Wet market: A live animal market, a common sight in many areas of the world and a source of influenza viruses and other infectious disease agents for human beings. SARS outbreaks have been traced to wet markets in southern China.

Wet markets sell live poultry, fish, reptiles, and mammals of every kind. Animals may stay from days to weeks. Daily introduction of new animals provides optimum conditions for the development of disease agents such as influenza. Add the daily human contacts (including children) with the live animals, and conditions are optimal for the transfer and evolution of infectious disease agents.

Refraction test: Also termed vision test, the refraction test is an examination that tests an individual's ability to see an object at a specific distance. The test is performed by an optometrist or ophthalmologist in the doctor's office. The refraction test involves looking through a device to read letters or recognize symbols on a wall chart through lenses of differing strength which are moved into and out of the device. This test is performed as part of a normal examination of the eye to determine whether an individual has normal vision. It is also used to determine the prescription for eyeglasses or contact lenses.

Hereditary angioneurotic edema: A genetic form of angioedema. (Angioedema is also referred to as Quinke's disease.) Persons with it are born lacking an inhibitor protein (called C1 esterase inhibitor) that normally prevents activation of a cascade of proteins leading to the swelling of angioedema. Patients can develop recurrent attacks of swollen tissues, pain in the abdomen, and swelling of the voice box (larynx) which can compromise breathing. The diagnosis is suspected with a history of recurrent angioedema. It is confirmed by finding abnormally low levels of C1 esterase inhibitor in the blood. Treatment options include antihistamines and male steroids (androgens) that can also prevent the recurrent attacks. Also called hereditary angioedema.

Empyema: The presence of pus in the pleural space which is between the outer surface of the lung and the chest wall. Empyema is often a complication of pneumonia caused by bacteria such as Streptococcus pneumonia, Staphylococcus aureus, or Haemophilus influenza (H. flu) type b.

The formation of the empyema is conventionally divided into three phases: exudative, fibrinopurulent and organizing. During the exudative phase, the pus accumulates. This is followed by the fibrinopurulent phase in which there is loculation of the pleural fluid (the creation of grapelike pockets of pus). In the final organizing phase there is the potential for lung entrapment by scarring.

The Greek philosopher, Aristotle, recognized empyema and described the drainage of pus with incision and a metal tube as early as 300 BC. The word "empyema" is Greek. It comes from "pyon" meaning pus.

Kalemia: The presence of potassium in the blood. The word "kalemia" is seldom used today although it is the basis for the terms for abnormally high blood potassium (hyperkalemia) and low blood potassium (hypokalemia). See also: Potassium balance.

Acidophilus: Bacteria found in yogurt that can help restore a supportive bacterial environment to an intestinal tract whose normal intestinal bacterial population ("flora") has been disturbed by disease or antibiotics.

Eating yogurt with acidophilus may also be useful in preventing candidiasis (thrush), including in the vagina.

Large saphenous vein: The larger of the two saphenous veins, the principal veins that run up the leg superficially (near the surface).

The large saphenous vein goes from the foot all the way up to the saphenous opening, an oval aperture in the broad fascia of the thigh, a fibrous membrane through which the vein passes.

The other saphenous vein, termed (not too surprisingly) the small saphenous vein, runs behind the outer malleolus (the protuberance on the outside of the ankle joint), comes up the back of the leg and joins the popliteal vein in the space behind the knee (the popliteal space).

The large saphenous vein is also called the great saphenous vein.

Beckwith-Wiedemann syndrome: An overgrowth syndrome, whose clinical manifestations typically include macrosomia (large body size), macroglossia (large tongue), omphalocele (exomphalos), organomegaly (enlarged organs), hemihypertrophy (overgrowth of one side of the body), neonatal hypoglycemia (low blood sugar in the newborn period), and ear creases and ear pits.

Patients with this syndrome have an increased risk of embryonal malignancies such as Wilms tumor, hepatoblastoma, neuroblastoma, adrenocortical cancer, and rhabdomyosarcoma.

The majority (about 85%) of patients with Beckwith-Wiedemann syndrome (BWS) have no family history of it while a minority (about 15%) of patients have a family history with autosomal dominant transmission of the syndrome.

The genetics of BWS appear complex, in part no doubt because the underlying causes of the syndrome are still not entirely clear. In 50% of patients, there is loss of methylation at the KCNQ1OT1 gene in chromosome 11p15 while in 10-20% of patients, there is paternal uniparental disomy of chromosome 11p15. There are mutations in the CDKN1C gene in chromosome 11p15 in 5-10% of cases with no known family history of the syndrome and 40% of familial cases of the syndrome.

The syndrome is named for the American pediatric pathologist J. Bruce Beckwith (1933-) and the German pediatrician Hans-Rudolf Wiedemann (1915-). In 1964, Wiedemann reported a familial form of omphalocele with macroglossia in Germany and then in 1969, Beckwith described a similar series of patients in the US. Wiedemann coined the term EMG syndrome to describe the combination of exomphalos, macroglossia, and gigantism. In time, the condition was renamed Beckwith-Wiedemann syndrome. It is also sometimes called the Wiedemann-Beckwith syndrome (WBS) because Wiedemann recognized the syndrome before Beckwith.

Jewett staging system: A system for determining the stage of a prostate cancer. The system uses ABCD. The letters "A" and "B" designate cancers that are confined to the prostate. The letter "C" applies to cancers that have grown out of the prostate but have not yet metastasized (spread) to lymph nodes or other sites. And the letter "D" refers to prostate cancer that has spread to lymph nodes or to other sites.

The Jewett staging system is also sometimes called the ABCD rating or the Whitmore-Jewett staging system.

Coronary angiography: The most accurate method (the "gold standard") for evaluating and defining coronary artery disease (CAD). Coronary angiography is used to identify the exact location and severity of CAD.

During coronary angiography, a small catheter (a thin hollow tube with a diameter of 2-3 mm) is inserted through the skin into an artery in the groin or the arm. Guided with the assistance of a fluoroscope (a special x-ray viewing instrument), the catheter is then advanced to the opening of the coronary arteries, the blood vessels supplying blood to the heart. Next, a small amount of radiographic contrast (a solution containing iodine, which is easily visualized with x-ray images) is injected into each coronary artery. The images that are produced are called the angiogram. Angiographic images accurately reveal the extent and severity of all coronary arterial blockages.

Coronary angiography is performed with the use of local anesthesia and intravenous sedation, and is generally not terribly uncomfortable. The procedure takes approximately 20-30 minutes. After the procedure, the catheter is removed and the artery in the leg or arm is sutured, "sealed," or treated with manual compression to prevent bleeding. There is a small risk of serious complications from coronary angiography, as it is an "invasive" test, but in the hands of an experienced physician, this risk is quite small (well below one per cent).

In patients for whom the test is appropriate, the therapeutic information learned from the coronary angiogram is far more valuable than the relatively small risk of the procedure. For patients with severe angina or myocardial infarction, or those who have markedly abnormal noninvasive tests for CAD, the angiogram also helps the doctor select the optimal treatment, which may include medications, balloon angioplasty, coronary stenting, atherectomy ("roto-rooter"), or coronary bypass surgery.

The coronary angiogram is the only test which allows the precise quantification of the extent and severity of CAD to optimally make these treatment decisions.

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F (symbol): A much used symbol, F stands for fractional concentration; free energy; Fahrenheit; visual field; fluorine; force; filial generation, followed by subscript numerals indicating specified matings such as F1); the amino acid phenylalanine; the coefficient of inbreeding , etc.

OAE (Otoacoustic emission test) : OAE is an abbreviation for "otoacoustic emission test" which measures an acoustic response that is produced by the inner ear (cochlea), which in essence bounces back out of the ear in response to a sound stimulus. The test is performed by placing a small probe that contains a microphone and speaker into the infant's ear. As the infant rests quietly, sounds are generated in the probe and responses that come back from the cochlea are recorded. Once the cochlea processes the sound, an electrical stimulus is sent to the brainstem. In addition, there is a second and separate sound that does not travel up the nerve, but comes back out into the infant's ear canal. This "byproduct" is the otoacoustic emission. The emission is then recorded with the microphone probe and represented pictorially on a computer screen. The audiologist can determine which sounds yielded a response/emission and the strength of those responses. If there is an emission present for those sounds that are critical to speech comprehension, then the infant has "passed" the hearing screen.

Snowblindness: A burn of the cornea (the clear front surface of the eye) by ultraviolet B rays (UVB). Also called radiation keratitis or photokeratitis.

The condition typically occurs at high altitudes on highly reflective snow fields or, less often, with a solar eclipse. Artificial sources of UVB can also cause snowblindness. These sources include suntanning beds, a welder's arc (flash burn, welder's flash, or arc eye), carbon arcs, photographic flood lamps, lightning, electric sparks, and halogen desk lamps.

Symptoms include tearing, pain, redness, swollen eyelids, headache, a gritty feeling in the eyes, halos around lights, hazy vision, and temporary loss of vision. These symptoms may not appear until 6-12 hours after the UBV exposure.

Treatment consists mainly of keeping the eye closed with patches, after instilling a few drops of ophthalmic antibiotic solution, such as sulfacetamide sodium 10% with methylcellulose or gentamicin. Vision usually returns after 18 hours. The surface of the cornea usually regenerates in 24 to 48 hours.

Prevention involves sunglasses with adequate UVB protection and full coverage of the eyes (side shields).

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Becker muscular dystrophy: A chronic, progressive muscle degeneration disease. A form of muscular dystrophy that is quite similar to Duchenne muscular dystrophy, except that patients with Becker do produce some of the key protein, dystrophin, whereas those with Duchenne do not. Progression of the disease in Becker type is slower than in Duchenne, and symptoms may appear as late as the mid-twenties.

Becker muscular dystrophy is a mild version of Duchenne. Both diseases result from mutations in the huge gene in region Xp21.2 on the X chromosome that encodes dystrophin. (The other principal form of X-linked, late-onset muscular dystrophy is Emery-Dreifuss muscular dystrophy, which results from mutation in the gene encoding emerin on Xq28.)

Scabies, crusted: A severe form of scabies caused by delayed treatment of the initial infestation, characterized by mite-filled lesions covered with scabs. These lesions often fall victim to secondary infections, as with Staphylococcus bacteria. Crusted scabies is most common in people with immune-system problems, including AIDS, diabetes, and lupus. Also known as keratotic scabies, Norwegian scabies.

Oligoastrocytoma: A type of malignant brain tumor that belongs to the category of "mixed" gliomas. Gliomas are brain tumors that begin in glial, or supportive, cells in the brain or spinal cord. Malignant gliomas are the most common primary tumors of the central nervous system (the brain and spinal cord). Mixed gliomas are gliomas that contain more than one type of cell. An oligoastrocytoma is a mixed glioma composed of cells that resemble two different kinds of brain cells known as astrocytes and oligodendrocytes.

Malabsorption: The impaired absorption by the intestines of nutrients from food. Malabsorption can be specific and involve sugars, fats, proteins, or vitamins. Alternatively, malabsorption can be general and nonspecific.

The causes of malabsorption include cystic fibrosis (from lack of pancreatic enzymes to digest food), lactose intolerance, celiac disease (gluten-induced-enteropathy, sprue), Whipple disease, acrodermatitis enteropathica (zinc malabsorption), biliary atresia, pernicious anemia, and the parasites Giardia lamblia (giardiasis), Strongyloides stercoralis (threadworm), and Necator americanus (the hookworm).

The signs and symptoms depend on the type of malabsorption and may include failure to thrive (in infancy and childhood), diarrhea, cramping, frequent bulky stools, bloating, flatulence (gas), and abdominal distention. Treatment depends on the exact cause.

Acaricide: An agent, usually a chemical, that kills mites. This class of pesticides is large and includes antibiotic acaricides, carbamate acaricides, formamidine acaricides, mite growth regulators, organophosphate acaricides, and many others. From the Latin acarus, a mite + -cide, to kill.

Hecht syndrome: A striking genetic disorder in which abnormally short muscles in the jaw make it impossible to open the mouth fully (trismus) and abnormally short muscles in the hands keep the fingers straight when the hand is flexed back (pseudocamptodactyly). The difficulty in opening the mouth fully can cause severe infant feeding problems. It also complicates dental care and intubation for anesthesia. The hands may be so tightly fisted the infant crawls on his or her knuckles. The pseudocamptodactyly impairs manual dexterity and causes occupational and social disability. Many patients require surgical correction of contractures. The syndrome is considered a type of distal arthrogryposis.

The gene for the syndrome is transmitted as an autosomal dominant trait passing from parent to child, irrespective of sex. There is variable expressivity but high penetrance.

The Hecht syndrome has been served as an historic marker. For example, a large American family with the syndrome was traced to a Dutch girl who migrated to Tennessee soon after the American Revolution. A large Dutch family with many affected members has also been described. The Dutch and American families are now believed to be related.

Hecht syndrome was first described by the pediatrician/geneticist Frederick Hecht and orthopedist Rodney K. Beals of the Oregon Health Sciences University. They called the syndrome "Inability to Open the Mouth Fully." It now also goes by the precise but hard-to-remember name of trismus pseudocamptodactyly syndrome. It has also been called the Hecht-Beals syndrome and the Dutch-Kentucky syndrome.

Tetraethyl lead: An anti-knock compound added to motor fuel. Also known as tetraethylplumbane, tetraethyl lead has highly adverse effects on human health. It causes lead poisoning.

The History of Tetraethyl Lead

In 1921 three General Motors (GM) engineers -- Charles Kettering, Thomas Midgeley, and Thomas Boyd -- reported success with adding tetraethyl lead to improve engine performance and reduce engine knock. Through the Ethyl corporation, then a GM subsidiary, GM quickly began touting this lead compound as the virtual savior of the American automobile industry. The discovery was indeed extremely important. It paved the way for the development of the high-power, high-compression internal combustion engines.

The first danger sign was the mysterious illness that forced Thomas Midgeley to spend weeks convalescing in the winter of 1923. Midgeley had been experimenting rather recklessly with the various methods of manufacturing tetraethyl lead, and he did not at first realize just how dangerous the substance was in its concentrated liquid state. The deadliness of tetraethyl lead was sadly confirmed in the summer of 1924. Workers engaged in producing the additive fell sick and died at several refineries in New Jersey and Ohio. Banner headlines greeted each new fatality until a total of 15 workers had lost their minds and then their lives.

In 1925, the US Surgeon General temporarily suspended the production and sale of leaded gasoline. He appointed a panel of experts to investigate the recent fatalities that had "occurred in the manufacture and mixing of the concentrated tetraethyl lead." The panel was also asked to weigh "the possible danger" that might arise "from...wide distribution of a lead compound" through its sale as a gasoline additive.

Industry dominated the Surgeon General's investigatory committee, which included only one genuine environmental visionary, Dr. Alice Hamilton of Harvard University. The Coolidge Administration gave the panel just seven months to design, run, and analyze its tests. The committee's final report, published in June 1926, complained of the time constraints under which it had been forced to operate. Seven months was "not sufficient," argued the panel, "to produce detectable symptoms of lead poisoning" in experimental subjects because of the very slow gestation of that toxicological syndrome.

Nevertheless, the Surgeon General's panel ruled that there were "no good grounds for prohibiting the use of ethyl gasoline...as a motor fuel, provided that its distribution and use are controlled by proper regulations." The coming decades of Depression, total war, and post-war boom were hardly conducive to the implementation of "proper regulations" for leaded gasoline. Indeed, no compulsory standards were set for the industry until the early 1970s when EPA began its long, hard struggle to phase down lead levels in US gasoline.

One saturnine prophecy marred the otherwise sanguine 1926 report to the Surgeon General. By 1985 these words were to reverberate with particular resonance down the corridors of time: "It remains possible that, if the use of leaded gasolines becomes widespread, conditions may arise very different from those studied by us which would render its use more of a hazard than would appear to be the case from this investigation. Longer experience may show that even such slight storage of lead as was observed [among human guinea pigs] in these [1925] studies may lead eventually to recognizable lead poisoning or to chronic degenerative diseases of a less obvious character. In view of such possibilities the committee feels that the investigation begun under their direction must not be allowed to lapse.... With the experience obtained and the exact methods now available, it should be possible to follow closely the outcome of a more extended use of this fuel and to determine whether or not it may constitute a menace to the health of the general public after prolonged use or under conditions not now foreseen.... The vast increase in the number of automobiles throughout the country makes the study of all such questions a matter of real importance from the standpoint of public health." Needless to say, this advice fell on deaf ears.

In 1927 the Surgeon General set a voluntary standard for the oil industry to follow in mixing tetraethyl lead with gasoline. This standard -- 3 cubic centimeters per gallon (cc/g) -- corresponded to the maximum then in use among refiners, and thus imposed no real restraint. Even without prodding, however, the industry did take giant strides toward instituting safer working conditions in oil refineries, thereby protecting individual laborers in the microcosm of the workplace.

Three decades later, the Surgeon General actually raised the lead standard to 4 cc/g (equivalent of 4.23 grams per gallon). This voluntary standard once again represented the outside range of industry practice. Nevertheless, the Surgeon General concluded in 1958 that a loosening of the voluntary standard posed no threat to the health of the average American: "During the past 11 years, during which the greatest expansion of tetraethyl lead has occurred, there has been no sign that the average individual in the U.S. has sustained any measurable increase in the concentration of lead in his blood or in the daily output of lead in his urine."

The actual industry average during the 1950s and the 1960s hovered in the vicinity of 2.4 grams per total gallon. The Department of Health, Education and Welfare (HEW), which was home to the Surgeon General starting with the Kennedy Administration, had authority over lead emissions under the Clean Air Act of 1963. The criteria mandated by this statute were still in the draft stage when the Act was reauthorized in 1970 and a new agency called EPA came into existence.

By then, the adverse effects of America's decades-old addiction to fossil fuel in general and leaded fuel in particular were becoming obvious to all. In 1971, the EPA's first Administrator, William D. Ruckelshaus, declared that "an extensive body of information exists which indicates that the addition of alkyl lead to gasoline...results in lead particles that pose a threat to public health."

It should be emphasized, however, that scientific evidence capable of documenting this conclusion did not exist in previous decades. Only very recently have scientists been able to prove that low-level lead exposure resulting from automobile emissions is harmful to human health in general, but especially to the health of children and pregnant women.

EPA took an emphatic stand on the issue in its final health document on the subject, "EPA's Position on the Health Implications of Airborne Lead," which was released on November 28, 1973. This study confirmed what preliminary studies had already suggested: namely, that lead from automobile exhaust was posing a direct threat to public health. Under the Clean Air Amendments of 1970, that conclusion left EPA with no option but to control the use of lead as a fuel additive known to "endanger the public health or welfare."

The very next month, in December 1973, EPA issued regulations calling for a gradual reduction in the lead content of the total gasoline pool, which includes all grades of gasoline. The restrictions were scheduled to be implemented starting on January 1, 1975, and to extend over a five-year period. The average lead content of the total gasoline pool of each refinery was to be reduced from the level of approximately 2.0 grams per total gallon that prevailed in 1973 to a maximum of 0.5 grams per total gallon after January 1, 1979. Litigation was to postpone implementation of this phasedown for two years.

Starting with the 1975 model year, US automakers responded to EPA's lead phasedown timetable by equipping new cars with pollution-reducing catalytic converters designed to run only on unleaded fuel. Fittingly, a key component of these catalysts that were to be the undoing of lead was that noblest of noble metals, platinum.

Although over 40% of all pump sales are still leaded as of today, the market share of leaded vehicle is steadily diminishing. And with it, so is the noxious cloud of lead-polluted air we have grown accustomed to breathing. EPA estimates that ambient lead levels dropped 64 percent between 1975 and 1982.

In 1982, with the introduction of unleaded gasoline well underway, EPA developed a new standard intended to apply strictly to leaded gasoline.

On the basis of all that is known about the history of lead and its adverse effects on human health, it is impossible not to welcome EPA's lead phasedown initiative as well as the agency's decision to consider banning lead altogether from US gasoline.