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Biomedical subjects

R Garry

Publications and source records attributed to R Garry.

71 records · Page 4Linked to original sources

Human immunodeficiency virus-induced cytotoxicity for CD8 cells from some normal donors and virus-specific induction of a suppressor factor.

Several aspects of human immunodeficiency virus (HIV)-induced pathology in vitro warrant close examination to ascertain their role in the development of disease in vivo. The ability of HIV to produce cytopathology of CD4 cells has been well documented, although the extent and mechanism(s) may be varied. Further, immune suppression by HIV envelope (env) is well documented in vitro, but its importance in vivo remains unknown and the role of other HIV components in immune suppression has not been examined. We have exposed peripheral blood mononuclear cells (PBMC) from normal donors to ultraviolet-irradiated HIV (uv-HIV) at concentrations similar to those found in AIDS patient serum and determined that in some normal donors (3/7) depletion of CD8 cells as well as CD4 cells is demonstrable. Abrogation of phytohemagglutinin (PHA)-induced proliferation by uv-HIV was also examined in the same normal donors. Immune suppression, unlike CD4 cell killing, does not require intact virus and occurs at physiologically relevant concentrations of HIV. Furthermore, PBMC exposed to uv-HIV in the presence of PHA produce a heat- and protease-labile suppressor factor(s) following removal of virus, whether or not they are reexposed to PHA. Our results suggest that cell killing may be a more broad event than previously described, including the killing of at least CD8 cells either directly or indirectly. In addition, suppressor factors produced following exposure of patient lymphocytes to agents that induce proliferation may exacerbate the development of opportunistic infection.

Animals↗

Relationship between cervical condylomata, pregnancy and subclinical papillomavirus infection.

From a retrospective study of 415 sets of colpophotographs, 25 clinically obvious condylomata of the cervix were identified. Two morphologically distinct forms were found and termed erythrocondylomata and leukocondylomata on the basis of their colposcopic appearance. Erythrocondylomata are red, raised lesions with diagnostic large capillary loops. Those lesions were found in young women (mean age, 22 years) and associated with pregnancy in 72% of cases. They were observed to involute and disappear to the naked eye within a few months of the diagnosis. Colposcopic and histologic studies, however, indicated that the lesions could persist in subclinical form. Of eight such lesions studied, five showed histologic and colposcopic features of subclinical papillomavirus infection, and two showed histologic features compatible with cervical intraepithelial neoplasia (CIN). Leukocondylomata are brilliant white lesions associated histologically with a thick layer of keratin over a typical condylomatous base. Those lesions occurred at a later age (mean, 32 years), were not associated with pregnancy and tended to increase rather than involute with time. Epidemiologic studies have indicated that it is the young and sexually active who are at most risk of developing cervical cancer. This study indicated that it is this same group that is also at highest risk of developing erythrocondylomata of the cervix. Such lesions have been shown to involve the squamocolumnar junction and transformation zone when that area is most active and vulnerable. The progression of such lesions to subclinical papillomavirus infection and CIN suggests that they may be involved in the initiation of the cervical neoplastic process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A potential systematic error in using lysivane as inhibitor in the measurement of amniotic fluid acetylcholinesterase by the Ellman method.

The measurement of low levels of cholinesterase or acetylcholinesterase by the Ellman method requires correction for a non-enzymatic increase in absorption at 412 millimicron that is due both to non-enzymatic hydrolysis of the acetylthiocholine substrate and to modification of the colour reagent. The rate of increase in absorption is dependent on temperature and pH. Addition of an acidic solution of lysivane to the assay solution for selective measurement of amniotic fluid acetylcholinesterase gives rise to a shift in pH; the use of methanol is suggested as an easier method of dissolving the inhibitor and does not affect the pH of the assay, obviating any need to redetermine the background absorption. There is, however, no improvement in ability of the method to predict pregnancies associated with neural-tube defects.

Acetylcholinesterase↗

Particulate acetylcholinesterase in amniotic fluid and its implications for neural tube defect screening.

Acetylcholinesterase activity in mid-trimester amniotic fluid has been determined by a quantitative spectrophotometric method and a qualitative electrophoretic technique in a limited (76 samples) retrospective study. Differential centrifugation studies on amniotic fluid from normal pregnancies demonstrated the presence of particle-associated acetylcholinesterase sedimenting only at relatively high centrifugal forces. It is postulated that this particle-associated activity was a contributory factor to an observed false-positive incidence of 6.6% when quantitative acetylcholinesterase measurement was used to discriminate between normal pregnancies and those associated with neural tube defects. Discrimination on the basis of electrophoretic analysis of acetylcholinesterase resulted in no misclassification of pregnancies. Particulate acetylcholinesterase would not be expected to influence the interpretation of the electrophoretic pattern due to its size-related exclusion from gel pores. The implication of these observations in the accurate prenatal diagnosis of neural tube defects is discussed.

Acetylcholinesterase↗

Further observations on the effect of synthetic thyrotropin-releasing hormone in man.

Synthetic thyrotrophin-releasing hormone (TRH) given intravenously in doses of 50 mug or more causes a significant rise in serum thyroid-stimulating hormone (TSH) levels but has no effect on serum growth hormone, plasma luteinizing hormone, or plasma 11-hydroxycorticosteroids under carefully controlled basal conditions.The peak TSH response to intravenous TRH occurs at 20 minutes. The mild and transient side effects, which occur only after intravenous TRH, include nausea, a flushing sensation, a desire to micturate, a peculiar taste, and tightness in the chest. There is considerable variability in response to a given dose of TRH in the same subject on different occasions and in different subjects. Oral administration of TRH in doses of 1 mg and above causes a rise in serum TSH, maximal at two hours, a consistent response being obtained at doses of 20 mg and above. A rise in serum protein-bound iodine (P.B.I.) follows that of TSH, a consistent response being observed at 40-mg doses of TRH orally. Measurements of serum TSH after intravenous administration of TRH or of serum TSH or serum P.B.I. after oral TRH should prove useful tests of pituitary TSH reserve.

Administration, Oral↗

Thyroid-stimulating hormone response to synthetic thyrotrophin releasing hormone in man.

Synthetic thyrotrophin-releasing hormone, L-pyroglutamyl-L-histidyl-L-proline-amide, has been administered intravenously to euthyroid subjects in doses ranging from 1 to 200 mug. Its effect was assessed by serial measurements of serum thyroid-stimulating hormone (T.S.H.). A rise in serum T.S.H. was detectable five minutes after administration of 50 mug. of thyrotrophin-releasing hormone, reaching a maximum in 15 to 30 minutes, and then gradually declining over the next 120 minutes. Doses of 100 and 200 mug. of thyrotrophin-releasing hormone produced even greater rises of T.S.H. in some cases. The only side-effect noted was transient nausea with doses greater than 50 mug. Measurement of serum T.S.H. levels after administration of thyrotrophin-releasing hormone should prove a useful test of pituitary T.S.H. release and may help to distinguish pituitary and hypothalamic lesions.

Adult↗