[The short-term effect of a television programme on premenstrual symptoms assessed in general practice].
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Biomedical subjects
Publications and source records attributed to C Pedersen.
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Sister chromatid exchange points (SCE points) on individual chromosomes were studied in cultured lymphocytes from 11 monozygotic (MZ) and nine dizygotic (DZ) same-sexed pairs by means of sequential Q-banding and BUdR-Giemsa techniques. No statistically significant variation between unrelated individuals with respect to SCE points on specific chromosomes was found. Intrapair differences in the number of SCE points on specific chromosomes were not significantly smaller between MZ twin partners as compared with DZ partners. The results suggest that genetic factors do not play any major role in the frequency and distribution of SCE in normal subjects.
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An inbred sibship with corneal opacities and deficient alpha-L-iduronidase activity showed signs of a Hurler/Scheie phenotype. The children were of normal intelligence. In one of the children, electron microscopy of the conjunctiva showed membrane-bound intracellular vacuoles and the electroretinogram was extinguished. The consanguinity of the parents is taken to indicate the presence of homozygosity of a mutant gene different from both the Hurler and Scheie mutants, thus rejecting the concept of a genetic compound in our patients.
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The presence of antibodies to HTLV-III and markers of active hepatitis B virus replication was examined in a longitudinal study of 33 consecutive male homosexual HBsAg carriers. The mean follow-up time was 37 months (range = 4 to 109 months). All patients were initially hepatitis B virus DNA-positive and HBeAg positive. Antibodies to HTLV-III were detectable in eight patients while they were positive for both of these markers. One of them cleared hepatitis B virus DNA and seroconverted from HBeAg to anti-HBe. This corresponds to an annual clearance/seroconversion rate of 4% (95% confidence limits = 0 to 15%). In two patients, antibodies to HTLV-III appeared after clearance of hepatitis B virus DNA and HBeAg, and in one of them, hepatitis B virus DNA reappeared. Among the 25 patients negative for HTLV-III antibodies, the annual hepatitis B virus DNA clearance rate was 20% and HBeAg to anti-HBe seroconversion rate was 11% (95% confidence limits = 11 to 31% and 4 to 20% respectively). The observed hepatitis B virus DNA clearance rates in the two groups were significantly different (p less than 0.05). Disease activity, as determined by transaminase levels, was significantly lower in HTLV-III-infected individuals as compared to individuals without HTLV-III infection (p less than 0.05). Infection with HTLV-III may extend the period of active viral replication or even reactivate hepatitis B virus replication and seems to diminish inflammatory disease activity in chronic HBsAg carriers.
Traditional Giemsa-stained thick blood films were compared with 2 fluorescence microscopy techniques, acridine orange (AO) staining of thin blood films and the quantitative buffy coat (QBC) method, for the microscopical diagnosis of malaria. Of 200 samples examined, 141 were positive by Giemsa staining, 146 by AO and 137 by QBC. Overall sensitivities for the 2 fluorescence techniques compared to Giemsa staining were good: AO 97.9% and QBC 93.6%. However, with parasitaemias < 100/microL the QBC sensitivity fell to 41.7% whereas that of AO was 83.3%. Both AO and QBC were unable to differentiate accurately between individual malaria species. We conclude that the QBC technique alone cannot replace Giemsa-stained thick blood films for most purposes in an African setting. However, apart from species differentiation, the AO method is an appropriate technique for the laboratory diagnosis of malaria in developing countries.
Twenty-two insulin-dependent diabetic patients participated in a double-blind, cross-over study, where treatment with semisynthetic human NPH insulin (Novo Industri) was compared with porcine NPH insulin (Nordisk). Each treatment period lasted 8 weeks. Blood glucose level, glycosylated haemoglobin, insulin requirements, and frequency of hypoglycaemic events were compared. No difference was found in 24-hour blood glucose profiles. Fasting blood glucose level was 8.3 mmol/l during treatment with human insulin and 8.7 mmol/l during treatment with porcine insulin (p less than 0.1). Mean HbA1c was 7.7% at the end of study compared to 9.5% at baseline (p less than 0.01), but this decline in HbA1c was independent of the treatment regimen. Forty-six hypoglycaemic events occurred during treatment with human insulin compared to 39 events during treatment with porcine insulin. No difference was found regarding insulin requirements during the study. It is concluded that semisynthetic human NPH insulin is indistinguishable from porcine NPH insulin with respect to 24-hour blood glucose profile, HbA1c level and insulin dose requirements.
Human immunodeficiency virus type 1 (HIV1) is neurotropic. One of the morphological changes that is seen in patients with acquired immunodeficiency syndrome (AIDS) is cerebral atrophy affecting various structures including the neocortex. The cause of atrophy is not known. The total number of neocortical neurons was estimated in formalin fixed brains of 12 males with AIDS and 12 male controls matched for age and height. The mean number of neocortical neurons was 16.0 x 10(9) (coefficient of variation = 0.11) in the AIDS patients compared with 21.9 x 10(9) (coefficient of variation = 0.22) in the controls, a difference of approximately six billion (p < 0.005, 2-tailed). The global neuronal loss was 37%, and affected all four neocortical lobes. Ten patients did not have a history of central nervous system symptoms; two patients had a history of dementia. The number of neurons in the AIDS cases was not associated with dementia. AIDS is the first disease in which a global loss of neocortical neurons has been demonstrated using unbiased stereological methods. The loss of more than one third of the neurons may partly explain the cortical atrophy. Focal neuron loss has been reported by several authors, but none have been based on unbiased methods. In this group of AIDS patients the severe loss of neurons did not correspond to neurological deficits.
PURPOSE: To assess the effect of changing antiretroviral therapy in patients initially treated with saquinavir hard gel capsule (hgc). METHOD: A retrospective cohort study comparing the virological and immunological responses in antiretroviral-naïve patients initially treated with a regimen of saquinavir-hgc, zidovudine, and lamivudine, with patients receiving either ritonavir or indinavir on a background of zidovudine and lamivudine. RESULTS: Twenty-nine patients starting with saquinavir-hgc as the protease inhibitor (PI) component were compared to 58 patients starting with ritonavir (n = 16) or indinavir (n = 42). Median follow-up time was 30 and 33 months, respectively. Twelve, 18, 24, and 30 months after starting a regimen including saquinavir-hgc, 72%, 50%, 4%, and 0% of patients still received this PI. At these time points, 35%, 24%, 59%, and 74% of the patients in the saquinavir group obtained an HIV-RNA <500 copies/mL compared to 76%, 72%, 66%, and 65% in the indinavir/ritonavir group. No significant difference in CD4 count between the two groups was observed. CONCLUSION: We found that saquinavir-hgc, in combination with nucleoside reverse transcriptase inhibitors, suppressed viral load insufficiently in HIV patients naïve to antiretroviral therapy. However, the suboptimal effect of saquinavir-hgc seems reversible after optimizing the antiretroviral regimen, at least for the short term.
PURPOSE: Previous studies have shown that agents modulating the cAMP/PKA pathway have a beneficial effect on immune reconstitution in HIV-infected individuals. Here we evaluate the effect of buspirone on immune function as measured by CD4 and CD8 T-cell counts, CD4/CD8 T-cell ratio, HIV viral load, and response to pokeweed mitogen (PWM) in antiretroviral naive HIV-1-infected individuals. METHOD: Twenty-three HIV-infected patients with CD4 T-cell counts above 300 per microL were enrolled in a 6-month double-blinded placebo controlled trial. No patients received antiretroviral therapy during the study. Blood samples were drawn prior to treatment, after 1 week, 1 month, 3 months, and 6 months, and as a follow-up sample 1 month after completion of study. RESULTS: A significant decrease in CD8+ T-cell counts (p =.02) and an increase in CD4/CD8 ratio (p =.0003) in buspirone-treated patients compared to placebo-treated patients was observed. There were no significant differences in CD4 T-cell counts, HIV viral load, or proliferative response to PWM between those receiving placebo and those receiving buspirone. CONCLUSION: Buspirone treatment leads to significant changes in CD8 T-cell count and in CD4/CD8 ratio. Thus, agents affecting the adenosine 3', 5'-cyclic monophosphate/protein kinase A type 1 (cAMP/PKA-1) pathway may be candidates for positive immune modulation in patients with HIV-1 infection.
Previous immunocytochemical studies of pleomorphic adenomas have demonstrated consistent labeling with glial fibrillary acidic protein (GFAP). Cross-reactivity with other intermediate filaments of similar structure and chemical composition has been suggested to account for this seemingly inappropriate pattern of immunoreactivity. To investigate further this phenomenon, we examined five pleomorphic adenomas by immunoelectron microscopy. Ultrastructural features were similar to those described by other investigators, with ductal epithelium being surrounded by myoepithelial cells and modified cells becoming detached to form the isolated stellate and spindle cells of the stroma. As part of this process, many neoplastic myoepithelial cells appeared to lose their specialized ultrastructural features, assuming a rather undifferentiated appearance. Single and double immunoelectron microscopic labeling showed vimentin filaments in all these neoplastic myoepithelial cells. In contrast, GFAP filaments were identified only in the most undifferentiated cells. Such restriction of GFAP filaments to an ultrastructurally definable subset of neoplastic cells provides strong evidence against nonspecific staining due to cross-reactivity. Given the previously described coexpression of vimentin and GFAP by neoplastic cartilage, it appears likely that this immunophenotype in neoplastic myoepithelial cells reflects early chondroid differentiation.