GTP-stimulated binding of initiator-tRNA to ribosomes directed by f2 bacteriophage RNA.
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Biomedical subjects
Publications and source records attributed to M Revel.
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Study of the mechanisms by which interferon (IFN) treatment of cells induces resistance to virus infections has been complicated by the multiple biochemical changes induced. Over 20 proteins are increased by IFN, including the double-stranded (ds) RNA-activated protein kinase, (2'-5') oligo A synthetase, surface proteins such as the major histocompatibility complex (MHC) proteins, and various proteins with unknown functions. The availability of cloned complementary DNAs for several IFN-induced proteins now allows us to probe their roles in IFN action. For instance, the murine Mx protein has been shown to confer resistance, to influenza virus. We studied chinese hamster ovary (CHO) cell clones expressing high constitutive levels of (2'-5') A synthetase as a result of transfection with the cDNA encoding the enzyme form which has a relative molecular mass (Mr) of 40K. Elevated enzyme correlates directly with resistance to infection by a picornavirus such as Mengo, but does not make the cells resistant to vesicular stomatitis virus (VSV).
An experimental model of disc herniation in tail discs of rats is described. Constant result on nucleus hernia and intervertebral narrowing were obtained by an easy manipulation on numerous rats. Intradiscal injection of aprotinin produced a widening of the disc height. Trypsin, collagenase, chymopapain, and hyaluronidase induced a narrowing of disc height; trypsin induced macroscopic necrosis of the soft surrounding tissues; and collagenase had a destructive effect on nucleus pulposus, annulus fibrosus, and even on end-plates. Chymopapain and hyaluronidase acted mainly on nucleus pulposus. Hyaluronidase could be of interest as a nucleolytic drug and needs further studies on optimal dosage and lack of side effects in the surrounding tissues before injecting it into human discs.
Pure recombinant human IL-6 inhibits growth of T47D, MCF-7 and SK-BR-3 human breast carcinoma and OVCAR-3 ovarian carcinoma cells in cultures. Subcloning of the breast ductal carcinoma T47D cells yields clones with high and low sensitivity to the growth inhibitory effect of IL-6. The subclones vary 40 fold in their sensitivity for inhibition of colony formation in sparse cultures and 200 fold for inhibition of thymidine incorporation in subconfluent cultures. Binding studies with 125I-rIL6 show that T47D cells and their subclones, as well as SK-BR-3 and MCF-7 cells, express high-affinity receptors for IL-6. The number and affinity constant of these receptors are comparable to those on lymphocytic and myeloid cells, and show no correlation with the high or low sensitivity phenotype. Proliferation of the breast cancer cells is inhibited by IL-6 in a cell density dependent manner, and is not due to a cytotoxic effect. In addition, IL-6 induces a morphological change with loss of epithelial characteristics and of cell-cell adhesion. Sensitivity to growth inhibition by IL-6 is independent from that of IFN-beta 1, IFN-gamma or TNF.
Human skin fibroblasts synthesize and secrete complement Factor B, a component of the complement alternative pathway, when stimulated by mediators of inflammation such as lipopolysaccharide and various cytokines. Recombinant IL-6/IFN-beta 2 (E. coli) stimulates Factor B synthesis in fibroblasts but the effect is strongly potentiated by the addition of IFN-gamma. When both cytokines are added, the skin fibroblasts secrete significant amounts of biologically active Factor B detectable in a hemolysis test. This cooperative effect of IL-6, which is made by most tissue cells and monocytes and of IFN-gamma which is made by T-lymphocytes may play a role in local inflammatory processes. IL-6 and IFN-gamma also cooperate in the induction of (2'-5') A synthetase, a mediator of IFN action.
From the tomodensitometric examination of 9 cases of hollow foot, the authors present their methodology, reminding the difficulties encountered, and they analyze the results. After a first tomodensitometric study including 16 cases of normal feet, confirming the existence of a suro-achilleo-plantar system by studying correlations between plantar intrinsic muscles and muscles of the posterior compartment of the leg, they establish: the advantage of this method of evaluation of section areas and evaluation of the maximum traction force of the intrinsic muscles of the foot (reproducibility), the disorganization of this anatomo-functional unit in hollow foot syndromes.
Historical aspects and anatomophysiologic features of posterior lumbar vertebral joints are summarized and results of arthrography of 55 joints presented, together with a simple, original method for performing this examination. Normal anatomic appearances condition understanding of principal lesions encountered, particularly with respect to compression of adjacent nerve structures.
Findings on arthrography of posterior lumbar spine joints in 55 patients were compared with those reported in the literature. Two major degenerative lesions of these joints, diverticula and cysts, can provoke back pain and symptomatic nerve compression. Whereas diagnosis of a cyst is dependent mainly on computed tomography imaging, that of a diverticulum is ensured by arthrography, an investigation which also has a therapeutic aim since it allows infiltrations to be performed.
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The clinical studies reviewed here indicated the usefulness of topical application of Human-fibroblast-derived (Beta) interferon (Hu1FN-B) in treatment of Adeno-8 Epidemic-keratoconjunctivitis. A week treatment with 2-5 x 10(5) reference units daily doses, starting early as possible, reduced the length of the disease from 22 day to a week, and almost totally prevented the appearance of subepithelial keratitis which occurred in 57% of the control group. Possibly interferon should be given also prophylactically to individuals exposed to contagion. Our results encourage further investigation on the Hu1 FN-B use as a drug for treatment and prevention of viral infection.