[Plastic surgery of the eyelids in small animals. I. Injuries, scar contractures, tumors].
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Biomedical subjects
Publications and source records attributed to M Keller.
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Depressed inpatients with psychotic features were compared to those without them in terms of demographic features, depressive symptoms at intake and family history. These variables were then used to compare patients with mood-congruent psychotic features to those with mood-incongruent psychotic features. Patterns of familial psychopathology were similar for psychotic and non-psychotic patients. In accord with other studies, the families of mood-incongruent patients had slightly more schizophrenia and significantly less depression than did the families of mood-congruent patients. Depressive symptoms, particularly those used to define major depression and melancholia, were more severe in psychotic patients. Moreover, these particular depressive symptoms were more likely to distinguish mood-congruent from mood-incongruent patients than were other depressive symptoms. Thus mood-congruent psychotic features accompanied a more typical depressive syndrome than did mood-incongruent psychotic features.
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An earlier report described symptoms and background features in depressed probands grouped by polarity: bipolar I, bipolar II, and nonbipolar. The present study made similar comparisons among relatives with a lifetime history of major depression. The 73 relatives with bipolar II disorder had the highest rates of marital disruption, psychopathology in the previous month, nonserious suicide attempts, and nonaffective syndromes and were the youngest when first treated.
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In the National Institute of Mental Health Collaborative Study of the Psychobiology of Depression, six-month follow-up evaluations are available for 24 patients with schizoaffective disorder (depressed type), 56 with psychotic depression, and 274 with nonpsychotic major depression. Outcome for patients with schizoaffective depression was significantly worse than for patients with nonpsychotic depression. The psychotic depression group held an intermediate position on most outcome measures and on psychosocial measures had outcomes significantly worse than those of the nonpsychotic group. Recovery rates assumed a very similar pattern in another cohort admitted more than 40 years ago and followed up without somatic treatment. Follow-ups of 12, 18, and 24 months are available for proportions of each diagnostic group. Survival curves suggest similar outcomes in psychotic depression and nonpsychotic depression, whereas outcomes in schizoaffective depression remain disparate. These trends together with family history studies suggest that a small proportion of patients with schizoaffective disorder, depressed type, will have a long-term course consistent with schizophrenia. Moreover, these data show that outcome studies of schizoaffective disorder must control for follow-up length and the effects of psychosis per se.
The functional capability of antigen-stimulated breast milk cells to produce an immunologic mediator was examined. Colostrum and comparison peripheral blood samples were obtained from ten women, two to four days postpartum, and supernatants from PPD-stimulated mononuclear cell cultures were assayed for the lymphokine, monocyte chemotactic factor. Five of the ten women studied had a history of a positive tuberculin skin test and one had received BCG immunization. Peripheral blood lymphocyte cultures and colostrum cell cultures from four of these six women produced monocyte chemotactic factor. These results demonstrated the functional capability of antigen-stimulated colostral cells to produce immunologic mediators.
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Professional raters who were blind to proband diagnosis used the schedule for affective disorders and schizophrenia (SADS-L) and the Research Diagnostic Criteria (RDC) to evaluate 1,210 first-degree relatives of 327 probands with primary major depression, participating in the family sub-study of the NIMH Collaborative Study of the Affective Disorders--Clinical Branch. Bipolar II probands were significantly more likely to have bipolar II relatives than were non-bipolar or bipolar I probands. Bipolar II probands were slightly more likely than non-bipolar probands and slightly less likely than bipolar I probands to have relatives with bipolar I illness. Similar patterns have emerged in two other recently reported family studies of bipolar II illness. Taken together, these data suggest heterogeneity among patients with bipolar II depression. Some appear to be genotypes for bipolar I illness, while a small proportion may be genotypes for non-bipolar illness. A third group, of undetermined size, may breed true.
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A variety of pretreatment-treatment protocols were applied to rats with ARF induced by the subcutaneous injection of 6 mg of HgCl2 per kilogram body weight. Renin depletion induced by DOCA-saline pretreatment was associated with protection against HgCl2-induced ARF only when the saline diuresis was maintained by drinking 1% NaCl after injury. Twenty-four dehydration followed by free access to tap water annihilated the protective effect of DOCA-saline pretreatment despite maintained depletion of renal renin. Continuous intravenous loading with saline and furosemide, although increasing renal renin levels, afforded as much protection as saline loading alone. Ethacrynic acid, which did not increase salt excretion in our rats, as well as water diuresis, failed to be protective. A loose correlation was found between he amount of histological damage to the convoluted parts of the proximal tubules and the degree of renal functional impairment. Thus protection against HgCl2-induced ARF was independent of the renal renin level but closely related to urinary NaCl excretion after the injury. Saline diuresis could act by relieving or preventing tubular obstruction.
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The effect of bezafibrate on serum lipids, lipoproteins and the apoproteins A-I, A-II and B was studied in 18 patients with primary hypercholesterolaemia. Total cholesterol was lowered by 20% (P less than 0.05), LDL-cholesterol by 24% (P less than 0.05), and apo B by 14% (P less than 0.05), which is comparable to the effect obtained with anion exchange resins but with far fewer side-effects. HDL increased significantly during bezafibrate treatment both by measurement of HDL-cholesterol (+54%, P less than 0.05) and by the determination of HDL-apoproteins A-I (+ 19%, P less than 0.05) and A-II (+ 23%, P less than 0.05). This increase of HDL and the decrease of triglycerides was maintained for 6 weeks of placebo treatment after cessation of bezafibrate, while serum total and LDL cholesterol as well as apo B returned to their baseline levels.