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151.
Nodular regenerative hyperplasia was found in nine patients who had hematological disease including polycythemia vera, agnogenic myeloid metaplasia, primary thrombocythemia, rheumatoid arthritis with thrombocytosis, multiple myeloma, and erythrocytosis associated with polycystic renal disease. Portal hypertension was suspected in three and features of hypersplenism were present in four. 2. Nodular regenerative hyperplasia occurred in livers which had widespread obliteration of portal vein radicals (obliterative portal venopathy). Morphometric analysis indicated that the portal vein lesions were predominately located in veins up to 0.2 mm in diameter and were significantly more frequent than similar lesions occurring in elderly persons. 3. The following pathogenesis of nodular regenerative hyperplasia is proposed: Thrombi, perhaps largely composed of platelet aggregates formed in the portal venous circulation or spleen, embolize to the liver and results in obliterative vascular lesions. Atrophy and regenerative nodule formation occur in response to the interruption of the portal blood supply. 相似文献
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IR Bariliak 《Canadian Metallurgical Quarterly》1977,40(5):606-609
On the 13th day of pregnancy chloridine (50 mg/kg) or 6-mercaptopurine (60 mg/kg) was administered to rats. Thirty minutes before this the anomals received insulin (40 IU/kg), pentoxyl (100 mg/kg), ethonium (15 mg/kg), dimexide (5500 mg/kg), or magnesium sulphate (250 mg/kg). Oi the 20th day of preganancy the animals were sacrificed. While chloridine and 6-mercaptopurine caused abnormal development in all live embryos, their damaging (teratogenic and embryolethal) and action was sharply reduced when teratogens were used in combination with other drugs. The author feels that the normalizing effect of the study agents is due to the influence of these compounds on the functioning of the lysosome-segregational system. 相似文献
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Further genetic mapping to two- and three-factor crosses show that the ush gene is closely linked to two other genes hemG and pisA, and that the probable gene order is proC-hemG-plsA-ush-gal. 相似文献
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DA Sanderson MA Wilcox IR Johnson 《Canadian Metallurgical Quarterly》1994,101(1):87; author reply 87-87; author reply 88
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1. Simultaneous recordings of tension and [Ca2+]i during NANC-mediated relaxation were made in the rat anococcygeus muscle under various conditions. 2. In muscles precontracted with guanethidine, nitrergic stimulations at 2 Hz produced a rapid decrease in both the tension and [Ca2+]i. 3. The nitric oxide synthase inhibitor, NG-nitro-L-Arginine (NOLA, 100 mumol/L) completely abolished the decreases in the [Ca2+]i and force response of the NANC-mediated relaxation. 4. Noradrenergic-mediated contractions elicited by electrical field stimulation were potentiated by the addition of NOLA. In the absence of NOLA, the motor responses were larger in magnitude at 10 Hz stimulation than at 2 Hz. After NOLA, both the force response and the associated rise in [Ca2+]i were substantially increased in comparison to the control stimulations. Proportionately the potentiation of the 2 Hz response was of a far greater magnitude than that of the 10 Hz response. 5. The guanylate cyclase inhibitor methylene blue (10 mumol/L), partially inhibited the force and [Ca2+]i response of the NANC relaxation. 6. Following exposure of the muscles to the sarcoplasmic reticulum Ca(2+)-ATPase inhibitor, cyclopiazonic acid, (10 mumol/L) the responses to NANC stimulation were inhibited. The attenuated relaxation response displayed a bi-phasic timecourse and the Ca2+ change in comparison to that of the control was markedly smaller. In some cases, a relaxation was observed with no detectable change in the [Ca2+]i. 7. The results suggest that part of the relaxation response observed with NANC-mediated relaxation in the rat anococcygeus is dependent on Ca2+ sequestration into the sarcoplasmic reticulum. However, other Ca2+ lowering mechanisms and possible Ca2+ independent mechanisms may also contribute to the NANC relaxation response. 相似文献