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11.
Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C. 相似文献
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13.
Localization of a gene for otosclerosis to chromosome 15q25-q26 总被引:5,自引:0,他引:5
Tomek MS; Brown MR; Mani SR; Ramesh A; Srisailapathy CR; Coucke P; Zbar RI; Bell AM; McGuirt WT; Fukushima K; Willems PJ; Van Camp G; Smith RJ 《Human molecular genetics》1998,7(2):285-290
Among white adults otosclerosis is the single most common cause of hearing
impairment. Although the genetics of this disease are controversial, the
majority of studies indicate autosomal dominant inheritance with reduced
penetrance. We studied a large multi- generational family in which
otosclerosis has been inherited in an autosomal dominant pattern. Five of16
affected persons have surgically confirmed otosclerosis; the remaining nine
have a conductive hearing loss but have not undergone corrective surgery.
To locate the disease- causing gene we completed genetic linkage analysis
using short tandem repeat polymorphisms (STRPs) distributed over the entire
genome. Multipoint linkage analysis showed that only one genomic region, on
chromosome 15q, generated a lod score >2.0. Additional STRPs were typed
in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and
D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis
gene.
相似文献
14.
Duncan WC; Illingworth PJ; Young FM; Fraser HM 《Human reproduction (Oxford, England)》1998,13(9):2532-2540
The molecular mechanisms involved in luteolysis are still unclear in the
primate. This study aimed to investigate the effect of induced luteolysis
on the ovarian luteinizing hormone (LH) receptor and the steroidogenic
enzyme, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in the marmoset
monkey. Luteolysis was induced in the mid-luteal phase either directly by
systemic prostaglandin F2alpha (PGF2alpha), or indirectly by LH withdrawal
using systemic gonadotrophin releasing hormone antagonist (GnRHant)
treatment. The LH receptor was studied by isotopic mRNA in-situ
hybridization and in-situ ligand binding and 3beta-HSD expression was
studied using isotopic mRNA in-situ hybridization and immunohistochemistry.
Induced luteolysis was associated with a reduction in the expression of LH
receptor (P < 0.0001) and 3beta-HSD mRNA, closely followed by a
reduction in the LH receptor (P < 0.05) and 3beta-HSD protein
concentrations within 24 h. There were no differences in the findings
whether luteolysis was induced with PGF2alpha or GnRHant. This study shows
that disparate mechanisms to induce luteolysis in the primate result in an
identical rapid loss of the LH receptor and 3beta-HSD. In conclusion,
induced luteolysis leads to rapid loss of the steroidogenic pathway in
luteal cells.
相似文献
15.
Hendrickx J; Dams E; Coucke P; Lee P; Fernandes J; Willems PJ 《Human molecular genetics》1996,5(5):649-652
X-linked liver glycogenosis type II (XLG II) is a recently described X-
linked liver glycogen storage disease, mainly characterized by enlarged
liver and growth retardation. These clinical symptoms are very similar to
those of XLG I. In contrast to XLG I patients, however, XLG II patients do
not show an in vitro enzymatic deficiency of phosphorylase kinase (PHK).
Recently, mutations were identified in the gene encoding the liver alpha
subunit of PHK (PHKA2) in XLG I patients. We have now studied the PHKA2
gene of four unrelated XLG II patients and identified four different
mutations in the open reading frame, including a deletion of three
nucleotides, an insertion of six nucleotides and two missense mutations.
These results indicate that XLG II is due to mutations in PHKA2. In
contrast to XLG I, XLG II is caused by mutations that lead to minor
structural abnormalities in the primary structure of the liver alpha
subunit of PHK. These mutations are found in a conserved RXX(X)T motif,
resembling known phosphorylation sites that might be involved in the
regulation of PHK. These findings might explain why the in vitro PHK
enzymatic activity is not deficient in XLG II, whereas it is in XLG I.
相似文献
16.
17.
Chlorozotocin, an anti-tumour agent lacking bone marrow toxicity at therapeutic doses: effects on lymphocyte subpopulations in mice. 下载免费PDF全文
R I Fisher G L Mandell F Bostick M G McMenamin T Anderson 《Clinical and experimental immunology》1980,39(2):416-425
Chlorozotocin is a new nitrosourea anti-tumour drug that does not produce bone marrow suppression at therapeutic doses in mice. CDF1 mice which were injected i.p. with a dose lethal to 10% of animals within 60 days (LD10), 20 mg/kg, developed a 50% reduction in circulating peripheral blood lymphocytes without a decrease in circulating granulocytes by day 3. Spleen weight also decreased markedly. The percentage of spleen B and T cells, determined by immunofluorescence with goat anti-mouse IgG and rabbit anti-mouse brain antisera, did not differ in control and chlorozotocin-treated mice. However, the ability of residual spleen cells to proliferate in response to phytohaemagglutinin, concanavalin A, pokeweed mitogen, and allogeneic cells was significantly suppressed although the lipopolysaccharide response was not reduced. The ability of the mice to respond to a primary immunization with sheep red blood cells was not significantly impaired. Therefore, chlorozotocin has a cytotoxic effect on both B and T cells but selectively inhibits the proliferative capacity of T cells. B cell proliferation and B cell function as measured in a primary antibody response were not reduced. These studies suggest chlorozotocin may be useful as an immunosuppressive drug as well as an anti-tumour agent. 相似文献
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20.
B M Weichman L S Hostelley S P Bostick R Levi L W Chakrin 《International archives of allergy and applied immunology》1981,64(4):456-463
Immunologic histamine release was evoked from the sensitized fragmented cardiac and pulmonary tissue of the cynomolgus monkey by a reverse anaphylactic reaction. Ventricular and pulmonary tissue released a similar fraction (approximately 6%) of the total tissue histamine when challenged with antihuman IgE, presumably reflecting the 'active' sensitization of the monkey in vivo. Passive sensitization of these tissues in vitro resulted in significantly greater immunologic histamine release in 6 of the 14 ventricles and d a similar fraction (approximately 6%) of the total tissue histamine when challenged with antihuman IgE, presumably reflecting the 'active' sensitization of the monkey in vivo. Passive sensitization of these tissues in vitro resulted in significantly greater immunologic histamine release in 6 of the 14 ventricles and d a similar fraction (approximately 6%) of the total tissue histamine when challenged with antihuman IgE, presumably reflecting the 'active' sensitization of the monkey in vivo. Passive sensitization of these tissues in vitro resulted in significantly greater immunologic histamine release in 6 of the 14 ventricles and in the lungs. The antiallergic compounds, disodium cromoglycate and SK&F 64398, inhibited immunologic histamine release from passively sensitized monkey ventricular tissue. These results demonstrate that ventricular histamine may be immunologically released and that this release process can be pharmacologically inhibited in a manner similar to that of pulmonary tissue. 相似文献