Faculty Bibliography

The host response to Mycobacterium tuberculosis is characterized by interactions between mononuclear cells, with recruitment and fusion of these cells culminating in granuloma formation. In addition, the host response to M. tuberculosis requires CD4+ T-cell reactivity, mediated by antigen-independent as well as antigen-dependent mechanisms. Thus, we hypothesized that cell adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1; CD54) would participate in the response to infection with M. tuberculosis. Exposure of THP-1 cells derived from a monocyte/macrophage cell line to M. tuberculosis (1:1 bacterium/cell ratio) elicited a sustained increase (660% +/- 49% above resting level) in the expression of ICAM-1 that continued for at least 72 h. Neither the expression of vascular cell adhesion molecule 1 (VCAM-1; CD106) nor that of the integrins lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18) or CR3 (CD11b/CD18) was increased to a similar extent at corresponding time points. The increase in ICAM-1 protein expression was accompanied by an increase in steady-state mRNA (Northern [RNA] analysis). Neutralizing monoclonal antibodies directed against tumor necrosis factor alpha but not interleukin 1 alpha or interleukin 1 beta substantially abrogated the response to M. tuberculosis consistent with a paracrine or autocrine response. Continuous upregulation of the expression of ICAM-1 on mononuclear phagocytes induced by M. tuberculosis may mediate the recruitment of monocytes and enhance the antigen presentation of M. tuberculosis, thus permitting the generation and maintenance of the host response

The researchers said they had expected to learn that the most severe damage was in the cortex of Quinlan's brain, the gray outer layer where many higher brainfunctions take place, because autopsies on others in this condition had shown extensive damage in that area. Wide publicity about Quinlan's case in New Jersey prompted a national debate about life support for individuals in the persistent vegetative state. Her landmark case also spurred the development of living wills and similar medical-legal guidelines that allow proxy decisions to be made for people who develop a severe neurological or other illness

The researchers said they had expected to learn that the most severe damage was in the cortex of Quinlan's brain, the gray outer layer where many higher brain functions take place, because autopsies on others in this state had shown extensive damage in that area. Wide publicity about Quinlan's case in New Jersey prompted a national debate about life support for individuals in the persistent vegetative state. Her landmark case also spurred the development of living wills and similar medical-legal guidelines that allow proxy decisions to be made for people who develop a severe neurological or other illness

According to an autopsy performed on the brain of Karen Ann Quinlan, who died in a coma in 1985, 10 years after her family won a landmark court battle to remove her from a respirator, the major damage to her brain that caused her to fall into a persistent vegetative state was to the thalamus, not the cortex

The researchers said they had expected to learn that the most severe damage was in the cortex of [Julia Quinlan]'s brain, the gray outer layer where many higher brain functions take place, because autopsies on others in this condition had shown extensive damage in that area. Wide publicity about Quinlan's case in New Jersey prompted a national debate about life support for individuals in the persistent vegetative state. Her landmark case also spurred the development of living wills and similar medical-legal guidelines that allow proxy decisions to be made for people who develop a severe neurological or other illness

The researchers said they had expected to learn that the most severe damage was in the cortex of Quinlan's brain, the gray outer layer where many higher brain functions take place, because autopsies on others in this state had shown extensive damage in that area. Quinlan, who was put on life support after an accident that left her in a persistent vegetative state, survived in a coma for 10 years after her family won a court battle to have the respirator removed. Wide publicity about Quinlan's case in New Jersey prompted a debate about life support for individuals in the persistent vegetative state. Her landmark case also spurred the development of living wills and similar medical-legal guidelines that allow proxy decisions to be made for people who develop a severe neurological or other illness

The researchers said they had expected to learn that the most severe damage was in the cortex of [Karen Ann Quinlan]'s brain, the grey outer layer where many higher brain functions take place, because autopsies on others in this state had shown extensive damage in that area

Doctors have long arbitrarily divided lymphomas into two types: Hodgkin's disease and a dozen other forms grouped as non-Hodgkin's lymphomas. Hodgkin's disease is named for Thomas Hodgkin, a 19th century physician in London who distinguished the cancer from tuberculosis. Through such tests, lymphomas are often divided into T-cell and B-cell types. Tests showed that Mrs. [Jacqueline Kennedy Onassis]' lymphoma was of neither type and that it was Ki-1, which is named for Kiel, Germany, where the test was developed. Attempts to correlate such markers with specific therapies for lymphomas is a promising area of research. But Mrs. Onassis' rapid demise clearly shows that there is a long way to go in cancer research. 'A Cancer's Rise' shows incidence and mortality rate of cases of non-hodgkin's lymphoma andHodgkin's disease from '73-'90. (Source: American Cancer Society, 'The Human Body,' Arch Cape Press) (pg. C3)

Experts are stymied about why this should be. But three factors can explain part of the overall rise. One is HIV, the virus that causes AIDS, which somehow increases the risk of lymphoma. A second is the growing number of people with transplanted organs, who are at increased risk for developing lymphoma because of the immunosuppressant drugs used to prevent rejection of donated organs. A third is improved diagnostic techniques

These diseases join a list that includes, among others, AIDS, legionnaire's disease, Lyme disease, Lassa fever and bleeding and fever from the Ebola and Marburg viruses. Some were unknown or minor hazards only a decade or two ago. Others increased significantly in incidence over the last 20 years. Still others threaten to become bigger hazards in the near future. Successful surveillance hinges on the accuracy of statistical analyses, and they hinge on the accuracy of reports that doctors and hospitals are supposed to mail to local health departments about specified infections. But many diseases are notoriously underreported in the United States.One of the most astonishing discoveries in recent years is that a bacterium, Helicobacter pylori, can cause ulcers and other stomach ailments including possibly some forms of stomach cancer. Last February, the bacterium's causative role for ulcers was given widespread acceptance by a government-appointed panel of experts that made antibiotics a required component of ulcer treatment. Scientists in the United States and South Africa have reported evidence linking a microbe, Chlamydia pneumoniae, to coronary artery disease. C. pneumoniae, which is also known as TAWR, is a common cause of pneumonia, bronchitis and sinusitis. The findings suggest but do not prove a link between C. pneumoniae infections and atherosclerosis, the underlying cause of heart attacks