata: Patchy areas of baldness.
Hair loss as a result of chemotherapy, the resultant hair loss usually being temporary.
Hair loss as a result of radiation therapy administered to the head, the hair loss usually being permanent, due to irreversible damage to the hair follicles.
Bald pate: Common male-pattern baldness localized to the front and top of the head, due to genetic (hereditary) factors.
Alopecia areata: A patchy baldness which
typically begins with patchy hair loss on the scalp and sometimes
progresses to complete baldness and even loss of body hair. The hair
loss tends to be rather rapid and asymmetrical and is different than
male pattern baldness.
Alopecia areata affects both males and females. It tends to occur
most often in children and young adults but older individuals can
also be affected.
The most common pattern of alopecia areata is one or more spots
of hair loss on the scalp. There is also a form of more generalized
thinning. When all of the scalp hair is lost, it is referred to as
alopecia totalis. Loss of all of the hairs on the body is called
alopecia universalis.
The cause appears to involve an autoimmune mechanism. The body's
own immune system attacks the hair follicles and disrupts normal hair
formation. Biopsies of affected skin show lymphocytes (one of the
body's immune system cells) inside of hair follicles where
lymphocytes normally are not present. What causes this is unknown.
Alopecia areata is sometimes associated with other
conditions (allergic disorders, thyroid disease, vitiligo, lupus,
rheumatoid arthritis, ulcerative colitis). Some cases occur within
family members and indicate a genetic basis.
The characteristic diagnostic finding of alopecia areata is the
exclamation point hair. These can be found in areas of hair loss and
are short broken off hairs that are narrower closer to the scalp and
therefore mimic an exclamation point. In some cases a biopsy is
necessary for diagnosis.
In about half of those affected, the hair regrows within a year
without any
treatment. The longer the period of time of hair loss, the less
chance that it will regrow and a variety of treatments can be tied.
Steroid injections and cream to the scalp have been used for many
years. Other drugs include minoxidil, irritants, and topical
immunotherapy which may be used in different combinations.
A study reported in the journal Archives of Dermatology
(Vol 134, 1998;1349-52) showed effectiveness of aromatherapy
essential oils (cedarwood, lavender, thyme, and rosemary oils) in
some patients. As with many disorders for which there is no clear cut
beneficial treatment, a variety of remedies are promoted which in
fact have no benefit.
typically begins with patchy hair loss on the scalp and sometimes
progresses to complete baldness and even loss of body hair. The hair
loss tends to be rather rapid and asymmetrical and is different than
male pattern baldness.
Alopecia areata affects both males and females. It tends to occur
most often in children and young adults but older individuals can
also be affected.
The most common pattern of alopecia areata is one or more spots
of hair loss on the scalp. There is also a form of more generalized
thinning. When all of the scalp hair is lost, it is referred to as
alopecia totalis. Loss of all of the hairs on the body is called
alopecia universalis.
The cause appears to involve an autoimmune mechanism. The body's
own immune system attacks the hair follicles and disrupts normal hair
formation. Biopsies of affected skin show lymphocytes (one of the
body's immune system cells) inside of hair follicles where
lymphocytes normally are not present. What causes this is unknown.
Alopecia areata is sometimes associated with other
conditions (allergic disorders, thyroid disease, vitiligo, lupus,
rheumatoid arthritis, ulcerative colitis). Some cases occur within
family members and indicate a genetic basis.
The characteristic diagnostic finding of alopecia areata is the
exclamation point hair. These can be found in areas of hair loss and
are short broken off hairs that are narrower closer to the scalp and
therefore mimic an exclamation point. In some cases a biopsy is
necessary for diagnosis.
In about half of those affected, the hair regrows within a year
without any
treatment. The longer the period of time of hair loss, the less
chance that it will regrow and a variety of treatments can be tied.
Steroid injections and cream to the scalp have been used for many
years. Other drugs include minoxidil, irritants, and topical
immunotherapy which may be used in different combinations.
A study reported in the journal Archives of Dermatology
(Vol 134, 1998;1349-52) showed effectiveness of aromatherapy
essential oils (cedarwood, lavender, thyme, and rosemary oils) in
some patients. As with many disorders for which there is no clear cut
beneficial treatment, a variety of remedies are promoted which in
fact have no benefit.
Definition of Alopecia
Alopecia: Baldness. There are many types of
alopecia, each with a
different cause. Alopecia may be localized to the front and top of
the head as in common male pattern baldness. It may be patchy as in a
condition called alopecia areata. Or it can involve the entire head
as in alopecia capitis totalis. The word "alopecia" comes from the
Greek "alopex" for "fox." Foxes are less furry when afflicted with a
skin disease (the "mange") which causes them to lose their hair.
When a fancier word for "baldness" was sought, the mangy fox supplied
it -- "alopecia" or, if you wish, "fox-mange" -- not a very positive
image to associate with baldness!
alopecia, each with a
different cause. Alopecia may be localized to the front and top of
the head as in common male pattern baldness. It may be patchy as in a
condition called alopecia areata. Or it can involve the entire head
as in alopecia capitis totalis. The word "alopecia" comes from the
Greek "alopex" for "fox." Foxes are less furry when afflicted with a
skin disease (the "mange") which causes them to lose their hair.
When a fancier word for "baldness" was sought, the mangy fox supplied
it -- "alopecia" or, if you wish, "fox-mange" -- not a very positive
image to associate with baldness!
Definition of Alogia
Alogia: 1. Complete lack of speech, as in profound mental retardation or advanced dementia. Alogia is synonymous in this sense with aphasia.
2. Poverty of speech, as commonly occurs in schizophrenia.
From the Greek a-, without + logos, speech.
2. Poverty of speech, as commonly occurs in schizophrenia.
From the Greek a-, without + logos, speech.
Definition of Allopathy
Allopathy: The system of medical practice which treats disease by the use of remedies which produce effects different from those produced by the disease under treatment. MDs practice allopathic medicine.
The term "allopathy" was coined in 1842 by C.F.S. Hahnemann to designate the usual practice of medicine (allopathy) as opposed to homeopathy, the system of therapy that he founded based on the concept that disease can be treated with drugs (in minute doses) thought capable of producing the same symptoms in healthy people as the disease itself.
The term "allopathy" was coined in 1842 by C.F.S. Hahnemann to designate the usual practice of medicine (allopathy) as opposed to homeopathy, the system of therapy that he founded based on the concept that disease can be treated with drugs (in minute doses) thought capable of producing the same symptoms in healthy people as the disease itself.
Definition of Allopathic medicine
Allopathic medicine: The system of medical practice which treats disease by the use of remedies which produce effects different from those produced by the disease under treatment. MDs practice allopathic medicine. Also called conventional medicine.
The term "allopathy" was coined in 1842 by C.F.S. Hahnemann to designate the usual practice of medicine (allopathy) as opposed to homeopathy, the system of therapy that he founded based on the concept that disease can be treated with drugs (in minute doses) thought capable of producing the same symptoms in healthy people as the disease itself.
The term "allopathy" was coined in 1842 by C.F.S. Hahnemann to designate the usual practice of medicine (allopathy) as opposed to homeopathy, the system of therapy that he founded based on the concept that disease can be treated with drugs (in minute doses) thought capable of producing the same symptoms in healthy people as the disease itself.
Tuesday, July 14, 2009
Definition of Allopathic
Allopathic: Pertaining to allopathy (conventional medicine). The term was coined in 1842 by C.F.S. Hahnemann to designate the usual practice of medicine as opposed to homeopathy, the system of therapy that he founded.
Definition of Allopath
Allopath: Or allopathist. A term sometimes applied to a physician who practices conventional medicine (allopathy).
Monday, July 13, 2009
Definition of Allelic
Allelic: Pertaining to an allele, an alternative form of a gene. A single allele is inherited from each parent.
Definition of Allele
Allele: An alternative form of a gene. One of the different forms of a gene that can exist at a single locus (spot on a chromosome). Also one of the different forms of any segment of a chromosome.
Definition of ALL (acute lymphoblastic leukemia)
ALL (acute lymphoblastic leukemia): Acute lymphoblastic leukemia, also less often called acute lymphocytic leukemia. See: Acute lymphoblastic leukemia.
Definition of Alkyl group
Alkyl group: In chemistry, a group of atoms derived from an alkane (a hydrocarbon with no carbon-to-carbon multiple bonds) by the loss of a hydrogen atom.
Alkaptonuria: A genetic metabolic disorder due to deficiency of the enzyme homogentisic acid (HGA) dioxygenase. Deficiency of this enzyme leads to the three cardinal features of alkaptonuria --the presence of homogentisic acid in the urine, ochronosis (bluish-black pigmentation in connective tissue), and arthritis.
The presence of HGA in the urine causes it to turn black upon standing when exposed to air. (Alkaptonuria was easily diagnosed among the nomadic Bedouin peoples because people with the disease left a characteristic dark spot in the sand marking the spot where they had urinated).
The ochronosis is due to the accumulation of a bluish-black pigment in connective tissues that darkly discolors them. Ochronosis occurs only after 30 years.
The pigment also accumulates in the cartilage of the joints and results in early-onset osteoarthritis. The arthritis often begins in the third decade of life when the patient is in their twenties.
Other less common features of the alkaptonuria include pigment deposition (aortic or mitral valve calcification or regurgitation and occasionally aortic dilatation), renal stones, and prostate stones.
The diagnosis of alkaptonuria is based upon the detection of excess HGA in the urine by gas chromatography and mass spectrometry analysis. Alkaptonuria results from mutations in the gene called HGD which encodes the enzyme homogentisic acid dioxygenase. This gene has been mapped to chromosome 3 in the region of bands 3q21-q23.
More than 40 mutations in the HGD gene have been identified in people with alkaptonuria. Many of these mutations change single amino acids in the homogentisate oxidase protein. For example, a substitution of the amino acid valine for methionine at position 368 (also written as Met368Val) is the most common HGD mutation in European populations. Mutations in the HGD gene probably inactivate the enzyme by changing its structure.
Alkaptonuria is inherited in an autosomal recessive manner. The brothers and sisters of someone with alkaptonuria have a 25% chance of also being affected, a 50% chance of being an unaffected carrier, and a 25% chance of being unaffected and not being a carrier. Prenatal testing is feasible.
Alkaptonuria enjoys the historic distinction of being one of the
conditions for which autosomal recessive inheritance was first proposed. This prescient proposal was made in 1902 by the English physician Archibald Garrod, later Sir Archibald. In a series of brilliant lectures in 1908 Garrod set forth the charter group of what he called "inborn errors of metabolism." The 4 conditions he labeled as inborn errors were albinism, cystinuria, pentosuria and, of course,
alkaptonuria.
The presence of HGA in the urine causes it to turn black upon standing when exposed to air. (Alkaptonuria was easily diagnosed among the nomadic Bedouin peoples because people with the disease left a characteristic dark spot in the sand marking the spot where they had urinated).
The ochronosis is due to the accumulation of a bluish-black pigment in connective tissues that darkly discolors them. Ochronosis occurs only after 30 years.
The pigment also accumulates in the cartilage of the joints and results in early-onset osteoarthritis. The arthritis often begins in the third decade of life when the patient is in their twenties.
Other less common features of the alkaptonuria include pigment deposition (aortic or mitral valve calcification or regurgitation and occasionally aortic dilatation), renal stones, and prostate stones.
The diagnosis of alkaptonuria is based upon the detection of excess HGA in the urine by gas chromatography and mass spectrometry analysis. Alkaptonuria results from mutations in the gene called HGD which encodes the enzyme homogentisic acid dioxygenase. This gene has been mapped to chromosome 3 in the region of bands 3q21-q23.
More than 40 mutations in the HGD gene have been identified in people with alkaptonuria. Many of these mutations change single amino acids in the homogentisate oxidase protein. For example, a substitution of the amino acid valine for methionine at position 368 (also written as Met368Val) is the most common HGD mutation in European populations. Mutations in the HGD gene probably inactivate the enzyme by changing its structure.
Alkaptonuria is inherited in an autosomal recessive manner. The brothers and sisters of someone with alkaptonuria have a 25% chance of also being affected, a 50% chance of being an unaffected carrier, and a 25% chance of being unaffected and not being a carrier. Prenatal testing is feasible.
Alkaptonuria enjoys the historic distinction of being one of the
conditions for which autosomal recessive inheritance was first proposed. This prescient proposal was made in 1902 by the English physician Archibald Garrod, later Sir Archibald. In a series of brilliant lectures in 1908 Garrod set forth the charter group of what he called "inborn errors of metabolism." The 4 conditions he labeled as inborn errors were albinism, cystinuria, pentosuria and, of course,
alkaptonuria.
Definition of Alkalosis
Alkalosis: A dangerous decrease in the normal acidity
of the blood. There is too much base in the blood and body. This is a
distinctly abnormal condition. It results from the accumulation of
base or from the depletion of acid. The pH of the alkalotic body is
above normal. Alkalosis can be caused by high altitudes, hyperventilation, and excessive vomiting. The opposite of alkalosis is acidosis in which there is too low a pH due to excess acid or insufficient base in the body.
of the blood. There is too much base in the blood and body. This is a
distinctly abnormal condition. It results from the accumulation of
base or from the depletion of acid. The pH of the alkalotic body is
above normal. Alkalosis can be caused by high altitudes, hyperventilation, and excessive vomiting. The opposite of alkalosis is acidosis in which there is too low a pH due to excess acid or insufficient base in the body.
Definition of Alkaloid
Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Many alkaloids possess potent pharmacologic effects. The alkaloids include cocaine, nicotine, strychnine, piperine, caffeine, morphine, pilocarpine, atropine, methamphetamine, mescaline, ephedrine, and tryptamine.
Sunday, July 12, 2009
Definition of Alexander technique
Alexander technique: A process that teaches how to properly coordinate body and mind to release harmful tension and to improve posture, coordination and general health. The technique is named for the Australian Frederick Matthias Alexander (1869-1955) who developed it. An actor, Alexander began his career as a Shakespearean orator. He developed chronic laryngitis while performing. Determined to restore the full use of his voice, he carefully watched himself while speaking, and observed that undue muscular tension accounted for his vocal problem. He sought a way to eliminate that restriction. Over time, he discovered and articulated a principle that he believed profoundly influenced health and well-being: when neck tension is reduced, the head no longer compresses the spine and the spine is free to lengthen. Alexander restored his own natural capacity for ease by changing the way he thought while initiating an action. From this work on himself and others, he evolved a hands-on teaching method that encouraged all the body's processes to work more efficiently -- as an integrated, dynamic whole. Today the Alexander technique is usually considered to be within the context of complementary and alternative medicine (CAM).
Definition of Alexander disease
Alexander disease: A slowly progressive and ultimately fatal brain disorder that most commonly occurs in children. The infantile form of the disease is characterized by megalencephaly (an abnormally large head), seizures, spasticity and developmental retardation. It leads to death usually within the first decade. Patients with the juvenile and adult forms of Alexander disease typically experience ataxia and spasticity and a more slowly progressive course. The classic hallmark of all forms of Alexander disease is the presence of Rosenthal fibers, abnormal inclusions in astrocytes that contain the intermediate filament protein GFAP. Mutations in the gene for GFAP (glial fibrillary acidic protein) cause Alexander disease, the first known example of a primary genetic disorder of astrocytes, one of the major cell types in the vertebrate CNS. The disease was first described by W. Stewart Alexander, a New Zealand pathologist, in 1949.
Rosenthal fibers are homogeneous masses which form elongated tapered rods scattered throughout the cortex and white matter of the brain. Rosenthal fibers are located in the astrocytes. Demyelination (loss of myelin, the insulation around nerves) is also a prominent feature of the disease.
Alexander disease is classified as one of the leukodystrophies, the diseases of the white matter of the brain.
Rosenthal fibers are homogeneous masses which form elongated tapered rods scattered throughout the cortex and white matter of the brain. Rosenthal fibers are located in the astrocytes. Demyelination (loss of myelin, the insulation around nerves) is also a prominent feature of the disease.
Alexander disease is classified as one of the leukodystrophies, the diseases of the white matter of the brain.
Definition of Alcoholism
Alcoholism: Physical dependence on alcohol to the
extent that stopping alcohol use will bring on withdrawal
symptoms. In popular and therapeutic parlance, the term may
also be used to refer to ingrained drinking habits that
cause health or social problems. Treatment requires first
ending the physical dependence, then making lifestyle
changes that help the individual avoid relapse. In some
cases, medication or hospitalization are needed. Alcohol
dependence can have many serious effects on the brain,
liver, and other organs of the body.
extent that stopping alcohol use will bring on withdrawal
symptoms. In popular and therapeutic parlance, the term may
also be used to refer to ingrained drinking habits that
cause health or social problems. Treatment requires first
ending the physical dependence, then making lifestyle
changes that help the individual avoid relapse. In some
cases, medication or hospitalization are needed. Alcohol
dependence can have many serious effects on the brain,
liver, and other organs of the body.
Definition of Alcohol Abuse and Alcoholism, National Institute
Alcohol Abuse and Alcoholism, National Institute on
(NIAAA): One of the National Institutes of Health, NIAAA's
mission is to "conduct research focused on improving the treatment
and prevention of alcoholism and alcohol-related problems to reduce
the enormous health, social, and economic consequences of this
disease."
(NIAAA): One of the National Institutes of Health, NIAAA's
mission is to "conduct research focused on improving the treatment
and prevention of alcoholism and alcohol-related problems to reduce
the enormous health, social, and economic consequences of this
disease."
Definition of Alcohol abuse
Alcohol abuse: Use of alcoholic beverages to
excess, either on individual occasions ("binge drinking")
or as a regular practice. For some individuals-children or
pregnant women, for example-almost any amount of alcohol
use may be legally considered "alcohol abuse," depending on
local laws. Heavy alcohol abuse can cause physical damage
and death.
excess, either on individual occasions ("binge drinking")
or as a regular practice. For some individuals-children or
pregnant women, for example-almost any amount of alcohol
use may be legally considered "alcohol abuse," depending on
local laws. Heavy alcohol abuse can cause physical damage
and death.
Definition of ALCAM
ALCAM: A receptor expressed on T cells which
is involved in the adhesion of cells. ALCAM stands for activated leukocyte cell adhesion molecule. The gene encoding ALCAM is on chromosome 3 in region 3q13.1-q13.2. The ALCAM gene has been reported to be less active in breast tumors with a poor prognosis.
is involved in the adhesion of cells. ALCAM stands for activated leukocyte cell adhesion molecule. The gene encoding ALCAM is on chromosome 3 in region 3q13.1-q13.2. The ALCAM gene has been reported to be less active in breast tumors with a poor prognosis.
Definition of Albuminuria
Albuminuria: More than the normal amount of albumin in the urine. Albumin is the predominant protein in human blood and it is the key to the regulation of the osmotic pressure of blood.
It is normal to have some albumin in urine. But too much albumin indicates that protein is leaking through the kidney. Albuminuria can mean many things. For example, albuminuria may be a sign of significant kidney disease or it may simply be a
sequel of vigorous exercise. Albuminuria is a form of
proteinuria.
See also: Microalbuminuria.
It is normal to have some albumin in urine. But too much albumin indicates that protein is leaking through the kidney. Albuminuria can mean many things. For example, albuminuria may be a sign of significant kidney disease or it may simply be a
sequel of vigorous exercise. Albuminuria is a form of
proteinuria.
See also: Microalbuminuria.
Saturday, July 11, 2009
Definition of Albinism, oculocutaneous
Albinism, oculocutaneous: An hereditary disorder characterized by deficiency of the pigment melanin in the eyes, skin and hair. The lack of eye pigment causes photophobia (sensitivity to light), nystagmus, and decreased visual acuity.
Oculocutaneous albinism is conventionally classified as to whether it is tyrosinase-negative or tyrosinase-positive. In the tyrosinase-negative class, there is absence of the enzyme tyrosinase. In the tyrosinase-positive class, tyrosinase is present but it cannot enter pigment cells to do its job and make melanin. There are a number of specific types of oculocutaneous albinism, all of which are inherited in an autosomal recessive manner:
Type IA is characterized by absence of tyrosinase with complete absence of melanin, marked photophobia, and nystagmus. It is due to mutation of the tyrosinase gene (TYR) on chromosome 11q.
Type IB has reduced activity of tyrosinase. It has been called yellow albinism. The child looks "dead white" at birth and has the usual eye problems, but soon develops normal skin pigmentation and yellow hair.
Type II has normal tyrosinase activity. It is the most common type of oculocutaneous albinism. The hair darkens and freckles and nevi (moles) develop normally on the skin. The disorder is due to mutation of the oculocutaneous albinism gene (OCA2) on chromosome 15q.
Type III is characterized by absence of tyrosinase with the presence of pigmentation of the iris in the first decade of life. It is due to mutation of the tyrosine-related protein-1 gene (TYRP1) on chromosome 9p.
Type IV is characterized by normal tyrosinase and is due to mutation of the MATP gene on chromosome 5p. MATP stands for membrane-associated transporter protein.
Oculocutaneous albinism is also a feature of certain other genetic conditions including the Hermansky-Pudlak syndrome and Chediak-Higashi syndrome.
Oculocutaneous albinism is conventionally classified as to whether it is tyrosinase-negative or tyrosinase-positive. In the tyrosinase-negative class, there is absence of the enzyme tyrosinase. In the tyrosinase-positive class, tyrosinase is present but it cannot enter pigment cells to do its job and make melanin. There are a number of specific types of oculocutaneous albinism, all of which are inherited in an autosomal recessive manner:
Type IA is characterized by absence of tyrosinase with complete absence of melanin, marked photophobia, and nystagmus. It is due to mutation of the tyrosinase gene (TYR) on chromosome 11q.
Type IB has reduced activity of tyrosinase. It has been called yellow albinism. The child looks "dead white" at birth and has the usual eye problems, but soon develops normal skin pigmentation and yellow hair.
Type II has normal tyrosinase activity. It is the most common type of oculocutaneous albinism. The hair darkens and freckles and nevi (moles) develop normally on the skin. The disorder is due to mutation of the oculocutaneous albinism gene (OCA2) on chromosome 15q.
Type III is characterized by absence of tyrosinase with the presence of pigmentation of the iris in the first decade of life. It is due to mutation of the tyrosine-related protein-1 gene (TYRP1) on chromosome 9p.
Type IV is characterized by normal tyrosinase and is due to mutation of the MATP gene on chromosome 5p. MATP stands for membrane-associated transporter protein.
Oculocutaneous albinism is also a feature of certain other genetic conditions including the Hermansky-Pudlak syndrome and Chediak-Higashi syndrome.
Definition of Alanine
Alanine: An amino acid, one of the 20 building blocks of protein. Alanine is not an "essential" amino acid. It is not essential to the diet, but can be made by the body from other substances. Alanine was discovered in protein in 1875. Symbol: Ala.
Definition of Akinetic mutism
Akinetic mutism: A state in which a person is
unspeaking (mute) and unmoving
(akinetic). A textbook on clinical neurology observes that
a person with
akinetic mutism has "sleep-waking cycles but, when
apparently awake, with
eyes open, lies mute. immobile and unresponsive." Akinetic
mutism is often
due to damage to the frontal lobes of the brain. The
disorder was the
subject of a front-page story in The New York Times on
Aug. 30, 1998. The
story concerned a 14-year-old girl in Worcester, Mass.
named Audrey Santo,
bedridden for 11 years, "inert and unspeaking, the legacy
of an accidental
fall into a backyard swimming pool" in 1987. "She has had a
steady stream of
visitors to her home," according to the Times, "including
priests and some
people who claim that they were miraculously healed by
her." According to
Audrey's pediatrician, Dr. John W. Harding, "She kind of
gives you the
impression at various times that she sees, hears, and knows
who you are."
unspeaking (mute) and unmoving
(akinetic). A textbook on clinical neurology observes that
a person with
akinetic mutism has "sleep-waking cycles but, when
apparently awake, with
eyes open, lies mute. immobile and unresponsive." Akinetic
mutism is often
due to damage to the frontal lobes of the brain. The
disorder was the
subject of a front-page story in The New York Times on
Aug. 30, 1998. The
story concerned a 14-year-old girl in Worcester, Mass.
named Audrey Santo,
bedridden for 11 years, "inert and unspeaking, the legacy
of an accidental
fall into a backyard swimming pool" in 1987. "She has had a
steady stream of
visitors to her home," according to the Times, "including
priests and some
people who claim that they were miraculously healed by
her." According to
Audrey's pediatrician, Dr. John W. Harding, "She kind of
gives you the
impression at various times that she sees, hears, and knows
who you are."
Definition of Akinetic
Akinetic: Without movement (or without much
movement). A term used in neurology to denote the absence (or
poverty) of movement.
The word "akinetic" comes from the prefix "a-" meaning "without"
+ the Greek word "kinesis" meaning motion = without motion.
For example, a
person in coma is akinetic. For another example, akinetic mutism is a
condition in which a person is both mute and akinetic. A textbook on
clinical neurology observes that a person with akinetic mutism
has "sleep-waking cycles but, when apparently awake, with eyes open,
lies mute. immobile and unresponsive."
movement). A term used in neurology to denote the absence (or
poverty) of movement.
The word "akinetic" comes from the prefix "a-" meaning "without"
+ the Greek word "kinesis" meaning motion = without motion.
For example, a
person in coma is akinetic. For another example, akinetic mutism is a
condition in which a person is both mute and akinetic. A textbook on
clinical neurology observes that a person with akinetic mutism
has "sleep-waking cycles but, when apparently awake, with eyes open,
lies mute. immobile and unresponsive."
Definition of Akathisia
Akathisia: A movement disorder characterized by a feeling of inner restlessness and a compelling need to be in constant motion as well as by actions such as rocking while standing or sitting, lifting the feet as if marching on the spot and crossing and uncrossing the legs while sitting. People with akathisia are unable to sit or keep still, complain of restlessness, fidget, rock from foot to foot, and pace.
Akathisia is often a side effect of certain drugs. The drugs that can cause akathisia include neuroleptic (antipsychotic) agents, serotonin receptor antagonists, lithium, L-dopa,, calcium channel blockers and phenothiazine antiemetics such as prochlorperazine or metoclopropamide. Also spelled acathisia. From the Greek a- + kathisis, a sitting.
Akathisia is often a side effect of certain drugs. The drugs that can cause akathisia include neuroleptic (antipsychotic) agents, serotonin receptor antagonists, lithium, L-dopa,, calcium channel blockers and phenothiazine antiemetics such as prochlorperazine or metoclopropamide. Also spelled acathisia. From the Greek a- + kathisis, a sitting.
Friday, July 10, 2009
Definition of Airway obstruction
Airway obstruction: Partial or complete blockage of the breathing tubes to the lungs. Obstruction of the airway can be due to different causes including foreign bodies, allergic reactions, infections, anatomical abnormalities and trauma.
The onset of respiratory distress may be sudden with cough. There is often agitation in the early stage of airway obstruction. The signs of respiratory distress include labored, ineffective breathing until the person is not longer breathing (apneic). Loss of consciousness occurs if the obstruction is not relieved.
Treatment of airway obstruction due to a foreign body includes:
Adults: The Heimlich maneuver.
Children over 1 year of age: A series of 5 abdominal thrusts (a children's version of the Heimlich maneuver
Infants under 1 year of age: A combination of 5 back blows (with the flat of the hand) and 5 abdominal thrusts (with 2 fingers on the upper abdomen).
The onset of respiratory distress may be sudden with cough. There is often agitation in the early stage of airway obstruction. The signs of respiratory distress include labored, ineffective breathing until the person is not longer breathing (apneic). Loss of consciousness occurs if the obstruction is not relieved.
Treatment of airway obstruction due to a foreign body includes:
Adults: The Heimlich maneuver.
Children over 1 year of age: A series of 5 abdominal thrusts (a children's version of the Heimlich maneuver
Infants under 1 year of age: A combination of 5 back blows (with the flat of the hand) and 5 abdominal thrusts (with 2 fingers on the upper abdomen).
Definition of Air bag
Air bag: A bag that fills with air, designed for frontal impact crashes, the kind of crashes which account for more than half of all passenger vehicle occupant deaths. Air bags are designed to limit head and chest injuries. But they only supplement safety belts, they do not replace them.
During pre-crash braking of a motor vehicle, an unrestrained passenger may be thrown against the dashboard area, in immediate proximity to an air bag. Since air bags inflate in less than 1/25th of a second, faster than the blink of an eye, drivers and passengers who are unrestrained or are wearing only the lap portion of their safety belt can receive serious or even fatal injuries from deploying air bags.
The National Highway Traffic Safety Administration estimates that the combination of an air bag in addition to a lap and shoulder belt reduces the risk of serious head injury by about 80%, compared with 60% reduction for belts alone.
Infants should NEVER ride in the front seat of a vehicle with a passenger air bag.
Children ages 12 and under should always be properly restrained in a child safety seat or safety belt and ride in the back seat. Even if there isn't a passenger air bag in the motor vehicle, the safest place for infants and children is properly secured and buckled up in the back seat.
According to the Insurance Institute for Highway Safety, over 95 million (46.8%) of the over 200 million cars and light trucks on U.S. roads have driver air bags. More than 68 million (33.4%) of these also have passenger air bags. Another one million new vehicles are being sold each month. By law, beginning with model year 1998, all new passenger cars were required to have driver and passenger air bags and safety belts. Light trucks were subject to the same requirement beginning with the 1999 model year.
During pre-crash braking of a motor vehicle, an unrestrained passenger may be thrown against the dashboard area, in immediate proximity to an air bag. Since air bags inflate in less than 1/25th of a second, faster than the blink of an eye, drivers and passengers who are unrestrained or are wearing only the lap portion of their safety belt can receive serious or even fatal injuries from deploying air bags.
The National Highway Traffic Safety Administration estimates that the combination of an air bag in addition to a lap and shoulder belt reduces the risk of serious head injury by about 80%, compared with 60% reduction for belts alone.
Infants should NEVER ride in the front seat of a vehicle with a passenger air bag.
Children ages 12 and under should always be properly restrained in a child safety seat or safety belt and ride in the back seat. Even if there isn't a passenger air bag in the motor vehicle, the safest place for infants and children is properly secured and buckled up in the back seat.
According to the Insurance Institute for Highway Safety, over 95 million (46.8%) of the over 200 million cars and light trucks on U.S. roads have driver air bags. More than 68 million (33.4%) of these also have passenger air bags. Another one million new vehicles are being sold each month. By law, beginning with model year 1998, all new passenger cars were required to have driver and passenger air bags and safety belts. Light trucks were subject to the same requirement beginning with the 1999 model year.
Definition of Aicardi syndrome
Aicardi syndrome: A genetic disorder characterized by the partial or complete agenesis of the corpus callosum (the structure that links the 2 hemispheres of the brain), infantile spasms (a characteristic form of childhood seizures), mental retardation, and an ocular (eye) abnormality called chorioretinal lacunae in which there are lacunae (holes) in the retina of the eye.
Aicardi syndrome may be associated with other brain defects such as microcephaly (small brain) or porencephalic cysts (cerebrospinal fluid-filled cavities or gaps in the brain). Features associated with Aicardi syndrome include cleft lip and/or palate, fatty tumors (lipomas) of the scalp, blood vessel malformations (cavernous hemangiomas), rib and vertebral defects and scoliosis (curved spine).
The genetics of Aicardi syndrome are extraordinary. The disorder affects only females. It is an X-linked dominant trait lethal in males. In a hemizygous male (whose only X chromosome contains the Aicardi gene), the Aicardi gene is fatal before birth. In a heterozygous female (with the Aicardi gene on one of her two X chromosomes), the Aicardi gene causes Aicardi syndrome. The Aicardi gene has been charted to the short (p) arm of the X chromosome and is in band Xp22.
There is no cure for Aicardi syndrome. Nor is there a standard course of treatment. Treatment is purely symptomatic. It generally involves management of seizures and programs for the mental retardation.
The prognosis for individuals with Aicardi syndrome varies according to the presence and severity of symptoms.
Aicardi syndrome may be associated with other brain defects such as microcephaly (small brain) or porencephalic cysts (cerebrospinal fluid-filled cavities or gaps in the brain). Features associated with Aicardi syndrome include cleft lip and/or palate, fatty tumors (lipomas) of the scalp, blood vessel malformations (cavernous hemangiomas), rib and vertebral defects and scoliosis (curved spine).
The genetics of Aicardi syndrome are extraordinary. The disorder affects only females. It is an X-linked dominant trait lethal in males. In a hemizygous male (whose only X chromosome contains the Aicardi gene), the Aicardi gene is fatal before birth. In a heterozygous female (with the Aicardi gene on one of her two X chromosomes), the Aicardi gene causes Aicardi syndrome. The Aicardi gene has been charted to the short (p) arm of the X chromosome and is in band Xp22.
There is no cure for Aicardi syndrome. Nor is there a standard course of treatment. Treatment is purely symptomatic. It generally involves management of seizures and programs for the mental retardation.
The prognosis for individuals with Aicardi syndrome varies according to the presence and severity of symptoms.
Definition of AHD
AHD: Abbreviation for alveolar hydatid disease; American Hospital Directory; and atherosclerotic heart disease.
Definition of Agranulocytosis, infantile genetic
Agranulocytosis, infantile genetic: Children born with this condition lack neutrophils (a type of white blood cell that is important in fighting infection). These children suffer frequent infections from bacteria which in the past led to death in three-quarters of cases before 3 years of age. This disease is also known as severe congenital neutropenia (SCN).
Children with SCN have no special problems with viral or fungal infections. They do, however, have an increased risk of developing acute myelogenous leukemia or myelodysplasia, a bone marrow disorder. Aside from agranulocytosis, the bone marrow and blood show a number of other abnormalities (including maturational arrest of neutrophil precursors at the promyelocyte stage, absolute monocytosis, eosinophilia and thrombocytosis). The gamma globulin level in blood is low.
The inheritance of the disease is autosomal recessive. Both seemingly-normal parents carry an SCN gene while each of their children, boys and girls alike, has a 1 in 4 (25%) risk of receiving both SCN genes and having the disease: severe congenital neutropenia (SCN).
SCN was first clearly described by Kostmann in 1956. It is now known to be caused by a defect in a gene on chromosome 1 (in 1p35-p34.3) that codes for what is called the granulocyte colony-stimulating factor receptor (GCSFR).
Treatment with recombinant human granulocyte colony-stimulating factor (GCSF) elevates the granulocyte counts, helps resolve preexisting infections, diminishes the number of new infections and results in significant improvements in survival and quality of life. Some patients have developed leukemia or myelodysplastic syndrome following treatment with GCSF.
Congenital neutropenia is due to diverse causes. Not all patients with congenital neutropenia have mutations in the GCSFR gene.
Alternative names for severe congenital neutropenia (SCN) include: Kostmann's disease or syndrome, infantile genetic agranulocytosis and genetic infantile agranulocytosis.
Children with SCN have no special problems with viral or fungal infections. They do, however, have an increased risk of developing acute myelogenous leukemia or myelodysplasia, a bone marrow disorder. Aside from agranulocytosis, the bone marrow and blood show a number of other abnormalities (including maturational arrest of neutrophil precursors at the promyelocyte stage, absolute monocytosis, eosinophilia and thrombocytosis). The gamma globulin level in blood is low.
The inheritance of the disease is autosomal recessive. Both seemingly-normal parents carry an SCN gene while each of their children, boys and girls alike, has a 1 in 4 (25%) risk of receiving both SCN genes and having the disease: severe congenital neutropenia (SCN).
SCN was first clearly described by Kostmann in 1956. It is now known to be caused by a defect in a gene on chromosome 1 (in 1p35-p34.3) that codes for what is called the granulocyte colony-stimulating factor receptor (GCSFR).
Treatment with recombinant human granulocyte colony-stimulating factor (GCSF) elevates the granulocyte counts, helps resolve preexisting infections, diminishes the number of new infections and results in significant improvements in survival and quality of life. Some patients have developed leukemia or myelodysplastic syndrome following treatment with GCSF.
Congenital neutropenia is due to diverse causes. Not all patients with congenital neutropenia have mutations in the GCSFR gene.
Alternative names for severe congenital neutropenia (SCN) include: Kostmann's disease or syndrome, infantile genetic agranulocytosis and genetic infantile agranulocytosis.
Definition of Agranulocytosis
Agranulocytosis: A marked decrease in the number of granulocytes. Granulocytes are a type of white blood cell filled with microscopic granules that are little sacs containing enzymes that digest microorganisms.
Granulocytes are part of the innate, somewhat non specific infection-fighting immune system. They do not respond exclusively to specific antigens, as do B-cells and T-cells.
Agranulocytosis results in a syndrome of frequent chronic bacterial infections of the skin, lungs, throat, etc. Although "agranulocytosis" literally means no granulocytes, there may, in fact, be some granulocytes but too few of them, i.e. granulocytopenia. Agranulocytosis can be genetic and inherited or it can be acquired as, for example, an aspect of leukemia.
Neutrophils, eosinophils and basophils are all types of granulocytes. They are named by the staining features of their granules in the laboratory:
Neutrophils have "neutral" subtle granules; Eosinophils have prominent granules that stain readily with the acid dye eosin; and
Basophils have prominent granules that stain readily basic (non acidic) dyes.
This classification dates back to a time when certain structures could be identified in cells by histochemistry, but the functions of these intracellular structures were still not yet fathomed. However, the classification of granulocytes into neutrophils, eosinophils and basophils is still widely used (and quite useful).
Granulocytes are part of the innate, somewhat non specific infection-fighting immune system. They do not respond exclusively to specific antigens, as do B-cells and T-cells.
Agranulocytosis results in a syndrome of frequent chronic bacterial infections of the skin, lungs, throat, etc. Although "agranulocytosis" literally means no granulocytes, there may, in fact, be some granulocytes but too few of them, i.e. granulocytopenia. Agranulocytosis can be genetic and inherited or it can be acquired as, for example, an aspect of leukemia.
Neutrophils, eosinophils and basophils are all types of granulocytes. They are named by the staining features of their granules in the laboratory:
Neutrophils have "neutral" subtle granules; Eosinophils have prominent granules that stain readily with the acid dye eosin; and
Basophils have prominent granules that stain readily basic (non acidic) dyes.
This classification dates back to a time when certain structures could be identified in cells by histochemistry, but the functions of these intracellular structures were still not yet fathomed. However, the classification of granulocytes into neutrophils, eosinophils and basophils is still widely used (and quite useful).
Thursday, July 9, 2009
Definition of Agonist maintenance treatment
Agonist maintenance treatment: See: Methadone treatment program.
Definition of Agnate
Agnate: 1. As a noun, a relative on the father's side.
2. As an adjective, related on the father's side.
As opposed to enate (someone related on the mother's side) From the Latin agnatus, the past participle of agnasci (to issue forth), from ad+ nasci (to be born).
2. As an adjective, related on the father's side.
As opposed to enate (someone related on the mother's side) From the Latin agnatus, the past participle of agnasci (to issue forth), from ad+ nasci (to be born).
Definition of Aging, National Institute on
Aging, National Institute on (NIA): One of the US National Institutes of Health (NIH). The
mission of the National Institute on Aging is to "lead a national
program of research on
the biomedical, social, and behavioral aspects of the aging
process; the prevention of age-related diseases and
disabilities; and the promotion of a better quality of life
for all older Americans."
The National Institute on Aging was founded in 1974. It is
one of two institutes of the NIH based on life stages. The other
is the National Institute of Child Health and Human Development (NICHD).
mission of the National Institute on Aging is to "lead a national
program of research on
the biomedical, social, and behavioral aspects of the aging
process; the prevention of age-related diseases and
disabilities; and the promotion of a better quality of life
for all older Americans."
The National Institute on Aging was founded in 1974. It is
one of two institutes of the NIH based on life stages. The other
is the National Institute of Child Health and Human Development (NICHD).
Definition of Aging
Aging: The process of becoming older, a process that is genetically determined and environmentally modulated.
Research into aging: To sum up the state of research into aging is well beyond the confines of this space (and this writer's talents). However, here is one type of research into the genetics of aging.
A gene has been discovered that helps determine the life-span of the fruit fly Drosophila. When the gene is mutated (altered), it can extend the life-span of fruit flies. It doubles their life-span. The gene has been named Indy (for I'm not dead yet). It appears that the protein encoded by this gene transports and recycles metabolic byproducts. Defects in the gene may lead to production of a protein that renders metabolism less efficient so that its body functions as if the fruit fly were dieting, even though its eating habits are unchanged. Mutations in Indy thus appear to create a metabolic state that mimics caloric restriction, which has been shown to extend life-span.
Reference: Rogina B, Reenan RA, Nilsen SP, and Helfand SL. Extended life-span conferred by cotransporter gene mutations in Drosophila. Science Dec 15 2000: 2137-2140.
Some useful suggestions for extending life: No known substance can halt aging or extend life, but here are some useful tips for improving the chances of living a long time and staying healthy:
Eat a balanced diet, including five helpings of fruits and vegetables a day.
Exercise regularly (check with a doctor before starting an exercise program).
Get regular health check-ups.
Don't smoke (it's never too late to quit).
Practice safety habits at home to prevent falls and fractures.
Always wear your seatbelt in a car.
Stay in contact with family and friends.
Stay active through work, play, and community.
Avoid overexposure to the sun and the cold.
If you drink, moderation is the key.
When you drink, let someone else drive.
Keep personal and financial records in order to simplify budgeting and investing.
Plan long-term housing and money needs.
Keep a positive attitude toward life.
Do things that make you happy.
Research into aging: To sum up the state of research into aging is well beyond the confines of this space (and this writer's talents). However, here is one type of research into the genetics of aging.
A gene has been discovered that helps determine the life-span of the fruit fly Drosophila. When the gene is mutated (altered), it can extend the life-span of fruit flies. It doubles their life-span. The gene has been named Indy (for I'm not dead yet). It appears that the protein encoded by this gene transports and recycles metabolic byproducts. Defects in the gene may lead to production of a protein that renders metabolism less efficient so that its body functions as if the fruit fly were dieting, even though its eating habits are unchanged. Mutations in Indy thus appear to create a metabolic state that mimics caloric restriction, which has been shown to extend life-span.
Reference: Rogina B, Reenan RA, Nilsen SP, and Helfand SL. Extended life-span conferred by cotransporter gene mutations in Drosophila. Science Dec 15 2000: 2137-2140.
Some useful suggestions for extending life: No known substance can halt aging or extend life, but here are some useful tips for improving the chances of living a long time and staying healthy:
Eat a balanced diet, including five helpings of fruits and vegetables a day.
Exercise regularly (check with a doctor before starting an exercise program).
Get regular health check-ups.
Don't smoke (it's never too late to quit).
Practice safety habits at home to prevent falls and fractures.
Always wear your seatbelt in a car.
Stay in contact with family and friends.
Stay active through work, play, and community.
Avoid overexposure to the sun and the cold.
If you drink, moderation is the key.
When you drink, let someone else drive.
Keep personal and financial records in order to simplify budgeting and investing.
Plan long-term housing and money needs.
Keep a positive attitude toward life.
Do things that make you happy.
Definition of Ageusia
Ageusia: The inability to taste sweet, sour, bitter, or salty substances. Some people can taste but their ability to do so is reduced; they are said to have hypogeusia.
Definition of Agent, tocolytic
Agent, tocolytic: A medication that can inhibit labor, slow down or
halt the contractions of the uterus. Tocolytic agents are widely used today to treat
premature labor and permit pregnancy to proceed and so let the fetus gain in size and
maturity before being born.
halt the contractions of the uterus. Tocolytic agents are widely used today to treat
premature labor and permit pregnancy to proceed and so let the fetus gain in size and
maturity before being born.
Definition of Agent Orange
Agent Orange: An herbicide and defoliant containing 2,4-D and 2,4,5-T and trace amounts of dioxin. Agent Orange was used as a defoliant in the Vietnam War. There has been concern about Agent Orange as a carcinogen and teratogen (cause cancer and birth defects).
The Institute of Medicine of the National Academies in the US has found "sufficient evidence" of an association between exposure to Agent Orange and the risk of developing chronic lymphocytic leukemia (CLL), non-Hodgkin lymphoma (NHL), Hodgkin disease, and soft tissue sarcoma.
The Institute of Medicine of the National Academies in the US has found "sufficient evidence" of an association between exposure to Agent Orange and the risk of developing chronic lymphocytic leukemia (CLL), non-Hodgkin lymphoma (NHL), Hodgkin disease, and soft tissue sarcoma.
Definition of Agenesis, sacral
Agenesis, sacral: Failure of formation of all or part of the sacrum (the lowest section of the
spine).
Currarino syndrome is a condition characterized by the combination of:
Partial absence of the sacrum (the lowest portion of spine),
Anorectal (anal and rectal) abnormalities, and
An abnormal mass in front of the sacrum (due to a meningocoele or
teratoma).
The malformations in Currarino syndrome are all in tissues that have their
embryological origin in the tail bud and may reflect disturbances in its
formation during early embryonic life. A mutation (change) in a gene called the
HLXB9 homeobox gene has been identified as responsible for autosomal dominant
Currarino syndrome, also known as hereditary sacral agenesis.
spine).
Currarino syndrome is a condition characterized by the combination of:
Partial absence of the sacrum (the lowest portion of spine),
Anorectal (anal and rectal) abnormalities, and
An abnormal mass in front of the sacrum (due to a meningocoele or
teratoma).
The malformations in Currarino syndrome are all in tissues that have their
embryological origin in the tail bud and may reflect disturbances in its
formation during early embryonic life. A mutation (change) in a gene called the
HLXB9 homeobox gene has been identified as responsible for autosomal dominant
Currarino syndrome, also known as hereditary sacral agenesis.
Wednesday, July 8, 2009
Definition of Agenesis of the corpus callosum
Agenesis of the corpus callosum: A congenital abnormality (a birth defect) in which there is partial or complete absence (agenesis) of the corpus callosum, the area of the brain which connects the two cerebral hemispheres (the two halves of the brain).
Agenesis of the corpus callosum can occur as a severe syndrome in infancy or childhood, as a milder condition in young adults, or as an asymptomatic incidental finding.
If there are symptoms, the first ones are usually seizures followed by feeding problems and delays in holding the head erect, sitting, standing, and walking. The seizures may constitute a very common disorder called infantile spasms. There may also be retardation in mental and physical development and impairment of hand-eye coordination and visual and auditory memory. Hydrocephalus is also a complication. In mild cases, symptoms (such as seizures, repetitive speech, and/or headaches) may not appear for years.
Girls with agenesis of the corpus callosum may have a specific condition called Aicardi's syndrome in which there is severe mental retardation, infantile spasms and chorioretinal lacunae. Agenesis of the corpus callosum can occur as an isolated condition or in association with other cerebral anomalies (such as the Arnold-Chiari malformation and Dandy-Walker syndrome, Andermann syndrome with progressive neuropathy, schizencephaly, holoprosencephaly, and migrational anomalies). Agenesis of the corpus callosum is also associated with several chromosome anomalies, including trisomy 13 and trisomy 18.
There is no standard course of treatment for agenesis of the corpus callosum. Treatment usually involves management of signs and symptoms such as hydrocephalus and seizures if they occur.
The prognosis (outlook) with agenesis of the corpus callosum is variable. The condition does not cause death in the majority of patients. Although many children with the disorder lead normal lives and have average intelligence, careful neuropsychological testing reveals subtle differences in higher cortical function compared to individuals of the same age and education without ACC. Children with agenesis of the corpus callosum accompanied by developmental delay and/or seizure disorders should be screened for metabolic disorders. The mental retardation associated with agenesis of the corpus callosum is not progressive.
Agenesis of the corpus callosum can occur as a severe syndrome in infancy or childhood, as a milder condition in young adults, or as an asymptomatic incidental finding.
If there are symptoms, the first ones are usually seizures followed by feeding problems and delays in holding the head erect, sitting, standing, and walking. The seizures may constitute a very common disorder called infantile spasms. There may also be retardation in mental and physical development and impairment of hand-eye coordination and visual and auditory memory. Hydrocephalus is also a complication. In mild cases, symptoms (such as seizures, repetitive speech, and/or headaches) may not appear for years.
Girls with agenesis of the corpus callosum may have a specific condition called Aicardi's syndrome in which there is severe mental retardation, infantile spasms and chorioretinal lacunae. Agenesis of the corpus callosum can occur as an isolated condition or in association with other cerebral anomalies (such as the Arnold-Chiari malformation and Dandy-Walker syndrome, Andermann syndrome with progressive neuropathy, schizencephaly, holoprosencephaly, and migrational anomalies). Agenesis of the corpus callosum is also associated with several chromosome anomalies, including trisomy 13 and trisomy 18.
There is no standard course of treatment for agenesis of the corpus callosum. Treatment usually involves management of signs and symptoms such as hydrocephalus and seizures if they occur.
The prognosis (outlook) with agenesis of the corpus callosum is variable. The condition does not cause death in the majority of patients. Although many children with the disorder lead normal lives and have average intelligence, careful neuropsychological testing reveals subtle differences in higher cortical function compared to individuals of the same age and education without ACC. Children with agenesis of the corpus callosum accompanied by developmental delay and/or seizure disorders should be screened for metabolic disorders. The mental retardation associated with agenesis of the corpus callosum is not progressive.
Definition of Agenesis
Agenesis: Lack of development of something. For
example, agenesis of a toe means that toe failed to form.
example, agenesis of a toe means that toe failed to form.
Definition of Agency for Toxic Substances and Disease Registry
Agency for Toxic Substances and
Disease Registry: An agency of the U.S. Department of Health and Human Services under the Public Health Service that works with states and
other federal agencies to prevent exposure to hazardous substances from waste
sites. The agency conducts public health assessments, health studies,
surveillance activities, and health education training in communities around
waste sites on the U.S. Environmental Protection Agency's National Priorities
List. ATSDR also has developed toxicological profiles of hazardous chemicals found at these sites. Established: 1980. Headquarters: Atlanta, GA.
Disease Registry: An agency of the U.S. Department of Health and Human Services under the Public Health Service that works with states and
other federal agencies to prevent exposure to hazardous substances from waste
sites. The agency conducts public health assessments, health studies,
surveillance activities, and health education training in communities around
waste sites on the U.S. Environmental Protection Agency's National Priorities
List. ATSDR also has developed toxicological profiles of hazardous chemicals found at these sites. Established: 1980. Headquarters: Atlanta, GA.
Definition of Age-related macular degeneration
Age-related macular degeneration: An eye disease with its onset usually after age 60 that progressively destroys the macula, the central portion of the retina, impairing central vision. Age-related macular degeneration (AMD) rarely causes blindness because only the center of vision is affected. However, injury to the macula in the center of the retina can impair the ability to see straight ahead clearly and sometimes make it difficult to read, drive, or perform other daily activities that require fine central vision.
The macula is in the center of the retina at the back of the eye. As we read, light is focused onto the macula where millions of cells change the light into nerve signals that travel to the brain and tell it what we are seeing. This is our central vision. With normal central vision, we are able to read, drive, and perform other activities that require fine, sharp, straight-ahead vision.
There are two types of AMD -- the dry type and the far more frequent wet type. Neither type causes pain. An early symptom of wet AMD is that straight lines appear wavy. This happens because the newly formed blood vessels leak fluid under the macula. The fluid raises the macula from its normal place at the back of the eye and distorts vision. Another sign that a person may have wet AMD is rapid loss of central vision. This is different from dry AMD in which loss of central vision occurs slowly. In both dry and wet AMD, the person may also notice a blind spot. If any of these changes in vision is noticed, an ophthalmologist should be consulted without delay.
Supplements of zinc and the antioxidants vitamin C, vitamin E and beta-carotene reportedly slow the progression of wet AMD. In people with intermediate-stage disease, zinc reduced the risk of the disease progressing to the advanced stage by 11%, and the antioxidants reduced the risk by 10%. When the two were combined, the risk was reduced by 19%. The daily doses of the antioxidants used in the study were 500 milligrams of vitamin C, 400 milligrams of vitamin E and 15 milligrams of beta-carotene (a molecule the body converts to vitamin A). The daily dose of zinc was 80 milligrams with 2 milligrams of copper. These amounts are well above the usual levels recommended by the Food and Drug Administration (FDA): 3 times as much vitamin A, 8 times as much vitamin C, 13 times as much vitamin E and 5 times as much zinc.
For a fuller consideration of this disorder, see the article on Age-related macular degeneration.
The macula is in the center of the retina at the back of the eye. As we read, light is focused onto the macula where millions of cells change the light into nerve signals that travel to the brain and tell it what we are seeing. This is our central vision. With normal central vision, we are able to read, drive, and perform other activities that require fine, sharp, straight-ahead vision.
There are two types of AMD -- the dry type and the far more frequent wet type. Neither type causes pain. An early symptom of wet AMD is that straight lines appear wavy. This happens because the newly formed blood vessels leak fluid under the macula. The fluid raises the macula from its normal place at the back of the eye and distorts vision. Another sign that a person may have wet AMD is rapid loss of central vision. This is different from dry AMD in which loss of central vision occurs slowly. In both dry and wet AMD, the person may also notice a blind spot. If any of these changes in vision is noticed, an ophthalmologist should be consulted without delay.
Supplements of zinc and the antioxidants vitamin C, vitamin E and beta-carotene reportedly slow the progression of wet AMD. In people with intermediate-stage disease, zinc reduced the risk of the disease progressing to the advanced stage by 11%, and the antioxidants reduced the risk by 10%. When the two were combined, the risk was reduced by 19%. The daily doses of the antioxidants used in the study were 500 milligrams of vitamin C, 400 milligrams of vitamin E and 15 milligrams of beta-carotene (a molecule the body converts to vitamin A). The daily dose of zinc was 80 milligrams with 2 milligrams of copper. These amounts are well above the usual levels recommended by the Food and Drug Administration (FDA): 3 times as much vitamin A, 8 times as much vitamin C, 13 times as much vitamin E and 5 times as much zinc.
For a fuller consideration of this disorder, see the article on Age-related macular degeneration.
Definition of Age by decade
Age by decade: A term designating someone's age by decade. For example, a septuagenarian refers to someone in his or her seventies (age 70 to 79). The prefix in such terms is always from the Latin. For example, the Latin septuageni = seventy.
Denarian: Someone age 10 to 19.
Vicenarian: Someone in his or her twenties.
Tricenarian: Someone in his or her thirties.
Quadragenarian: Someone in his or her forties.
Quinquagenarian: Someone in his or her fifties.
Sexagenarian: Someone in his or her sixties.
Septuagenarian: Someone in his or her seventies.
Octogenarian: Someone in his or her eighties.
Nonagenarian: Someone in his or her nineties.
Centenarian: Someone 100 or more.
Supercentenarian: Someone 110 years old or more (no upper limit).
The terms denarian, vicenarian, tricenarian, and quadragenarian are not in common usage. The term supercentenarian was coined in 1991.
Denarian: Someone age 10 to 19.
Vicenarian: Someone in his or her twenties.
Tricenarian: Someone in his or her thirties.
Quadragenarian: Someone in his or her forties.
Quinquagenarian: Someone in his or her fifties.
Sexagenarian: Someone in his or her sixties.
Septuagenarian: Someone in his or her seventies.
Octogenarian: Someone in his or her eighties.
Nonagenarian: Someone in his or her nineties.
Centenarian: Someone 100 or more.
Supercentenarian: Someone 110 years old or more (no upper limit).
The terms denarian, vicenarian, tricenarian, and quadragenarian are not in common usage. The term supercentenarian was coined in 1991.
Definition of African tick typhus
African tick typhus: One of the tick-borne rickettsial
diseases of the eastern hemisphere, similar to Rocky Mountain spotted fever, but less
severe, with fever, a small ulcer (tache noire) at the site of the tick bite, swollen
glands nearby (satellite lymphadenopathy), and a red raised (maculopapular) rash. Also
called fievre boutonneuse.
diseases of the eastern hemisphere, similar to Rocky Mountain spotted fever, but less
severe, with fever, a small ulcer (tache noire) at the site of the tick bite, swollen
glands nearby (satellite lymphadenopathy), and a red raised (maculopapular) rash. Also
called fievre boutonneuse.
Definition of African sleeping sickness
African sleeping sickness: Also called African trypanosomiasis, a systemic disease caused by the parasite Trypanosoma brucei that is
transmitted by the bite of the tsetse fly, a gray-brown insect about the size of
a honeybee. African trypanosomiasis is confined to tropical Africa from north of
South Africa to south of Algeria, Libya, and Egypt. Tsetse flies inhabit rural
areas only, living in the woodland and thickets of the savannah and the dense
vegetation along streams. Although infection of international travelers was considered rare, the number of cases in travelers, primarily to East African game parks, has increased in recent years. Travelers visiting game parks and remote areas should take precautions. Travelers to urban areas are not at risk.
The signs and symptoms of the infection are initially nonspecific (high fever, rash, edema, or swollen glands) but
the disease progresses to encephalitis and meningitis. Symptoms generally appear
within 1 to 3 weeks of infection. Untreated cases are eventually fatal. People
who have had tsetse fly bites or become ill with high fever or other
manifestations of African trypanosomiasis are advised to seek early medical
attention. The infection can usually be cured by an appropriate course of
anti-trypanosomal therapy. Pentamidine isethionate and suramin are the drugs of
choice to treat the hemolymphatic stage of West and East African trypanosomiasis, respectively. Melarsoprol is the drug of choice for late disease with central nervous system involvement.
No vaccine is available to prevent this disease. Tsetse flies are attracted to moving vehicles and dark, contrasting colors. They are not affected by insect repellents and can bite through lightweight clothing. Areas of heavy infestation tend to be sporadically distributed and are usually well known to local residents. Avoidance of such areas is the best means of protection. Travelers at risk should be advised to wear clothing of wrist and ankle length that is made of
medium-weight fabric in neutral colors that blend with the background
environment.
transmitted by the bite of the tsetse fly, a gray-brown insect about the size of
a honeybee. African trypanosomiasis is confined to tropical Africa from north of
South Africa to south of Algeria, Libya, and Egypt. Tsetse flies inhabit rural
areas only, living in the woodland and thickets of the savannah and the dense
vegetation along streams. Although infection of international travelers was considered rare, the number of cases in travelers, primarily to East African game parks, has increased in recent years. Travelers visiting game parks and remote areas should take precautions. Travelers to urban areas are not at risk.
The signs and symptoms of the infection are initially nonspecific (high fever, rash, edema, or swollen glands) but
the disease progresses to encephalitis and meningitis. Symptoms generally appear
within 1 to 3 weeks of infection. Untreated cases are eventually fatal. People
who have had tsetse fly bites or become ill with high fever or other
manifestations of African trypanosomiasis are advised to seek early medical
attention. The infection can usually be cured by an appropriate course of
anti-trypanosomal therapy. Pentamidine isethionate and suramin are the drugs of
choice to treat the hemolymphatic stage of West and East African trypanosomiasis, respectively. Melarsoprol is the drug of choice for late disease with central nervous system involvement.
No vaccine is available to prevent this disease. Tsetse flies are attracted to moving vehicles and dark, contrasting colors. They are not affected by insect repellents and can bite through lightweight clothing. Areas of heavy infestation tend to be sporadically distributed and are usually well known to local residents. Avoidance of such areas is the best means of protection. Travelers at risk should be advised to wear clothing of wrist and ankle length that is made of
medium-weight fabric in neutral colors that blend with the background
environment.
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