Search PubMed⌕ Search

Biomedical subjects

M Kennedy

Publications and source records attributed to M Kennedy.

At least 127 records · Page 7Linked to original sources
PubMed1997

Ultraviolet irradiation induces the production of multiple cytokines by human corneal cells.

PURPOSE: Ultraviolet (UV) irradiation exposure represents a significant environmental and occupational hazard that can cause acute and chronic inflammatory changes in the exposed cornea. Acute exposure to solar UV irradiation or to UV irradiation from such artificial sources as tanning lamps can result in severe pain and inflammation in the cornea. Chronic exposure to solar UV irradiation is associated with several external eye diseases including pterygium and squamous metaplasia or carcinoma. In the skin, inflammatory responses to UV exposure appear to be mediated by the release of inflammatory cytokines. The role of corneal-derived cytokines in UV-mediated corneal inflammation has not been established. In this study, the effect of UV exposure on the production of proinflammatory cytokines by corneal cells was examined. METHODS: Cultured human corneal stroma cells and whole human corneas received UV irradiation (10 to 100 mJ/cm2), and the production of the proinflammatory cytokines interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor alpha (TNF alpha) was measured by Northern blot analysis, enzyme-linked immunosorbent assay, cytokine bioassays, and immunohistochemical analysis. RESULTS: The results indicate that acute UV exposure leads to a significant increase in the production of IL-1, IL-6, IL-8, and TNF alpha in human corneal stroma cells. Similarly, acute UV irradiation of whole human corneas ex vivo induces a significant increase in the production of IL-1, IL-6, IL-8, and TNF alpha. CONCLUSIONS: Acute UV irradiation exposure results in the induction of cornea-derived proinflammatory cytokines. The local release of these proinflammatory cytokines by cells in the irradiated cornea may be responsible for UV-mediated corneal inflammation.

Blotting, Northern↗
PubMed1996

BCR gene recombines with genomically distinct sites on band 11Q13 in complex BCR-ABL translocations of chronic myeloid leukemia.

We have analysed a cloned 11q13/3'BCR junction fragment, one recombination product of a complex t(9;11;22) translocation in a patient with chronic myeloid leukemia. 3'M-Bcr recombined with chromosome band 11q13 at a specific point between two Alu elements lying in opposite orientation. We present new molecular data comparing the genomic location of the 11q13 breakpoint in our patient with that of one other recently reported to lie within the GSTP1 gene. This is the first time that specific breakpoint sites within a chromosomal region highly involved in complex Ph translocations have been relatively mapped. These early results argue against a precise site in 11q13 with which M-Bcr preferentially recombines and favour instead a larger recombination-prone domain. Both of the 11q13 breakpoint regions show Alu repeat elements in close proximity to the site of recombination.

Base Sequence↗
PubMed1996

A prospective long-term study of fibromyalgia syndrome.

OBJECTIVE: To ascertain the long-term natural history of fibromyalgia syndrome (FMS). METHODS: Patients with a history of FMS, seen in an academic rheumatology referral practice, were originally surveyed soon after onset of symptoms, and then were reinterviewed 10 years later in a prospective followup cohort study. A validated telephone survey was administered that inquired into current symptoms, medical care and treatments used, and work disability. The results were compared with the prior surveys. RESULTS: Of the original 39 patients, there were 4 deaths. Of the remaining 35 patients, 29 (83%) were reinterviewed. Mean age at current survey was 55 years, and mean duration of symptoms was 15.8 years. All patients had persistence of some fibromyalgia symptoms, although almost half (48%) had not seen a doctor for them in the last year. Moderate to severe pain or stiffness was reported in 55% of patients; moderate to a lot of sleep difficulty was noted in 48%; and moderate to extreme fatigue was noted in 59%. These symptoms showed little change from earlier surveys. In 79% of patients, medications were still being taken to control FMS symptoms. Despite continuing symptoms, 66% of patients reported that FMS symptoms were a little or a lot better than when first diagnosed. Fifty-five percent of patients said they felt well or very well in terms of FMS symptoms, and only 7% felt they were doing poorly. With the exception of sleep trouble, which was persistent, baseline survey symptoms correlated poorly with symptoms at the 10-year followup. CONCLUSION: FMS symptoms last, on average, at least 15 years after illness onset. However, most patients experience some improvement in symptoms after FMS onset.

Adult↗
PubMed1996

Neuroendocrine (carcinoid) tumor of the mandible: a case report and review of the literature.

The aim of this article is to present a case of primary neuroendocrine tumor (typical carcinoid) of the mandible that occurred in a 46-year-old black woman who was seropositive for the human immunodeficiency virus. Radiologically the lesion presented as a poorly circumscribed honeycomb radiolucency that extended from tooth 21 to the ascending ramus. Histologically the tumor cells were variously arranged in small islands, trabeculae, follicles, and slitlike spaces lined by a single layer of palisaded low-columnar cells. The follicles contained an eosinophilic colloid-like substance. Immunocytochemical staining showed diffuse, intense positivity for MAK 6, pancytokeratin, S-100, and neuron-specific enolase and focal, intense, positive staining for chromogranin A. Electron microscopy showed the presence of interdigitating cell membranes, rudimentary cell attachments, and varying numbers of membrane-bound dense core granules. Special investigations failed to reveal a primary tumor, and no metastases were found. Urine and hematologic assessment did not show any evidence of functional activity. The tumor was resected, and no recurrence or spread has been seen for 2 years. Origin from foregut-derived, immature, and functionally uncommitted endocrine cells is presumed.

Carcinoid Tumor↗
PubMed1996

Drugs and brain death.

Brain death protocols facilitate early recognition of death in patients on life support systems. When the clinical situation has deteriorated to a level where brain death is to be considered, it is essential that the effects of drugs be excluded. Most centrally acting drugs depress respiration and would be expected to affect apnoea testing of brain stem function. However, the pharmacodynamic and pharmacokinetic properties of drugs are altered when patients are critically ill, so projections made from data derived from less ill patients or normal volunteers are inappropriate. The entry of drugs into the brain is also altered in some disease states, but there are few data relating to the effects of central depressant drugs in the situation of a disrupted blood-brain barrier or brain damage. Drug screens can assist in determining whether drugs are present, but correct interpretation of the results depends on close liaison between the clinical and laboratory staff. It is in the patient's interests to avoid termination of life support if any centrally active drug is present, unless there are other categorical factors consistent with irreversible brain death, such as demonstrated lack of cerebral blood flow.

Blood-Brain Barrier↗