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101.
J.M. Katz S.J.M. Skinner T. Wilson D.H. Gray 《Prostaglandins & other lipid mediators》1983,26(4):545-555
Mouse calvaria were maintained in organ culture without serum additives. Basal active resorption, as measured by 45Ca and hydroxyproline release, was significantly inhibited to 74% control levels by indomethacin (1.4 × 10−7 M). Prostaglandin F and prostaglandin E2 production, determined by radioimmunoassay, were both significantly lowered by this concentration of indomethacin. DNA, protein and hydroxyproline synthesis, as indices of cell toxicity, were unaffected by low concentrations of indomethacin, while concentrations of 1.4 × 10−6M inhibited protein synthesis (p<0.005). In the presence of indomethacin (1.4 × 10−7M) both PGE2 and PGF2α stimulated resorption in a dose-dependent manner, with PGE2 being the more potent. Neither prostaglandin affected hydroxyproline synthesis at low concentrations, but PGE2 had a marked inhibitory action at a higher concentration (10−6M). In combination, the effects of PGE2 and PGF2α showed no evidence of synergism or any antagonistic action. The study shows that in vitro calcium and hydroxyproline resorption in the unstimulated mouse calvaria are inhibited by indomethacin at concentrations measured in serum during human therapy. The decreased PGF and PGE2 production associated with this decreased bone resorption in the presence of non-toxic concentrations of indomethacin would suggest a role for these prostaglandins in maintaining the basal resorption of cultured bone. 相似文献
102.
103.
Collagen-induced arthritis in mice. Relationship of collagen-specific and total IgE synthesis to disease. 总被引:3,自引:0,他引:3
J F Marcelletti J Ohara D H Katz 《Journal of immunology (Baltimore, Md. : 1950)》1991,147(12):4185-4191
The relationship between production of IgE and collagen-induced arthritis in mice was examined. Collagen-specific IgE was produced as a consequence of immunization of DBA/1 mice with chicken type II collagen emulsified in CFA. We observed a rise in collagen-specific IgE antibody levels at the onset of CIA clinical and histologic signs in DBA/1 mice. This rise in IgE paralleled that of IgG2a anticollagen antibodies, an isotype implicated in the pathogenesis of CIA by other laboratories. The collagen-specific IgE contained in the plasma of mice with CIA could arm basophils for Ag- (collagen) dependent degranulation. Collagen-specific IgE may thus contribute to CIA by promoting mast cell degranulation in the synovia of susceptible mice immunized with chick type II collagen; but, further work is required to establish such a role for IgE in CIA. However, genetic differences in disease susceptibility could not be accounted for by quantitative differences in collagen-specific IgE production. Further, comparable levels of IgE anticollagen antibodies were observed in animals with active CIA and after spontaneous remission, thereby confirming that the presence of such antibodies is insufficient for disease. Total IgE levels peaked just before spontaneous remission indicating active production of IL-4. IL-4 was administered to animals with CIA to determine if this lymphokine could be involved in the remission process. IL-4 facilitated remission of CIA. Enhanced total IgE production may thus be a marker for activation of Th2 cells that produce lymphokines such as IL-4 and IL-10, factors that may be involved in the spontaneous remission process. 相似文献
104.
ADP-ribosylation of actin by Clostridium botulinum C2 toxin resulted in a depolymerization of filamentous F-actin and an increase of monomeric G-actin in cultured hepatocytes. Simultaneously the de novo synthesis of actin was largely reduced, while the synthesis of albumin and of other proteins was not significantly impaired. The specific decrease of actin mRNA to 30% of the control indicates a down-regulation of actin synthesis at a pretranslational level. On the other hand, treatment with the mycotoxin phalloidin resulted in an increase of F-actin and a decrease of monomeric G-actin. Under this condition the de novo synthesis of actin was specifically enhanced and the level of actin mRNA was increased to 600% of the control. The data suggest an autoregulatory control of the actin synthesis. 相似文献
105.
M Carey J Kolman D A Katz L Gradoville L Barberis G Miller 《Journal of virology》1992,66(8):4803-4813
106.
Identification and induction of keratinocyte-derived IL-10. 总被引:23,自引:0,他引:23
107.
Ellen S. Dierenfeld Nancy Katz Jack Pearson Frank Murru Edward D. Asper 《Zoo biology》1991,10(2):119-125
Retinol (n = 17 spp.) and α-tocopherol (n = 9 spp.) concentrations in whole fish utilized for captive animal feeding programs were determined by high-performance liquid chromatography (HPLC) following routine storage and preparation after commercial purchase by two zoological institutions. Vitamin A activity was calculated from retinol values and ranged from 55 IU/100 g (immature herring) to >2,000 IU/100 g (salmon) on an as-fed basis. α-Tocopherol values, a measure of vitamin E activity, ranged from 0.9 IU/100 g (butterfish) to 12.3 IU/100 g (tilapia) on a wet basis. Vitamin levels in whole fish were intermediate to values previously quantified for muscle or liver tissues alone. Vitamin concentrations in fish livers were quantified separately in seven of these species; liver contributed 35–63% of total retinol measured and 8–34% of total α-tocopherol. Based on these analyses, whole fish commonly fed in zoos, aquariums, and marine zoological parks would appear to meet vitamin A requirements established for most species without additional supplementation, whereas levels of vitamin E quantified indicate a need for supplementation of diets for piscivores. 相似文献
108.
Prostaglandin release by normal and osteomyelitic human bones 总被引:1,自引:0,他引:1
D Plotquin S Dekel S Katz A Danon 《Prostaglandins, leukotrienes, and essential fatty acids》1991,43(1):13-15
The release of prostaglandin E (PGE) and prostacyclin (as 6-keto PGF1 alpha) by human osteomyelitic bone, compared with normal (control) bone, incubated in vitro was evaluated. Prostacyclin was the main arachidonic acid metabolite released by normal human bone, and similar quantities were released by osteomyelitic bone. However, PGE production was 5-30-fold higher in osteomyelitic bone, compared with control, thus becoming the major prostanoid in this disease. It is concluded that PGE production is probably involved in the inflammatory and/or bone resorption processes that occur in osteomyelitis. 相似文献
109.
Skewed X inactivation in a female MZ twin results in Duchenne muscular dystrophy. 总被引:16,自引:7,他引:9 下载免费PDF全文
C S Richards S C Watkins E P Hoffman N R Schneider I W Milsark K S Katz J D Cook L M Kunkel J M Cortada 《American journal of human genetics》1990,46(4):672-681
One of female MZ twins presented with muscular dystrophy. Physical examination, creatine phosphokinase levels, and muscle biopsy were consistent with Duchenne muscular dystrophy (DMD). However, because of her sex she was diagnosed as having limb-girdle muscular dystrophy. With cDNA probes to the DMD gene, a gene deletion was detected in the twins and their mother. The de novo mutation which arose in the mother was shown by novel junction fragments generated by HindIII, PstI, or TaqI when probed with cDNA8. Additional evidence of a large gene deletion was given by novel SfiI junction fragments detected by probes p20, J-Bir, and J-66 on pulsed-field gel electrophoresis (PFGE). Immunoblot analysis of muscle from the affected twin showed dystrophin of normal size but of reduced amount. Immunofluorescent visualization of dystrophin revealed foci of dystrophin-positive fibers adjacent to foci of dystrophin-negative fibers. These data indicate that the affected twin is a manifesting carrier of an abnormal DMD gene, her myopathy being a direct result of underexpression of dystrophin. Cytogenetic analysis revealed normal karyotypes, eliminating the possibility of a translocation affecting DMD gene function. Both linkage analysis and DNA fingerprint analysis revealed that each twin has two different X chromosomes, eliminating the possibility of uniparental disomy as a mechanism for DMD expression. On the basis of methylation differences of the paternal and maternal X chromosomes in these MZ twins, we propose uneven lyonization (X chromosome inactivation) as the underlying mechanism for disease expression in the affected female. 相似文献
110.
Gary N. Cherr Ashley I. Yudin David F. Katz 《Development, growth & differentiation》1990,32(4):353-365
The mammalian oocyte-cumulus complex contains an extracellular matrix rich in hyaluronate. Recently, the microstructure of the hamster cumulus extracellular matrix was described (52). In the present work, we investigated the organization of this matrix. We employed freeze-substitution methodologies to investigate ultrastructural effects of various treatments, including sperm enzymes, on the matrix. Protease treatment resulted in disruption with a loss of the fibrillar structures and some expansion; in contrast, hyaluronidase treatment completely solubilized the matrix. EDTA extraction revealed that the fibrils are composed of fine filaments. A discrete region of the matrix immediately surrounding the oocyte, the corona radiata, was resistant to EDTA disruption. We found that hyaluronate is an ubiquitous constituent of the microstructural elements of this extracellular matrix. The matrix exhibits a carbohydrate:protein ratio of approximately 2:1. SDS-PAGE revealed that glycosylated polypeptides are bound to the matrix. The lectins LCA and WGA had differing affinities for these polypeptides, and bound ubiquitously to the intact matrix. The present data suggest that glycoprotein-hyaluronate interaction is critical for maintenance of the cumulus extracellular matrix microstructure and for its physical properties. 相似文献