Response to gamma radiation of mice with spontaneous chromosome instability (NZB mice).
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Biomedical subjects
Publications and source records attributed to C Bernard.
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Human embryonic cell cultures, infected with the Mouse sarcoma virus, complex (Moloney isolate), produced a virus that specifically transformed mink lung cells. The non-transforming helper virus could infect Mouse cells as well as a wide range of other mammalian cells. These observations could suggest the presence of either several viruses in the virus stock and/or stable recombinants.
1. An isolated frog semicircular canal was placed in a two-compartment perspex chamber which allowed the fluids bathing the inside (endolymph) and the outside (perilymph) of the canal to be replaced separately. Mechanical stimulation (MS) of the ampullar receptors was performed by sinusoidal cupular movement. 2. Streptomycin sulfate in the perilymph reduced promptly, strongly and reversibly nerve spontaneous activity (SA) recorded on the ampullar nerve. Streptomycin sulfate also reduced reversible and weakly the slow potentials recorded either near the crista ampullaris (Adc) or on the ampullar nerve (Ndc) and the modulation of firing rate (delta Fms) all these activities being evoked by a mechanical stimulation. 3. Streptomycin sulfate injected into ampullar endolymph reduced promptly and strongly the Adc, Ndc, and delta Fms. When its concentration was higher 0.2 mg/ml, the SA was also reduced about 40 min later. 4. It is concluded that streptomycin sulfate alters weakly and reversibly spike generation process and synaptic transmission; it inhibits strongly and reversibly the resting discharge and it inhibits strongly and may be partly reversibly the transduction mechanisms.
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Traumatic rupture of the descending thoracic aorta is lethal within 3 weeks in 95% of patients who do not undergo operation. In this series of 25 patients who were operated on, 84% have survived for 6 years and there have been no cases of paraplegia. The mechanism of injury is most important in the investigation of patients with traumatic injuries and must be sought either from the patient or from witnesses. A history of rapid deceleration (more than 60 km/h) following a highway collision was present in all our cases. Failure to wear seat-belts resulted in 70% of patients being ejected from a vehicle. A side-on collision resulting in lateral deceleration caused trauma to the intrathoracic aorta in 45% of cases. Vertical deceleration resulted from falls from great heights (bridge, overpass) in 25% of cases. Clinical signs of diagnostic importance were: arterial hypertension (60%), systolic murmur (35%) and the pseudocoarctation syndrome (25%). Pertinent signs on chest roentgenograms were present in 95% of cases and included widening of the mediastinum and blunting of the aortic knob. The authors conclude thoracic aortography should be carried out in trauma patients when two or more of the following are present: (a) history of rapid deceleration, ejection from a vehicle or lateral collision, (b) hypertension and (c) blunting or modification of the aortic knob. The presence of a pseudocoarctation syndrome is an absolute indication for aortography.
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A considerable increase in chromatid and chromosome breaks, as well as excessive fragmentation and "pulverization" of whole metaphase plates was observed in embryonic fibroblast cultures from New Zealand black mice. A C-type RNA virus with a xenotropic host range was isolated from the supernatant fluid of co-cultures of NZB cells and heterologous permissive cells (SIRC cell line). One of the NZB cultures produced this virus without amplification by co-cultivation after spontaneous transformation of the cells. NZB cells are supposed to lack normal restriction of complete xenotropic virus expression and to release this endogenous virus spontaneously at a high level. It is hypothesized that the excessive chromosome damage observed in these cell cultures is related to the permanent production of virus, thus indicating a chromosome breaking effect of endogenous viruses.
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We saw bone marrow necrosis in a case of acute myelomonocytic leukemia. The diagnosis was made during the patinet's life, and the bone marrow microcirculation was studied immediately postmortem. Histology and injection of the bone marrow arteries showed an acute microcirculation failure. The pathogenesis and possible relationship with soluble immune complexes was studied.
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The isoelectric point (PI) of the p30 polypeptide of members of the three known classes of mouse C-type endogenous viruses was determined both by column and by thin-layer gel isoelectric focusing. Each class was found to be characterized by a particular variant of p30 (isop30), with pI values of 6.1 for class I (ecotropic), 5.7 for class II (xenotropic), and 5.5 for class III (NZB, NIH, ATS124, also xenotropic). The 6.1-isop30 was found as a minor component of rat-grown NZB virus and of a number of laboratory strains of mouse C-type viruses.
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In order to study the distribution of somatostatin in the upper digestive tract in man, biopsies were taken through endoscopy or at surgery from the fundus, antrum, and duodenal bulb in 15 subjects with no gastroduodenal lesion, 12 patients with severe antral and/or fundic atrophy in the sampling area, 28 patients with an active duodenal ulcer, and 14 patients with a nonmalignant gastric ulcer. The specimens were extracted in 2 N acetic acid and tested for somatostatin content with a specific radioimmunoassay. In the control subjects, the somatostatin concentration (nanograms per milligram of wet weight) was 0.60 +/- 0.12 in the fundus, 1.68 +/- 0.33 in the antrum, and 1.35 +/- 0.30 in the duodenal bulb. Atrophy of the gastric mucosa was associated with a reduction of the somatostatin concentration in the fundus and the antrum. No significant variation was observed in the present series of patients with gastric ulcer. Duodenal ulcer was associated with a reduction of the somatostatin concentration in the antrum (P less than 0.02). These results indicate that somatostatin is widely distributed from fundus to duodenal bulb in adult human subjects, and that lower antral concentrations are observed in patients with duodenal ulcer.
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Cultures of cells derived from non-leukemic human tissues were submitted to treatments known to induce endogenous C-type viruses of a number of animal species. Virus expression was evaluated by reverse transcriptase (RT) assays in the growth medium. Of 20 cultures treated or untreated with bromodeoxyuridine, 18 were totally negative in RT assays. Of the 2 positive cultures, one was a human-mouse hybrid in which the induction of RT activity coincided with the expression of murine antigens. The other culture, a diploid strain which exhibited borderline enzymatic activity, was subjected to more detailed analysis after treatment with several chemical inducers and/or irradiation, but none of these procedures gave clearly positive results. The apparent lack of an endogenous virus synthesis in these human cells is discussed.
Delayed-type hypersensitivity (DTH) transfer to GAT was restricted by the I-A region of the major histocompatibility complex (MHC). Sensitized cells from F1 hybrid mice between responder and nonresponder strains transferred DTH to syngeneic F1 mice and to naive parental strain recipients of the responder but not of the nonresponder haplotypes. These results are interpreted to favor the postulate that the MHC-linked Ir genes exert their effects by coding for components which allow interactions between particular I region gene products and the region to form stable structures immunogenic for DTH T cells.
Endogenous ecotropic and xenotropic murine C-type viruses induced in K-Balb-3T3 cells treated with iododeoxyuridine (IdU) were selected by infection of appropriate indicator cells. The isoelectric point (p1) of the major viral polypeptide (p30) was found to be 6.1 for the ecotropic virus (class I), and 5.7 for the xenotropic virus (class II). An isoelectric form (iso p30) of pl 6.5 was observed in the initial induction peak. In addition, the pattern of cellular alteration in NRK cells at its onset varied according to the pseudotype, the class I pseudotype inducing round cell foci while the foci associated with the class II pseudotype consisted of fusiform cells.