Metallic mercury vapor poisoning simulating mucocutaneous lymph node syndrome.
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Biomedical subjects
Publications and source records attributed to R Adler.
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Incubation of herpes simplex virus type 1-infected cells with succinyl-concanavalin A, a derivative of the jack bean lectin concanavalin A, resulted in the decreased production of virus. The mode of inhibition by the lectin was unclear. No effect was apparent on the level of viral DNA synthesis. However, incubation of infected cells with increasing concentrations of the lectin appeared to result in a decrease in the quantity of viral protein produced within the cell. A reduction in the virus titer of 57 to 64% was observed upon direct incubation of extracellular virus in the presence of 50 to 100 micrograms of succinyl-concanavalin A per ml.
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An analysis of the etiology of acute viral hepatitis in 172 hospitalized patients showed that 70.9% suffered from hepatitis A (HA), 12.2% from hepatitis B (HB), 1.7% from infectious mononucleosis and 15.1% (26 cases) from non-A, non-B hepatitis. Patients who had received blood transfusions during the 6 mo preceding the onset of the disease were not included in the present survey. The male:female ratio in the patients with non-A, non-B hepatitis was 1:88; 73% were Ashkenazic and 27% non-Ashkenazic Jews. The ethnic distribution of patients with non-A, non-B hepatitis was similar to that of patients with HA but differed from that of HB patients (only 41% Ashkenazic). Thirty-eight percent of the non-A, non-B group had had contact with jaundiced patients during the 6 mo preceding the onset of the disease, and 46% were students or soldiers. The clinical course of the disease was, on the whole, milder than that of HB and similar to that of HA. Since many cases of non-A, non-B hepatitis are anicteric, it is concluded that the disease is a significant problem in Israel.
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A 19-year-old boy with congenital hypoplastic anemia (CHA) treated with long-term steroid therapy, presented with septic shock caused by Streptococcus pneumoniae. Peripheral blood smears revealed Howell-Jolly bodies and postmortem examination revealed the absence of the spleen, splenic vein and splenic artery. We have found no association of CHA and congenital asplenia previously reported in the literature or in a review of 12 additional patients with CHA at this institution. The case is reported to bring attention to the concurrence of these two rare conditions in one individual and to discuss the possible implications of this association.
Psychosocial adaption during or after somatic illness is relatively little studied--quite in difference to the better known psychosocial predictors of somatic illness. This study is concerned with a group of 31 female patients who suffered from a terminal vascular disease (primary vascular pulmonary hypertension)--an iatrogenic disease which with high probability is the consequence of a drug for weight reducing (Menocil), prescribed by their family doctors to these moderate overweight middle aged women. Psychosocial adaptions was assessed on a 5-point-scale, including the following dimensions: work-situation, socio-economic conditions, family adaption, social activities. Psychosocial adaption before illness was very good (just 10% below maximal values). Two or three years after illness started, however, there was a highly significant drop in all dimensions (most significant in "work" and "social activities"). To some extent success or failure of psychosocial adaption had a predictive power for the terminal course of this illness. Possible interaction between course of illness and psychosocial adaption is discussed and illustrated. There was also a significant correlation between psychosocial adaption and defense-processes.
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We have recently reported the existence within chick embryo heart cell conditioned medium (HCM) of two distinct and independently assayable factors. One agent, ciliary neuronotrophic factor (CNTF), supports the in vitro survival of 8-day chick embryo ciliary ganglionic (CG) neurons. The other factor, polyornithine-attachable neurite promoting factor (PNPF) is required for extensive neuritic growth from these same CNTF-supported CG neurons. In the present study we have examined the occurrence of PNPF activity within nearly 100 different conditioned media using our previously described chick CG bioassay system. From this screening we conclude that: (1) PNPF production is a rather widespread property of cultured neural as well as non-neural cells; and (2) the chick bioassay is sensitive to PNPF activity from all the species examined, including mouse, rat, human and chick cells. We next examined the effects of 3 representative PNPF-containing conditioned media (from chick heart, mouse Schwann and rat Schwannoma) on neurite production from 3 other peripheral ganglionic neuronal cultures (8-day chick dorsal root, 11-day chick sympathetic, and neonatal mouse dorsal root ganglia) as well as 4 central neuronal cultures (8-day chick embryo telencephalon, optic lobe and spinal cord and neonatal mouse cerebellum). The results of these studies indicate: (1) that the peripheral neurons exhibit a dramatic increase in neurite production in response to PNPF which can be easily recognized both qualitatively and quantitatively; whereas (2) the CNS neurons showed essentially no PNPF-induced increase in neurite production. The sole exception to the latter was the appearance within the chick spinal cord cultures of a neuronal population which extended very long neurites in response to PNPF.
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DNA levels were measured in synovial fluids and sera of 106 patients with rheumatoid arthritis (RA), osteoarthritis (OA), gout, pseudogout, and posttraumatic arthritis (TRA). In synovial fluids, the highest concentration was found in rheumatoid arthritis (mean +/- SE 18 +/- 3 microgram/ml for seropositive and 9 +/- 1 microgram/ml for seronegative variants), gout and pseudogout (17 +/- 3 microgram/ml). In contrast, the levels in patients with OA or acute TRA were very low: 0.8 +/- 0.1 microgram/ml an 1.1 +/- 0.2 microgram/ml, respectively. The differences between the means of the first disease group and OA or TRA is statistically significant. A similar pattern was observed for DNA levels in the circulation: in rheumatoid arthritis, the mean concentration was 135 +/- 28 ng/ml and 164 +/- 39 ng/ml for seropositive and seronegative RA, respectively. Again the levels in OA and TRA were much lower, 52 +/- 18 ng/ml and 0 ng/Ml, respectively. The latter are not significantly different from the mean levels of 95 normal, healthy controls (14 +/- 3 ng/ml), whereas the concentration of DNA in the serum of RA patients is significantly higher than in OA, TRA, or normal controls. Serial determinations of DNA and other criteria of disease activity (leukocytes and protein levels in synovial fluid, blood sedimentation rate) in individual patients revealed a strong correlation of elevated values with active episodes. THe results suggest that these parameters reflect tissue damage.
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