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Previous reports indicate that amphotericin B (AmB) and amphotericin methyl ester (AME) are potent adjuvants and polyclonal B-cell activators, and that most mouse strains can be classified as high or low responders to AmB and AME. In the present study, an inbred strain with very high plasma cholesterol concentration (HC strain) proved to be a low responder. Responses of HC mice to other immune stimuli were normal, suggesting that HC lymphoid cells expressed selectively weak responses to AmB and AME. Plasma levels of low-density lipoproteins (LDL), very-low-density lipoproteins (VLDL), and high-density lipoprotein subfraction (HDL2) were very much higher in HC mice than in AKR mice, an AmB-high responder strain. Low responses in vitro to AME were observed with lymphoid cells from HC mice and from AKR----HC bone marrow chimeras, i.e., AmB-high responder strain lymphocytes from a low responder host. However, enhanced AME responses were induced by a 2- or 48-hr preincubation of splenocytes from either HC or AKR mice in medium containing lipoprotein-depleted fetal calf serum. Taken together these studies indicate that plasma lipoproteins can inhibit lymphocyte responses to AME; this seems to account for the low AmB and AME responses of the HC strain. The mechanism of this lipoprotein-induced inhibition remains obscure, but it cannot be accounted for by competitive binding of AmB by lipoproteins. 相似文献
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F P Cappuccio N D Markandu G W Beynon A C Shore B Sampson G A MacGregor 《BMJ (Clinical research ed.)》1985,291(6490):235-238
Seventeen unselected patients with mild to moderate essential hypertension and whose average supine blood pressure after two months'' observation with no treatment was 154/100 mm Hg were entered into a double blind randomised crossover study of one month''s treatment with magnesium aspartate (15 mmol magnesium/day) and treatment with placebo for a further month. This preparation of magnesium was well tolerated and did not cause diarrhoea. Despite a significant increase in plasma magnesium concentration and a significant increase in urinary excretion of magnesium while taking magnesium aspartate there was no fall in blood pressure compared with either treatment with placebo or values before treatment. The results provide no evidence for a role of dietary magnesium in the regulation of high blood pressure and are contrary to recent speculations. 相似文献
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Endogenous prostaglandins modulate histamine-induced contraction in canine tracheal smooth muscle 总被引:1,自引:0,他引:1
We studied the role of endogenous prostaglandins in modulating the histamine response of canine tracheal smooth muscle (TSM) in vitro. Indomethacin (INDO) (10(-7) - 10(-5) M), a cyclooxygenase and prostaglandin synthesis inhibitor, significantly increased maximum histamine-induced tension (Tmax) and decreased the concentration of histamine required to produce 50% of Tmax (EC50). Acetylsalicylic acid (10(-5) -5 X 10(-4) M), another less potent cyclooxygenase inhibitor, also decreased EC50. Neither the lipoxygenase inhibitor nordihydroguaiaretic acid nor the leukotriene antagonist FPL 55712 had any effect on histamine-induced tension in INDO-pretreated TSM. INDO reduced the standard deviation of EC50 from 0.47 in control TSM (n = 51) to 0.26 in INDO-pretreated TSM (n = 31) (P less than 0.02). High-pressure liquid chromatography established prostacyclin (PGI2), through its degradation product 6-oxo-PGF1 alpha, as the predominant prostaglandin produced by canine TSM. Exogenous PGI2 caused a concentration-dependent relaxation of histamine-contracted TSM. In the tissue bath, spontaneous efflux of 6-oxo-PGF1 alpha from TSM, as measured by radioimmunoassay, averaged 4.7 ng . g muscle-1 . min-1 and increased to 10 ng/g muscle (n = 10, P less than 0.001) with administration of histamine. The isometric tension produced by histamine (10(-4) M) was inversely linearly correlated with the log concentration of endogenous 6-oxo-PGF1 alpha (r = 0.81, P less than 0.01). Our results are consistent with an important role for endogenous bronchodilating prostaglandins, probably prostacyclin, in determining both the histamine sensitivity of canine TSM in vitro and its variability among individual animals. 相似文献
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用放射免疫成斑法研究了甲型肝炎病毒FM-175株的理化稳定性和灭活条件,证明甲型肝炎病毒理化稳定性与其它肠道病毒相似,具有广范围的pH(2~10)稳定性;Mg~(++)和Ca可增强其热稳定性,不能抵抗冷冻干燥,但对热的抵抗力明显高于普通肠道病毒,可被紫外线迅速杀灭,也可被多种消毒剂如3~8%的甲醛液,50~90%的乙醇,2%的石炭酸及400ppm的有效氯等杀灭,但可抵抗0.1%甲醛液,2~5%的来苏儿及200ppm的有效氯1小时以上,本研究工作为甲型肝炎病毒的理化性状、保存及消毒条件等提供了实验数据。 相似文献
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Herpes simplex virus type 2 mutagenesis: characterization of mutants induced at the hprt locus of nonpermissive XC cells. 总被引:3,自引:1,他引:2
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In a previous report, herpes simplex virus type 2 (HSV-2) was shown to increase the frequency of mutation at the hypoxanthine phosphoribosyltransferase (hprt) locus of nonpermissive rat XC cells (L. Pilon, A. Royal, and Y. Langelier, J. Gen. Virol. 66:259-265, 1985). A series of 17 independent mutants were isolated after viral infection together with 12 spontaneous noninfected mutants to characterize the nature of the mutations induced by the virus at the molecular level. The DNA of the mutants isolated after viral infection was probed with cloned HSV-2 fragments representing the entire genome. In these mutants, no authentic HSV-2 hybridization could be detected. This was indicative of a mechanism of mutagenesis which did not require the permanent integration of viral sequences in the host genome. The structure of the hprt gene was determined by the method of Southern (J. Mol. Biol. 98:503-517, 1975), and the level of hprt mRNA was analyzed by Northern blots. Except for the identification of one deletion mutant in each of the two groups, the HPRT- clones showed no evidence of alteration in their hprt gene. A total of 7 of 12 spontaneous mutants and 11 of 15 mutants isolated from the infected population transcribed an hprt mRNA of the same size and abundance as did the wild-type cells. Thus, the majority of the mutants seemed to have a point mutation in their hprt structural gene. Interestingly, the proportion of the different types of mutations was similar in the two groups of mutants. This analysis revealed that HSV-2 infection did not increase the frequency of rearrangements but rather that it probably induced a general increase of the level of mutations in the cells. This type of response is thought to be compatible with the biology of the virus, and the possible mechanisms by which HSV-2 induces somatic mutations in mammalian cells are discussed. 相似文献