Biomedical subjects
Publications and source records attributed to L Perry.
Circulating levels of prolactin, dehydroepiandrosterone sulphate (DHEAS) and testosterone (T) were measured in single blood samples from 115 normal women throughout the menstrual cycle. There was an inverse relationship between prolactin and both DHEAS and T. Subjects with high serum prolactin levels had significantly lower levels of DHEAS and T.
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Single serum progesterone determinations were made in 79 apparently normal women with a regular menstrual cycle. A normal range (40 subjects) was derived from the concentrations in the follicular phase and used to define an "anovular" range for luteal phase values (nine out of 39 subjects). The remaining luteal phase values were used to construct an "ovular" range for the luteal phase and, within this range, to define a group of values (less than the 20th centile) which could be described as a "defective luteal phase." The cut off limits between ovular and anovular and between normal and defective luteal phases were respectively two and four times the follicular phase median. It is proposed that the numerical findings of this study may be used as a rule of thumb for defining normality and abnormality from a single serum progesterone determination.
Synthetic CRF-41 has been given to 43 patients with hypothalamic, pituitary or adrenal diseases and contrasted with the responses in 20 normal subjects. In the normal subjects the mean increment in serum cortisol (+/- SE) was 276 +/- 38 nmol/l; the increments showed a significant negative correlation with the basal serum cortisol levels (r = -0.56; P less than 0.02). The mean peak serum cortisol was 662 +/- 34 nmol/l and the mean peak corticosterone was 28.6 +/- 3.8 nmol/l. There was a significant positive correlation between the peak serum corticosterone and cortisol concentrations (r = 0.84; P less than 0.0001). Dexamethasone pretreatment abolished the rise in cortisol in response to CRF-41. The peak serum cortisol following CRF-41 was not significantly different between the normal subjects and those patients with pituitary disease who had normal cortisol responses to insulin-induced hypoglycaemia. However, in individual patients the peak cortisol levels induced by hypoglycaemia were greater than, but significantly correlated with, those induced by 100 micrograms of CRF-41. Seven patients were ACTH deficient in response to hypoglycaemia, and of these six responded normally to CRF-41. Only one of these patients had a lesion clearly originating in the hypothalamus; four had pituitary tumours with suprasellar extensions and the remaining patient had idiopathic GH and ACTH deficiency. Our data suggest that these patients have a functional defect of ACTH secretion due to the failure of CRF to reach the corticotroph. Of the four patients with pituitary-dependent Cushing's disease who were on no treatment at the time of testing, three showed an exaggerated and one a normal response to CRF-41. These normal or enhanced responses of hypercortisolaemic patients with Cushing's syndrome contrast with the complete inhibition of the responses to CRF-41 in normal subjects given dexamethasone. In the treated patients with Cushing's syndrome and normal serum cortisol levels, those with pituitary-dependent disease showed an enhanced ACTH response to CRF-41 as compared with the ectopic ACTH group, but there was some overlap between the two groups. Acromegalic patients did not show a GH response to CRF-41. We conclude that administration of CRF-41 is a safe new method for investigating disorders of the hypothalamo-pituitary axis.
In order to define surface antigens unique to ependymal cells, spleen cells from C57/B16 mice immunized with a suspension of 70-80% purified isolated ependymal cells from syngeneic animals were fused with NS-1 myeloma cells. Five hybridomas were found which secrete monoclonal antibodies that recognize ependymal cells both by indirect immunofluorescence and radioimmunoassay. One of them, Epenl, appears to be a relatively specific surface marker of murine and rat ependymal cells, whereas the 4 others also recognize neurons, astrocytes, and/or oligodendrocytes. Absorption of Epenl with murine cerebral cortex did not affect its binding, whereas absorption with ependymal cells abolished it. Labeling of in vivo sections with Epenl demonstrates prominent binding to ependymal cells lining ventricular cavities. Epenl does not bind to neurons or astrocytes in culture, and binds only minimally to isolated oligodendrocytes. It does, however, recognize an antigenic determinant present in lung tissue.
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A 65-year-old man who had had acne conglabata since early adult life was treated with buserelin for advanced prostatic cancer. Within 1 month of starting therapy, the inflammatory acne had completely resolved and this coincided with remission of the carcinoma. Gonadotrophin-releasing hormone analogues may be useful in the treatment of resistant acne.
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Chlamydia trachomatis LGV-434 was grown in HeLa 229 cells. Benzylpenicillin completely inhibited the formation of infectious elementary bodies (EBs) at a concentration of 19 pmol/ml or higher and produced abnormally large reticulate bodies (RBs) in the inclusions at 30 pmol/ml or higher. The possible targets for penicillin in C. trachomatis were three penicillin-binding proteins (PBPs) which were identified in the Sarkosyl-soluble fractions of both RBs and EBs. The apparent subunit molecular weights were 88,000 (PBP 1), 61,000 (BPB 2), and 36,000 (PBP 3). The 50% binding concentrations of [3H]penicillin for PBPs 1 to 3 in EBs and RBs were between 7 and 70 pmol/ml. Such high susceptibility to penicillin was shown by an organism that did not have detectable muramic acid (less than 0.02% by weight) in preparations of either whole cells or sodium dodecyl sulfate-insoluble residues.
OKT3 monoclonal antibody, a human T cell mitogen, induced interferon production by cultured mononuclear cells at 10(-11) M concentrations. Interferon was secreted only under conditions wherein OKT3 was mitogenic, and production was correlated with cell proliferation. Thus, like mitogenesis, interferon secretion reached a peak 3 days after OKT3 stimulation, was inhibited by a factor(s) in human serum, and required 1000 times higher concentrations of Fab and F(ab')2 fragments of OKT3 for induction. The interferon was most likely of "gamma" (immune) type, because pH 2 and 56 degrees C treatments denatured it, whereas anti-alpha or -beta interferon antibodies did not. Mononuclear cells were fractionated into subpopulations that contained OKT4+ cells (helper/inducer T cells), OKT8+ cells (cytotoxic/suppressor T cells), and OKM1+ cells (monocytes) by combining sheep red blood cell rosetting and complement-mediated lysis using monoclonal antibodies against specific cell types. Both OKT4+ and OKT8+ cells proliferated upon OKT3 stimulation with the absolute requirement of OKM1+ cells. However, OKT4+ cells plus OKM1+ cells were necessary for the secretion of interferon. Studies with selective pretreatments with mitomycin C suggested that gamma-interferon was secreted by the OKT4+ cells and that the OKM1+ population subserved an accessory function.
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Dysphagia represents a varying group of swallowing difficulties commonly encountered in patients in both acute and community settings. It accompanies a variety of disease states, can be neuromuscular or mechanical/obstructive in origin and encompasses varied prognoses and outcomes. Its consequences include dehydration, malnutrition, bronchospasm, airways obstruction, aspiration pneumonia and chronic chest infection, social isolation, depression and detrimental psychosocial effects. Current "best evidence" in screening, assessment and management is of variable quality but demonstrates that nurses have an important role to play in interventions entailing multiprofessional collaboration within individually tailored programmes. Clear benefits for patients have been indicated. There are gaps in the knowledge base, especially in relation to psychosocial effects and treatment strategies and the nursing contribution in this area.
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