The health services' connection: report from home care.
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Biomedical subjects
Publications and source records attributed to M Nelson.
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Supernatants from cultured mouse and human tumour cells, but not mouse or guinea-pig fibroblasts, inhibited the production of a lymphokine, macrophage chemotactic factor, by PHA-stimulated mouse spleen cells. The supernatants affected spleen cells from old, but not young, mice. They were most active if added at the start of the spleen cell culture and did not act by binding phytohaemagglutinin (PHA). The active material had an approximate molecular weight, on membrane filtration, of 1000-10,000 and could be bound to and eluted from Con A-Sepharose. Tumour supernatant factor(s) of similar molecular weight inhibited the production of interleukin 1 (lymphocyte activating factor) in response to lipopolysaccharide by stimulated thioglycollate-induced peritoneal exudate macrophages, but not by Corynebacterium parvum-activated macrophages. Similar tumour-produced material has been found to inhibit the early phase of delayed-type hypersensitivity reactions in older mice. It is suggested that this effect is due, at least in part, to inhibition of interleukin 1 production leading to inhibition of lymphokine production.
Psychological testing was done on 20 subjects at various altitudes (sea level, 3,8,10 m, and 5,000 m) during a 35-d mountaineering expedition to Denali (Mt. McKinley). Intellectual functioning and personality changes were studied. While little variation was noted at the lower altitude, at 5,000 m there was a marked deterioration in cognitive ability. This was accompanied by a sharp increase in paranoia and obsessive-compulsiveness and smaller increases in depression and hostility.
Mouse resident peritoneal macrophages were cultured with supernatants from cultures of tumor cells and normal cells, then tested for their capacity to phagocytose opsonized sheep erythrocytes (SRBC). Most tumor cells produced inhibitory material but some did not (HeLa, EL-4). Conversely, nonmalignant cells generally did not produce active material though some (Chang B cells) did. Inhibition was not noticeable until after 13 hr contact with tumor supernatant and then became progressively more pronounced at 24 and 48 hr. Phagocytic capacity recovered only partially on reincubation with fresh medium. Inhibition was caused by material of approximate M.W. less than 1,000 (by membrane filtration), which also inhibited macrophage migration in vitro but had no effect on delayed-type hypersensitivity reactions or tumor growth in vivo. There was no species specificity and normal macrophages from various sources were susceptible, although activated or stimulated macrophages were wholly or partly resistant. Tumor carriage was associated with an initial decrease in phagocytic capacity of resident peritoneal macrophages, followed by an increase then a second decrease, although the cells remained susceptible to the inhibitory effect of tumor supernatant in vitro. Depression of phagocytosis was more marked in the presence of normal mouse serum and less marked in the presence of human serum than in the presence of fetal calf serum. Phagocytosis of zymosan and pinocytosis of colloidal gold by mouse macrophages were also depressed by tumor cell products.
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Explored whether psychiatric diagnostic differences exist between male and female, black, white and Hispanic-American patients seen in the Department of Psychiatry/Community Mental Health Center of a major hospital in the South Bronx, New York. Admission data on almost 2,000 patients furnished demographic and diagnostic characteristics of the patients. Sex and ethnic differences were found. Suggestions are offered as to why various subpopulations are perceived differently.
Examined diagnostic differences between black, white, and Hispanic-American patients (N = 1968) seen in psychiatric outpatient clinics of a large hospital in the South Bronx. Distribution of diagnoses also was compared statistically in relation to the diagnostician's ethnicity. Results indicated statistical differences between the patient's ethnicity and psychiatric diagnosis, as well as interactions between the therapists' ethnicity and these variables. Implications of the findings were discussed, and suggestions were offered for future research.
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Clinical examinations and radiographic skeletal surveys have been carried out in 15 patients with foetal alcohol syndrome. Fusion of the capitate and hamate bones in the carpus was bilateral in one patient and unilateral in two. All three had accessory ossification centres at the proximal ends of both second metacarpals. Two of these patients also had radio-ulnar synostosis. Digital shortening, which was demonstrated by pattern profile analysis, was very variable in degree and anatomical distribution. Other skeletal changes of uncertain significance were a "beaten copper" appearance of the calvarium in four patients, and coxa valga in one other. Diagnosis of the foetal alcohol syndrome warrants consideration in any individual presenting with carpal fusion or with radio-ulnar synostosis.
Studies were made of the effects of various treatments on the growth in mouse feet of isografts of two methylcholanthrene-induced fibrosarcomas: C-4, of CBA/J mice, and A-2, of A/J mice. The isografts were prepared by pronase digestion of subcutaneous tumors and were injected as unseparated cell suspensions or as tumor-cell-enriched suspensions after depletion of infiltrating host inflammatory cells. The recipient mice were untreated or treated with reserpine, sublethal whole body irradiation, cyclophosphamide, or corticosteroids. Depletion of host cells from the inoculum resulted in increased growth from the same number of tumor cells. Reserpine treatment decreased the growth of both tumors, whether unseparated or tumor-cell-enriched, and whether injected into the foot or the flank. Irradiation, cyclophosphamide pretreatment, and corticosteroid pretreatment decreased the growth of normal inocula or enriched inocula or both. The effects of cyclophosphamide and corticosteroids were apparently not due to cytotoxicity to tumor cells. Normal resident peritoneal cells increased tritiated thymidine uptake by tumor cells in vitro. Sedimentation velocity separation showed the largest cells to be the most potent. It is suggested that some hot inflammatory reaction is necessary for optimal tumor growth and that murine hosts produce not only cells with antitumor effects but also cells, possibly a subpopulation of macrophages, that potentiate tumor growth.
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Experiments were carried out to determine whether the growth of tumors could be influenced by local inflammatory reactions induced by mitogens; Gram-negative bacterial lipopolysaccharide (LPS), concanavalin A (Con A) and phytohemagglutinin (PHA). Mice received injections, beneath the footpad or subcutaneously in the flank, of cells of syngeneic chemically induced fibrosarcomas with or without varying doses of mitogen. In the footpad (a) LPS caused a dose-dependent increase in the size; (b) Con A caused a decrease in the size of one of the three tumors, the decrease being inversely related to the dose of Con A; (c) PHA caused a dose-dependent decrease in the size of all three tumors: (d) PHA caused much smaller macroscopic inflammatory reactions than LPS or Con A. Subcutaneously injected tumor growth was inhibited by all three agents. Subcutaneous tumors contained a higher proportion of host inflammatory cells when mitogens had been mixed with the tumor inoculum. It is concluded that mitogens that can induce inflammatory reactions in mice can also bring about some suppression of tumor growth but that the depression is site-dependent and not clearly related to the apparent intensity of inflammation.