Systemic vasculitis and its renal lesions.
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Biomedical subjects
Publications and source records attributed to H Hashimoto.
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A mutant temperature-sensitive for R-plasmid replication, Rms201ts14, was isolated from composite plasmid Rms201 after mutagenesis of P1 transducing lysate with 100 mM hydroxylamine for 40 h at 37 degrees C. When Escherichia coli ML1410(Rms201ts14)(+) was grown at temperatures between 40 and 42 degrees C in L broth, antibiotic-sensitive cells were segregated. When the incubation temperature of ML1410(Rms201ts14)(+) in L-broth was shifted to 42 from 30 degrees C, the increase in the number of antibiotic-resistant cells ceased 90 min after the temperature shift. However, the total number of cells continuously increased, and only 3% of the cells retained the plasmid at 5 h after the temperature shift to 42 degrees C. At 30 degrees C the amounts of covalently closed circular deoxyribonucleic acid per chromosome of Rms201ts14 and Rms201 were 3.8 and 6.3%, respectively. Incorporation of radioactive thymidine into the covalently closed circular deoxyribonucleic acid of Rms201ts14 did not take place at 42 degrees C, whereas radioactive thymidine was incorporated into the covalently closed circular deoxyribonucleic acid of Rms201 at a rate of 4%/chromosome even at 42 degrees C. The synthesis of plasmid covalently closed circular deoxyribonucleic acid in a cell harboring Rms201ts14 was almost completely blocked at 42 degrees C. These results indicated that the gene(s) responsible for plasmid deoxyribonucleic acid replication was affected in the mutant Rms201ts14. Temperature-sensitive miniplasmid pMSts214, which has a molecular weight of 5.3 x 10(6) and encodes ampicillin resistance, was isolated from Rms201ts14. Similarly, miniplasmid pMS201, which encodes single ampicillin resistance, was isolated from its parent, Rms201, and its molecular weight was 4.7 x 10(6). These results indicate that the gene(s) causing temperature sensitivity for replication of Rms201 resides on the miniplasmid.
Plasmid Rms312, specifying resistance to tetracycline (Tc), chloramphenicol (Cm), streptomycin (Sm), sulfonamide (Su), and mercury chloride (Mer), deletes both Tc and Cm Sm Su Mer determinants at a high frequency in Salmonella typhimurium LT2. S. typhimurium mutants that were stable carriers of Rms312 were isolated by alternate culture of R-bearing cells in a medium containing either tetracycline or chloramphenicol. In one of these mutants the deletion frequency of drug resistance determinants was decreased by about 100-fold not only Rms312, but also in R100, R1, and R6-5. This mutation caused a slight reduction of ultraviolet resistance but did not affect generalized genetic recombination, indicating that the mutation is different from recA. The mutation, designated dor (deletion of r-determinants), was mapped to a position near 57 units in the new linkage map of S. typhimurijm LT2 (K. E. Sanderson and P. E. Hartman, Microbiol. Rev. 42:471-519, 1978). The dor mutation had no effect on IS1-mediated illegitimate deletion, indicating that the dor mutation is different from the del mutation described by Nevers and Saedler (P. Nevers and H. Saedler, Mol. Gen. Genet. 160:209-214, 1978).
A high incidence of autoantibody against the neutral glycolipid "asialo GM1" was observed in sera from patients with systemic lupus erythematosus (SLE) with neurological disorders, using an immunoflocculation test. The sera from 14 out of 17 cases of SLE with neurological disorders showed antibody activity against asialo GM1 but not against the following glycolipids: asialo GM2 GM1, and galactocerebroside. In another 87 cases of SLE without any history of seizures, as well as 61 cases of other autoimmune diseases (rheumatoid arthritis, progressive systemic sclerosis, mixed connective tissue disease, etc.) and 20 cases of various neurological diseases (epilepsy, multiple sclerosis, etc.), no antibody could be detected. In general, the antibody titer was high several months, even years, before and/or after the seizure, though the titer was low at the time that patients showed definite neurological symptoms. Immunochemical characterization with Sephadex G-200 chromatogrphy and protein A-Sepharose CL-4B affinity column indicated that the antiasialo GM1 was probably an autoantibody belonging to the immunoglobulin G class. The above results suggest that this newly found autoantibody plays a role in the pathogenesis of neurological disorders accompanying SLE.
The effects of prostacyclin (PGI2) were compared with those of prostaglandin E1 (PGE1) on the cardiac hemodynamics (coronary blood flow, systemic blood pressure, cardiac output and max dp/dt of the left ventricle) in closed-chest dogs. Moreover, the effects of PGI2 were compared with those of PGE1 on the concentrations of the coronary arterial and myocardial cyclic adenosine 3':5'-monophosphate (cyclic AMP) and cyclic guanosin 3':5'-monophosphate (cyclic GMP) in open-chest dogs. The intraventricular and intravenous injection of 0.1 to 4.0 microgram/kg of POGI2 increased the coronary blood flow and decreased the mean systemic blood pressure. Comparison of dose response curves for PGI2 and PGE1 in relation to the coronary blood flow indicated that PGI2 and 4 times as potent as PGE1. On the other hand, the effect of PGI2 on the systemic blood pressure was twice as potent as PGE1. The concentration of the coronary arterial cyclic AMP was significantly increased by the administration of PGI2 and PGE1 (control group: PGI2 group was 0.201 +/- 0.022 vs. 0.264 +/- 0.017 pmoles/mg tissue, p < 0.05; control: PGE1 was 0.201 +/- 0.022 vs. 0.286 +/- 0.027 pmoles/mg tissue, p < 0.05). The concentrations of the coronary arterial cyclic GMP were not significantly changed by the administration of PGI2 and PGE1, nor were those of myocardial cyclic AMP and cyclic GMP. The changes in cyclic nucleotide levels and cardiac hemodynamics induced by PGI2 were qualitatively similar to those induced by PGE1, but the change caused by PGI2 was greater than PGE1 in the coronary and systemic hemodynamics.
A comparative toxicity study with 6 alpha-methylprednisolone 21-sodium succinate (MPS) and hydrocortisone 21-sodium succinate (HCS) was carried out on male rats of the Wistar strain. MPS and HCS were administered intravenously to rats in dose levels of 20 or 100 mg/kg/day for 14 days. There were no significant differences in the pituitary weights in MPS and HCS groups, but weight of the adrenal glands decreased with increasing dose levels of MPS and HCS. Histopathological examination of MPS and HCS treated rats revealed atrophy of the zona fasiculata in the adrenal cortex which correlated with dose levels. The decline of serum corticosterone levels in rats correlated with increasing dose levels of MPS and HCS. It can be concluded that the inhibitory effect of MPS on the pituitary-adrenal system in rats was the same as HCS. No ulceration was observed in the gastro-intestinal tract of MPS of HCS treated rats.
The responses of renin release to three different stimuli, such as 1) head-up tilt, 2) administration of loop diuretics(bumetanide) and 3) low sodium diet + administration of bumetanide + ambulation were examined in essential hypertensive patients and normotensive subjects. Essential hypertensive patients were classified as stage I and II according to WHO stage classification. Groups studied were age-matched. The responses of renin release to three stimuli did not significantly differ in normotensive subjects (n = 13, 42 +/- 2(SEM) years old) and essential hypertensive patients of stage I (n = 15, 44 +/- 2). However, essential hypertensive patients of stage II (n = 20, 44 +/- 1) showed significantly lower responses of renin release to all three stimuli than essential hypertensive patients of stage I and normotensive subjects. The results suggest that the suppression of renin release is related in part to the development of hypertension.
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A clinicopathologic study of 130 cases of malignant fibrous histiocytoma (MFH) of the soft tissues is reported. This malignant neoplasm principally of middle and late adults occurred most often in the proximal portions of the extremities (48%) including the thigh and buttocks (35%). MFH may be subclassified into common (storiform and pleomorphic), myxoid, xanthogranulomatous, and giant cell types, the common type being accounted for 100 cases (77%) of the series. The prognosis was more favorable in patients with storiform and myxoid tumors than in patients with pleomorphic or other type tumors, the overall relative five-year survival rate being 48%. The depth of the tumor also affected prognosis with a significantly lower survival rate in deeply situated tumors. The rate of local recurrence of the tumor was 48%. Because of incomplete informations, metastasis was confirmed in only 26 patients and was most frequently to the lung (73%). In addition, electron microscopic, histochemical and tissue culture findings in limited cases are presented, concerning the histogenesis of the MFH.
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