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Biomedical subjects

G Knox

Publications and source records attributed to G Knox.

18 recordsLinked to original sources
PubMed1995

Country watch: Malawi.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Phenytoin as a countermeasure for motion sickness in NASA maritime operations.

Seasickness is the most prevalent form of motion sickness and is an operational problem during Space Shuttle Solid-fueled Rocket Booster (SRB) retrieval. Phenytoin has been shown to protect against motion sickness induced by Coriolis stress. We exposed SRB recovery personnel to off-vertical rotation and sea motion after phenytoin or placebo. Phenytoin blood levels of at least 9 micrograms/ml were protective against motion sickness at sea. No change in susceptibility to nitrogen narcosis was seen in divers in chamber tests at 460 KPa. Phenytoin was used during performance of critical and hazardous tasks during training and actual SRB recovery operations. Phenytoin is an effective operational countermeasure for motion sickness for selected SRB crewmembers.

Adult↗
PubMed1991

Unlinked surveillance of the prevalence of HIV infection in antenatal patients in the West Midlands, England.

In the course of an unlinked, anonymous survey of anti-HIV seroprevalence among antenatal patients in the West Midlands, carried out between November 1986 and March 1990, seven out of 202,012 patient samples were anti-HIV seropositive. Although the numbers of women infected by heterosexual contact are still low in this region, it is likely that HIV infection is no longer limited to well-defined, male risk groups. It is therefore increasingly important to monitor the course of the epidemic through large-scale unbiased surveys of the heterosexual population in order to plan future preventive and health-care strategies.

Adult↗
PubMed1991

Case-control studies of screening procedures.

Case-control studies of different screening procedures have been reported. Cases of the detectable disease, and controls without the disease, were compared with respect to their previous screening histories. Measures of the protective value of the test were calculated from the difference. The inductive basis of these studies is re-examined and it is concluded that all claims to have measured the protective value of a screening test through such means are potentially or actually flawed. The reasons for the inductive failures are: (a) The ratio between the retrospective screening frequencies depends critically upon unmeasured parameters other than procedural efficacy; the ratio is therefore not capable on its own of providing an estimate of the protection afforded: (b) Almost all screens among reported case and control groups have been negative, and it is a matter of prior fact that a negative test does not protect anyone. Only the positive tests protect. Direct analogies with drug and vaccine trials, from which the concept of a 'protective value' originates, are therefore false.

Case-Control Studies↗
PubMed1988

Beta-endorphin production by the fetal Leydig cell: regulation and implications for paracrine control of Sertoli cell function.

Immunohistochemical evidence has indicated that beta-endorphin (beta EP) is present in the Leydig cells of fetal, neonatal, and adult mice and hamsters. In vivo experiments suggest that hCG and/or testosterone may increase the synthesis and release of the peptide from the Leydig cell compartment. Since cultured fetal Leydig cells have considerable potential for long term studies and elucidation of trophic hormone actions in vitro, we evaluated beta EP production in this system. Fetal Leydig cells were maintained in culture for 5 days in medium with 1 microgram ovine LH added every third day in the presence or absence of inhibitors of cholesterol (aminoglutethimide) or pregnenolone metabolism (cyanoketone and spironolactone), or known regulators of beta EP production [dexamethasone (DEX)]. Media were assayed for testosterone and beta EP by RIA methods. Beta EP accumulation over 3 and 5 days was markedly increased by inhibitors of steroid biosynthesis (1.5-fold) and reduced by DEX only after treatment for 5 days (by 50%). Acute hCG stimulation significantly increased beta EP levels by 5- to 9-fold in all conditions tested. Inhibition of Leydig cell steroid biosynthesis markedly increased basal and hCG-stimulated beta EP output (by 150-200%). In contrast, DEX reduced basal and hCG-stimulated beta EP production (by approximately 50%). HPLC analysis of cultured pooled media revealed that the beta EP immunoreactivity eluted at the retention time of authentic rat beta EP. The pattern of beta EP stimulation was not reflected by testosterone levels that were low or undetectable in controls and under conditions in which spironolactone/cyanoketone or aminoglutethimide were present; most importantly, inhibition of steroid biosynthesis markedly increased beta EP levels. In addition, beta EP (10(-7) M) did not affect testosterone production, and opiate binding was not detected on Leydig cells. The lack of degradation of this opioid peptide in the fetal cultures contrasted with results from adult cultures and provided an ideal system for studies of the regulation of this peptide in Leydig cells. These results demonstrate that beta EP is released from fetal Leydig cells in culture and that acute stimulation of Leydig cells by hCG can enhance beta EP secretion. These changes are not mediated by testosterone. In contrast, testosterone or its metabolites may exert negative autocrine modulation of beta EP production.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Acquisition of estradiol-mediated regulatory mechanism of steroidogenesis in cultured fetal rat Leydig cells.

The inability of the fetal and immature Leydig cell to be desensitized by gonadotropin treatment, a characteristic of the adult cell, is attributed to the absence of an estrogen-mediated regulation of the androgen pathway. Cultures of fetal rat Leydig cells were employed to analyze this differential response. The fetal rat Leydig cells revealed low aromatization capacity, undetectable estradiol production, a low level of estrogen receptors, and a minimally detectable level of an estradiol-regulated protein. However, exogenous estradiol caused up-regulation of its own receptor, increase of an estradiol-regulated protein, and induction of a steroidogenic lesion at the microsomal level, resulting in decreased androgen production. This estrogen-mediated enzymatic inhibition resembles that observed in gonadotropin-desensitized adult Leydig cells. The absence of this regulation in fetal life is likely due to insufficient aromatase activity, with lack of consequent receptor-mediated estrogen action. The cultured fetal Leydig cell provides a useful model to elucidate the molecular mechanism involved in the development of estradiol-mediated desensitization.

Androgens↗
PubMed1984

Sorbitol accumulation is altered in type 1 (insulin-dependent) diabetes mellitus.

Intracellular sorbitol accumulation has been implicated as an aetiological factor for many of the complications of diabetes mellitus. Erythrocyte sorbitol is found in higher concentration in Type 1 (insulin-dependent) diabetic patients than in normal subjects. When sorbitol accumulation is corrected for its immediate precursor glucose (sorbitol/glucose ratio), the polyol accumulation remains significantly greater in erythrocytes from the Type 1 diabetic. Erythrocytes from Type 1 diabetic patients exposed to normal extracellular glucose concentrations for 3 h in vitro, accumulate more sorbitol and fructose than normal cells in the same incubation system. Near-normalization of plasma glucose in Type 1 diabetic patients for 12 h did not result in normal erythrocyte sorbitol levels. The increased sorbitol accumulation in erythrocytes from Type 1 diabetic subjects may reflect similar activity in the lens and nerve in long-standing diabetes. This increased sorbitol production was found in most, but not all, individuals with diabetes and appears to be an acquired characteristic. Those factors influencing enhanced tissue sorbitol accumulation may be important in the aetiology of diabetes-associated complications.

Adolescent↗
PubMed1980

Red cell sorbitol: an indicator of diabetic control.

Intact human erythrocytes accumulate intracellular sorbitol in response to the medium's glucose concentration during in vitro incubations. Sorbitol was identified and measured both enzymatically and by gas-liquid chromatography. The sorbitol produced is most likely a result of the activity of aldose reductase, since (1) a low glucose concentration in the medium elicits this response, and (2) this activity is completely blocked by tetramethylene glutaric acid, a specific inhibitor of aldose reductase. Erythrocyte sorbitol levels in insulin-dependent diabetics are clearly above those of nondiabetics after an 8 h fast. A good correlation exists between red cell sorbitol content and coincident plasma glucose concentrations. Individual exceptions to this rule exist, however, and suggest that red cell sorbitol levels may provide information about in vivo polyol pathway activity that may be important in the pathogenesis of diabetes-associated complications.

Blood Glucose↗
PubMed1978

Concentrations of 24,25-dihydroxyvitamin D and 25-hydroxyvitamin D in paired maternal-cord sera.

Mean serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)2D) and 25-hydroxyvitamin D (25OHD), measured by competitive radioassays, were significantly higher in maternal serum than in cord serum of term infants in both black and white subjects. There were positive correlations between maternal and cord levels of both metabolites of vitamin D. Serum concentrations of 24,25(OH)2D and 25OHD were significantly lower in white pregnant subjects than in nonpregnant women. In utero levels of 24,25(OH)2D and 25OHD probably reflect maternal stores of these metabolites.

Dihydroxycholecalciferols↗
PubMed1978

Transcatheter arterial embolization of a traumatic lumbar artery false aneurysm.

The case of a false aneurysm of a lumbar artery secondary to penetrating trauma is presented. Problems of diagnosis are outlined, emphasizing the value of ultrasound, computerized tomography, and angiography. The early use of angiography is strongly advocated in cases of suspected post-traumatic bleeding. The use and value of therapeutic transcatheter embolization is discussed.

Abdominal Muscles↗