Koro-like symptoms in a man infected with the human immunodeficiency virus.
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Biomedical subjects
Publications and source records attributed to I Heyman.
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Schizophrenia is characterised by the psychotic symptoms of hallucinations and delusions, accompanied by variable degrees of loss of insight. Whilst there is heterogeneity in the clinical profile, and presumably in the pathogenesis of what is currently called 'schizophrenia', it has become absolutely clear over the past decade that schizophrenic symptoms are consequent upon serious brain dysfunction. This new perspective has laid to rest a variety of 'crazy' theories, including the notion that mental illness was a myth, or that schizophrenia could be caused by faulty child rearing. The use of dopamine-blocking drugs has led to an improvement in symptom control, and diminished the need for prolonged hospital stays. It was hoped that the clear relationship between antipsychotic activity and dopamine blockade would help to elucidate the pathophysiology of schizophrenia, but to date no consistent abnormalities of the dopamine system have been found. Nevertheless, we have learned much about both the aetiology of schizophrenia and the origin of particular symptoms. Much of this has stemmed from increased understanding of the brain abnormalities underlying the disorder.
In 1987 a study was carried out at two upper secondary schools. The aim was to study the working conditions of teachers in a changing environment by interviewing different professionals in the school as well as students. In the last five years, the average age of students was found to have fallen by two to four years. Another finding was that the entrance requirements had been lowered. In the same five-year period the drop-out rates at one of the two schools had risen from 5/60 to 18/81. At the other school 5/30 dropped out in 1987. Many of the teachers interviewed reported their students to be open-minded and spontaneous but at the same time too immature to work in the medicare sector, especially in the psychiatric field. A tendency appeared for teachers to take on a more curative and supportive role. The teachers maintained certain minimum standards and students who did not pass their examinations were required to withdraw.
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Microelectrode recordings from the somata of rat dorsal root ganglion (DRG) cells were used to correlate their electrophysiological characteristics with sensitivity to locally applied capsaicin. Of the 80 cells tested, 17 responded to capsaicin by a rapid depolarization. These cells had low axonal conduction velocities (less than 1.4 m/s) and long duration action potentials, characteristic of C-cells. Some C-cells did not respond to capsaicin, and no A-cells, which had high conduction velocities and brief action potentials, did so. The effect of capsaicin on the current-voltage curve of C-cells suggested that it produced a conductance increase as well as a change in delayed rectification.
The presence of receptors for 1,25-dihydroxyvitamin D3 in the pituitary, pancreas, testis, and ovary has raised the question of a possible direct role for 1,25-dihydroxyvitamin D (1,25(OH)2D) in the regulation of hormone synthesis and secretion. To evaluate this problem, six children with the syndrome of resistance to 1,25(OH)2D with rickets and alopecia underwent dynamic tests of insulin, TSH, PRL, GH, and testosterone secretion. Oral glucose loading resulted in normal glucose curves, subnormal peak insulin responses of 12-20 microU/ml in three hypocalcemic patients, and normal peak serum insulin values of 30-40 microU/ml in two normocalcemic patients. Basal serum, TSH, PRL, T4, and T3 concentrations were normal in all patients. Peak serum TSH values after TRH were 11-17 and 16-32 microU/ml in the hypo- and normocalcemic patients, respectively. The PRL response to TRH stimulation in either hypocalcemic or normocalcemic patients was normal [mean 26.2 +/- 5.1 (SD) ng/ml]. Peak serum GH levels were greater than 8 ng/ml in all five patients studied after one or more of the various stimuli. Serum testosterone concentrations after hCG stimulation were normal in the three patients studied (4.1-8.0 ng/ml). Thus, in children with resistance to 1,25(OH)2D, we could find no significant abnormalities in hormone secretion from the pituitary, pancreas, and testis apart from those presumably due to the hypocalcemia itself.
Two boys suffering from the hemolytic-uremic syndrome (HUS) are presented. One of them developed four episodes of the disease beginning at infancy, the other one had at least two episodes which were associated with mild portal fibrosis of the liver. Between the attacks of the disease, the children were completely healthy, and no renal or hematological abnormalities were detected. Both patients are now physically and mentally well developed healthy young men. The relatioship between HUS and thrombotic thrombocytopenic purpura is briefly discussed.
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Substances that cause liver damage in humans were identified through a literature search conducted on Toxline and Medline. Using the same search strategy, species other than man were selected, in whom hepatic injury could be attributed to exposure to the identified substances. A total of 38 substances were identified as producing liver damage, manifested by either clinical chemistry or histopathology. The substances included 24 drugs, 9 industrial chemicals, 3 environmental agents, 1 pesticide, and ethanol. Twelve of the 36 compounds have been toxicologically evaluated in man, rodent, and non-rodent. Histopathologic liver damage was reported in all three species for 11 of these compounds. Only carbencillin produced histopathologic damage in man but not in either the rodent or non-rodent. Where clinical chemistry changes were reported for all three species categories, only eight substances induced similar reactions in all three species. Only with two substances did man and rodent react similarly (both positive), while the non-rodent was negative. The two substances were polychlorinated biphenyl (PCB) and tetrachlorethane. In the majority of the cases in which either or both histopathologic or clinical chemistry changes were reported for man or for the rodent or non-rodent, the changes that occurred were qualitatively similar. The rodent was as sensitive a predictor for hepatic effects as the non-rodent. Although it is impossible to predict how liver damage observed in a laboratory animal is correlated with human liver damage, hepatotoxicity in the rodent must be considered as indicative of potential hepatic damage in man.