T-cell responses in the thymus after hepatic transplantation in the rat.
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Biomedical subjects
Publications and source records attributed to Y Yamaguchi.
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The 3-glucosides of nonamidated lithocholic, chenodeoxycholic, ursodeoxycholic, deoxycholic, and cholic acids, and their double conjugate forms with glycine and taurine were synthesized. The key reactions used were 1) beta-D- glucosidation at C-3 by the Koenigs-Knorr condensation reaction of 3 alpha-hydroxylated bile acid methyl (or p-nitrophenyl) esters with 1 alpha-bromo-1-deoxy-2, 3, 4, 6-tetra-O-acetyl-D-glucopyranose in the presence of cadmium carbonate in refluxing benzene; 2) indirect and direct amidations at C-24 by the activated p-nitrophenyl ester and by the diethylphosphorylcyanide methods, respectively, using glycinate ester and taurine as coupling agents; and 3) simultaneous alkaline hydrolysis of the hydroxyl-protecting and ester groups in both the sugar and aglycone moieties.
We studied the cases of 60 patients who underwent magnetic resonance (MR) imaging evaluation after fixation with the titanium alloy pedicular screw system. Spine stabilization was required in the thoracic and lumbar region for various spinal disorders. The images were evaluated for the spinal and adjacent tissues. These pedicular screw systems were imaged safely and caused no particular clinical problems. The localized signal void artifacts were seen around the implants. This artifact did not interfere with the diagnosis for another disease. The spinal cord and dura mater appeared in midsagittal and in axial images except for regions lying close to the implants. After surgery MR imaging revealed the decompressed or the deformed spinal cord. However, the prognosis of spinal disorder could not be revealed by the intensity grade of MR imaging because of the distortion in the spinal cord.
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A Tuberculosis epidemic occurred in a hospital in Fukushima prefecture, 1993. It was detected after the diagnosis of two tuberculosis cases among nurses working in the hospital. A contact survey in the hospital revealed two another cases of tuberculosis, one from the nurse, and the other one from the patient admitted to the hospital. In addition, two more nurses in the same hospital were suspected of having tuberculosis, but they do not yet started treatment by the time of the survey. Though the source of the infection could not be identified, the doctor's delay in detecting cases was suspected on the background of the epidemic. Deficiency in the health care system of nursing school was also suspected.
The aim of this study was to show that ultraviolet (UV) irradiation to the skin around the catheter exit site (ES) could inhibit its infection. First, bacterial cultures of swabbed fluid from the ES were obtained from 68 continuous ambulatory peritoneal dialysis (CAPD) outpatients six times during the 24-month observation period. Second, the bactericidal effects of UV irradiation on the catheter ES were examined. The results were as follows: (1) In spite of disinfection of the catheter ES by the strict application of povidone-iodine once or twice a day, 23%-45% of the cases were found to be micro-organism positive. The most prevalent micro-organisms from the catheter ES were, in order of highest to lowest prevalence, Staphylococcus epidermidis (SE), Staphylococcus aureus (SA), and Pseudomonas aeruginosa (PA). (2) In the nasal cavity SA was detected in 20%-25% of patients. There was a high incidence of ES infection among the SA nasal carriers. (3) UV irradiation was performed in 18 cases that constantly revealed bacteria on culture at the catheter ES. Ten cases (55%) became culture-negative, 3 cases showed a microbial decrease, and 5 cases remained unchanged. These results suggest that UV irradiation can eliminate bacteria and can be of prophylactic use for ES infections.
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To elucidate the vascular endothelial function at pulmonary ischemia and reperfusion, cyclic GMP (cGMP) release in lung perfusate at reperfusion after ischemia was examined as a marker of nitric oxide (NO) release from the endothelium in an in situ perfused rabbit lung. The lung was perfused from the pulmonary artery with Krebs-Henselite buffer and cGMP in the lung effluent from the left ventricle was assayed in a time-dependent manner. The inhibition of cGMP release by NG-nitro-L-arginine methyl ester and the reversal of the effect by L-arginine indicated that cGMP released into the perfusate was elicited by NO from the endothelium. There was a significant decrease in cGMP release during reperfusion after warm ischemia (30 min and 60 min) compared with the immediately perfusion without intervening ischemia. These data suggest that NO release is impaired by the endothelial dysfunction at reperfusion after warm ischemia in the perfused rabbit lung and the biochemical studies of the perfusate is useful in assessing the vascular endothelial function.
The metabolism of (+)-S-145, a thromboxane A2 receptor antagonist, was investigated in vitro using isolated hepatocytes, liver homogenates, and subcellular fractions prepared from rats. The cofactor requirement and subcellular distribution of beta-oxidation and hydroxylation suggested that the chain shortening of the carboxyl side chain of (+)-S-145 was catalyzed by beta-oxidation enzyme systems in peroxisomes and hydroxylation at the C-5 and C-6 positions of the bicyclo ring was catalyzed by monooxygenases in microsomes, respectively. In the initial stage of metabolism of (+)-S-145, the potential of activation to its coenzyme A (CoA) thio ester was prominent, compared with that of the hydroxylation. The resulting (+)-S-145-CoA was beta-oxidized. There seems to be two metabolic pathways in the metabolism of (+)-S-145-CoA. One is the biotransformation of (+)-S-145-CoA to bisnor-(+)-S-145 and tetranor-(+)-S-145 in the beta-oxidation cycle, and the other is the reduction of (+)-S-145-CoA to dihydro-(+)-S-145-CoA by NADPH dependent delta 5-reductase followed by beta-oxidation to dihydrobisnor-(+)-S-145, which was scarcely beta-oxidized to tetranor-(+)-S-145. Finally, these beta-oxidized metabolites are hydroxylated by monooxygenases in microsomes at the 5- or 6-position of their bicyclo ring, whereas beta-oxidation activity of hydroxylated metabolites of (+)-S-145 was not observed in the light mitochondrial fraction nor in isolated hepatocytes.
Werner's syndrome is characterized by premature aging and frequent impaired glucose tolerance or overt diabetes. Insulin resistance may play an important role and may be caused by a post-receptor defect or dysfunctional insulin receptor. The present study was undertaken to investigate the insulin receptor gene mutation in Werner's syndrome. The genomic DNAs were obtained from four patients with Werner's syndrome. Exons 2-22 of the insulin receptor gene except exon 1 were amplified from genomic DNA by the polymerase chain reaction and screened for nucleotide variation by examining for single-stranded conformational polymorphisms. There were no nucleotide variations in exons 2, 4-->7, 9 and 12-->22. Variants were thus found in exons 3, 8, 10 and 11 and each were sequenced. The variant in exon 8 was due to a silent polymorphism (GAT-->GAC/T, Asp519) and other variants in exons 3, 10 and 11 were caused by nucleotide substitutions in introns. These results suggest that the patients with Werner's syndrome express normal insulin receptors and that the primary genetic lesion for insulin resistance is not in the insulin receptor gene. Insulin resistance in Werner's syndrome is thus likely by a post-receptor defect.
We isolated a binding protein for inositol 1,3,4,5-tetrakisphosphate (InsP4) from detergent-solubilized mouse cerebellar membrane fractions by sequential column chromatographies. Partial amino acid sequencing of the purified sample revealed that the protein is essentially identical to rat synaptotagmin II, an integral membrane protein of synaptic vesicles. Immunoprecipitation experiment of [3H]InsP4 binding activity of the purified protein using polyclonal antibody against the C2A domain of rat synaptotagmin II also revealed that mouse synaptotagmin II is the InsP4 binding protein (IP4BP). Scatchard analysis of InsP4 binding to the IP4BP/synaptotagmin indicates a single binding site with a Kd of 30 nM. The present finding that InsP4 binds strongly to synaptotagmin II suggests an important role for inositol polyphosphates in the regulation of neurotransmitter release.