Faculty Bibliography

Werner's syndrome affects about 10 people per million population throughout the world. The researchers focused on Japan and Syria because of a high frequency of intermarriage in the two countries. The syndrome is named after Otto Werner, who in Germany in 1904 reported a family affected by premature aging and said a genetic component was at work. Certain features set Werner's syndrome apart from the usual age- related diseases. For example, Werner's individuals generally do not develop high blood pressure or Alzheimer's disease. The osteoporosis that Werner's patients develop tends to damage the arms and legs, and not the vertebrae as in older people without the syndrome. Werner's syndrome individuals tend to develop certain cancers more often than those in the geriatric population who do not have the condition. For example, those with Werner's syndrome tend to develop cancers of muscle, connective tissue and the meninges, or membrane, covering the brain, while those who do not have the syndrome tend to develop cancers of the colon and prostate

Federal health officials said on Apr 8, 1996 that they would step up surveillance for a human version of mad cow disease by focusing initially on four states and then expanding their efforts elsewhere if necessary

Researchers said the week of Mar 31, 1996 that a study to determine whether a drug could help protect brain function during open-heart surgery had to be halted because it led to a relatively large number of deaths from bleeding. The drug is nimodipine, a member of a class known as calcium channel blockers that are widely used for treating high blood pressure and chest pains from angina

The epidemic of mad cow disease in England has focused worldwide attention on the human version of the ailment, the fatal malady known as Creutzfeldt-Jakob disease. Creutzfeldt-Jakob disease affects on average about one person in a million worldwide each year. Now that an expert British committee has tentatively linked it to mad cow disease, a question is raised: How many, if any, of these cases are caused by something in the diet or environment. The natural history of the mysterious malady may shed light on its cause, and may also help clarify the nature of other brain-destroying diseases such as Alzheimer's, to which Creutzfeldt-Jakob disease seems related by symptoms and pathology. With both diseases, waxy deposits known as amyloid plaques are seen under the microscope in stricken nerve cells

The epidemic of mad cow disease in England has focused worldwide attention on the human version of the ailment, the fatal malady known as Creutzfeldt-Jakob disease. It is one of a small group of obscure diseases called spongiform encephalopathies because they produce holes in various areas of the brain, giving it a pitted appearance like Swiss cheese. Creutzfeldt-Jakob disease affects on average about one person in a million worldwide each year. Now that an expert British committee has tentatively linked it to mad cow disease, a question is raised: how many, if any, of these cases are caused by something in the diet or environment? Creutzfeldt-Jakob disease usually strikes people in their 50s and 60s, after taking years or even decades to develop. But once symptoms begin, the course is swift and relentless. Destruction of brain cells impairs an individual's ability to think, see, speak and move. Muscles go into spasm, becoming rigid and jerky. Balance is lost. The dementia that develops mimics Alzheimer's disease, a related disorder that is not classified as a spongiform disease

Many of the 10 British patients afflicted with a new variant of a fatal brain disease possibly linked to mad cow disease had behavioral and emotional changes that initially fooled doctors into thinking they had psychiatric disorders, according to the first published scientific report about the cases, in Lancet on Apr 6, 1996. Brain wave tracings did not show the changes that are usually observed in traditional cases of the human brain disease, Creutzfeldt-Jakob Disease

Reacting to the epidemic of mad cow disease in Britain, the WHO on Apr 3, 1996 recommended a worldwide ban on feeding sheep, goat, cattle and other animal tissues to livestock as part of an effort to prevent the infectious agent that causes mad cow disease from expanding further in the animal or human food chain. The health agency also urged all countries to intensify efforts to monitor for mad cow disease and its human version, a fatal malady known as Creutzfeldt-Jakob disease

The epidemic of mad cow disease in England has focused attention on the human version of the ailment, the fatal malady known as Creutzfeldt-Jakob disease, one of a small group of obscure diseases called spongiform encephalopthies because they produce holes in various areas of the brain. Now that it has been tentatively linked to mad cow disease, the question has been raised of how many, if any, of these cases are caused by something in the diet or environment

The increasing emphasis in medicine on treating the whole patient has focused attention of the association between emotions and disease. However, physicians have long studied the connection between mind and body. One particularly interesting researcher in this area was Thomas Holmes, a charismatic and iconoclastic Seattle physician who studied the association between stress and tuberculosis in the 1950s. Although lacking the sophistication of modern biostatistics, several of Holmes' studies suggested that persons who had experienced stressful situations, such as divorce, death of a spouse, or loss of a job, were more likely to develop tuberculosis and less likely to recover from it. Holmes consciously used the same scientific methods as his peers, devising a numeric scale that quantified stressful events and doing prospective studies with control groups. Yet, he also emphasized the need to understand each patient's story and to view his or her tuberculosis as the culmination of a life of emotional hardship. Although Holmes' work was rudimentary, his basic supposition may have been correct. Recent research, benefiting from advances in both immunology and biostatistics, suggests that stress may lead to decreased immune function and thus to clinical disease. As studies of stress and disease become more statistically sophisticated, it will be important to retain Holmes' emphasis on understanding the lives of individual patients.

Two genes (rpsL and rrs) with mutations associated with streptomycin resistance in Mycobacterium tuberculosis were characterized in 78 streptomycin-resistant and 61 streptomycin-susceptible isolates recovered from patients living in the United States, South America, Europe, Africa, and Asia. Fifty-four percent of the 78 resistant organisms had missense mutations in codon 43 of rpsL resulting in a K-43-->R substitution. Mutations in codon 88 of rpsL were also identified in four Asian isolates