Leukocyte histamine release to thiopental.
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Biomedical subjects
Publications and source records attributed to J Peters.
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The combination of various concentrations of acyclovir and vidarabine or its 5'-monophosphate usually produced an additive interaction with various strains of herpes simplex virus types 1 and 2 in Vero cells. Similarly, certain combinations of these drugs were more effective than the individual drugs in decreasing the mortality and increasing the mean day of death of mice inoculated intracerebrally with herpes simplex virus type 2. Neither antagonism nor interference was noted for any of the in vitro or in vivo combinations. The increased antiviral activity was determined not to be secondary to toxic effects of the drugs. Although viruses resistant to either vidarabine or acyclovir developed readily in cell culture, no evidence of cross-resistance was obtained. Furthermore, in the presence of the two drugs, mutants resistant to vidarabine, acyclovir, or vidarabine/acyclovir could not be isolated. These findings suggest that combinations with these antivirals, which are currently being evaluated singly for the therapy of severe forms of herpetic infection, could prove clinically useful if increasing numbers of resistant viral strains are observed.
To evaluate the ability of gray-scale renal ultrasonography to distinguish cystic neoplasms from benign cysts, 182 cysts or cyst-like masses were reviewed retrospectively by three radiologists with varying degrees of experience in nephrosonography. All cases were proved by needle puncture or surgery. An unequivocal diagnosis of "cyst" based solely on ultrasonography was 98% accurate, with 2% being due to hematomas, localized hydronephrosis, or septa within the cyst. No cystic neoplasms were mistaken for benign cysts. These results indicate that experienced observers using proper technique will rarely be in error in distinguishing non-neoplastic cystic masses from cystic neoplasms by articulated-arm gray-scale ultrasonography, and that routine needle puncture may be unnecessary in such cases.
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We present here the initial characterization of a new repair system which is induced in actively growing cultures of Escherichia coli and which repairs a major fraction of lethal damage produced by near-UV (310-400 nm) light. This system is different from the error-prone 'SOS' repair system for DNA, known to be induced in E. coli by treatments which damage DNA and/or inhibit DNA replication, such as irradiation by far-UV (254 nm) light or X rays, thymine starvation or treatment with naladixic acid or mitomycin C. The SOS response requires induction of an 'X' protein, the product of the recA gene, whereas the inducible repair system described here utilizes proteins distinct from the X protein.
An electrophoretically detectable variant of pyruvate kinase (EC 2.7.1.40) has been found in the house mouse Mus musculus. The variant was seen in all tissues examined except liver and red cells. The gene (Pk-3) determining this electrophoretic variation is inherited as an autosomal codominant located on chromosome 9. Our data confirm that the genetic determination of pyruvate kinase in liver and red cells is separate from that in other tissues. In addition, our results indicate that the muscle (M1) and kidney (M2) pyruvate kinase isozymes share at least one genetic determinant and may in fact be determined by the same structural gene.
HSC and CFUs are not identical. HSC are no longer considered to be a homogeneous population but an age-structured spectrum of cells (Schofield, 1978). CFUs, which have been identified only in rodents and with certainty only in mice, may be a sub-set of HSC required by mice, perhaps controlled by the W locus and virtually eliminated in double W mutants. A dichotomy of CFUs and HSC has also been demonstrated by Wiktor-Jedrzejczak et al. (1977); ++ bone marrow treated with anti-Thy 1.2 serum lost its curative properties for W Wv anaemic mice with CFUs being unaffected.
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54 cases of retinal branch vein occlusion, 19 of which received photocoagulation treatment, were reviewed to assess the value of photocoagulation in this disease. Our results suggest that the effect of photocoagulation in the treatment of macular edema is not convincing. This finding is in contrast to the main stream in literature. On the other hand the treatment's beneficial effect in destroying or preventing neovascularisations in the course of RBVO seems established and may even be enhanced with the technique described. On the basis of our results and theoretical considerations, some guidelines for the care and treatment of RBVO patients are suggested.
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