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Biomedical subjects

T Asano

Publications and source records attributed to T Asano.

At least 721 records · Page 40Linked to original sources
PubMed1988

[Studies of the factors affecting the reduction of chronic subdural hematoma: effect of preoperative factors with special reference to cerebral atrophy].

The authors examined the preoperative factors affecting the reduction of chronic subdural hematoma (CSDH). A new method was developed to calculate the reduction rate of CSDH using CT volumetry technique. Postoperative serial CT films were examined and each hematoma volume was calculated by microcomputer. A postoperative exponential decrease of hematoma volume was observed, and the log-transformation of the hematoma volume turned the curve to a linear decrease. The least square method was used to fit an exponential curve, and the half reduction date (HRD) was calculated from the fitting curve. This HRD represents a mathematical indicator of the reduction rate of CSDH. Using this technique, the relationships between this HRD and the following parameters were examined in 61 patients. The preoperative factors examined are as follows; 1) patient's age, 2) preoperative hematoma volume, 3) CT number of the hematoma, 4) time interval between the head injury and the onset of symptom, and 5) the degree of cerebral atrophy. The degree of cerebral atrophy was calculated by means of a simple approximate formula as described by one of the authors (K.N.). Patient's age and the hematoma volume were correlated with HRD, and the correlation coefficients were 0.346 (p less than 0.01) and 0.298 (p less than 0.05) respectively. On the other hand, preoperative CT findings and the duration from the trauma had no correlation with HRD. Cerebral atrophy has hitherto been thought to affect the reduction of hematoma. However, our quantitative study revealed no correlation between cerebral atrophy and the reduction of hematoma rate. This unexpected result may be attributed to the difference between cerebral atrophy and cerebral elasticity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Evaluation of the nutritional management of patients with liver cancer and cirrhosis].

Ninety-five patients with liver cancer and cirrhosis who had undergone hepatic lobectomy or partial hepatectomy were studied. According to nutritional protocol based on experimental results, a large quantity of fresh frozen plasma (FFP), and BCAA-enriched amino acids at 30 kcal/kg/d as an energy source were administered postoperatively for 7-10 days with strict restriction of sodium and total fluid volume. An elemental diet for liver dysfunction (ED-H) was given to 13 patients at more than 1,500 kcal/d via a naso-duodenal feeding tube for 7-14 days. Six patients were given 15 g/d of BCAA granules after discharge for as long as possible. Serum levels of TP, Alb, T.Bil and PT were kept moderately high in the IVH and ED-H group. Although BCAA/AAA molar ratio was kept high when IVH or ED-H was provided, it gradually fell if nutritional management was discontinued. This ratio was maintained within normal limits by oral administration of BCAA granules. According to the Child classification, 1,2,3 and 5-year cumulative survival rates were 80.9, 62.9, 44.1 and 25.5% for Child A, 70.0, 43.1, 43.1 and 0% for Child B, and 50.0, 25.0, 0 and 0% for Child C, respectively. These data indicate the importance of nutritional support for improvement of nutritional status and for obtaining a better prognosis. Oral BCAA supplementation should be useful for the performance of long-term nutritional management for cancer patients with liver cirrhosis.

Amino Acids, Branched-Chain↗
PubMed1987

Production of the alpha subunit of guanine nucleotide-binding protein GO by neuroendocrine tumors.

We have found that neuroendocrine tumors (including neuroblastoma, ganglioneuroma, gut carcinoid, pheochromocytoma, medullary thyroid carcinoma, insulinoma, glucagonoma, prolactinoma, carotid body tumor, and small cell lung carcinoma) produce considerable amounts (about 1000-80,000 ng/g tissue) of the alpha subunit of guanine nucleotide-binding protein, GO (GO alpha), whereas nonneuroendocrine tumors contain less than 300 ng of GO alpha/g tissue. GO alpha in the neuroendocrine tumors was present both in the soluble fraction, and cholate-extractable membrane-bound fraction of tissues. Immunoblots of membrane fractions of neuroblastoma and carcinoid tissues confirmed that the immunoreactive substance in the tumor tissues was GO alpha. Immunohistochemically, GO alpha was localized consistently in the cell membrane and occasionally in the cytoplasm of neuroendocrine tumors. GO alpha was also detected in sera of 73% patients with neuroblastoma at diagnosis, whereas serum GO alpha concentrations in control children, or patients with nonneuroendocrine tumors were lower than the detection limit of the immunoassay method employed. Serum GO alpha concentrations in patients with neuroblastoma changed with the clinical course; they fell in patients responding to treatment and increased in patients who relapsed. Since GO alpha, a specific protein in the neural and neuroendocrine cells, was found to be produced in considerable amounts by all types of neuroendocrine tumors but not in nonneuroendocrine tumors, GO alpha might be a useful biomarker for neuroendocrine tumors.

Adrenal Gland Neoplasms↗
PubMed1987

A novel concept on the pathogenetic mechanism underlying ischaemic brain oedema: relevance of free radicals and eicosanoids.

A survey on literature reports and our own experimental studies on the pathogenetic mechanisms underlying ischaemic brain oedema is given and a new concept proposed. In regional incomplete ischaemia the lipoxygenase activity is enhanced, presumably caused by an increase of free radicals and hydroperoxides, leading to an enhancement of endothelial Na+, K+-AtPase and increased sodium and water transport from blood to brain. The aggravation of brain oedema and post-ischaemic hypoperfusion following recirculation appears to be mainly due to an activation of the cyclo-oxygenase pathway with release of oxidants from PGG2, which causes non-specific but detrimental damage to the endothelial and parenchymal cells. This new concept may open future perspectives in treatment which are briefly discussed.

Animals↗
PubMed1987

Differential purification by immunoaffinity chromatography of two carboxy-terminal portion-deleted derivatives of recombinant human interferon-gamma from Escherichia coli.

Two lower-molecular-weight derivatives of recombinant human interferon-gamma (rIFN-gamma) were purified concurrently from a lysozyme-EDTA extract of Escherichia coli cells by immunoaffinity chromatography using a monoclonal antibody (MAb) against a synthetic carboxy-terminal peptide (Lys-131-Gln-146). The two derivatives, 15K rIFN-gamma and 17K rIFN-gamma, were regarded to have been generated at the extraction step. They were successfully separated from each other by using another MAb against the same synthetic peptide with higher binding affinity than the first. The results of protein-chemical analyses indicate that 15K rIFN-gamma and 17K rIFN-gamma lack 15 (Arg 132-Gln-146) and 4 (Arg-143-Gln-146) carboxy-terminal amino acid residues, respectively. All the data suggest that the two derivatives form a noncovalent dimer and that 15K rIFN-gamma binds indirectly to the MAb column via 17K rIFN-gamma.

Amino Acids↗
PubMed1987

Studies of the induction and maintenance of long-term graft acceptance by treatment with FK506 in heterotopic cardiac allotransplantation in rats.

Immunosuppressive activities of the newly discovered FK506, isolated from Streptomyces tsukubaensis, were examined by using cardiac allotransplantation in the rat, and the mechanisms underlying induction and maintenance of FK506-induced long-term allograft survival were studied. Male rats of WKA (RT1k) and F344 (RT1lvl) strains were used as recipients and donors, respectively, and those of BN (RT1n) strain were used as third-party donors. Treatment with FK506, beginning from the day of allografting for 14, 10, or as few as 4 days, prolonged allograft survival significantly across the major histocompatibility barrier. The minimum doses for prolonging graft survival were 0.1 mg/kg/day by intramuscular treatment and 1.0 mg/kg/day by oral treatment. Treatment with FK506 at a dose of 0.32 mg/kg/day from day 4 until day 10 resulted in all the grafts surviving indefinitely and from days 5 to 10, half the grafts survived indefinitely, suggesting that the agent inhibited ongoing rejection. On the other hand, cyclosporine treatment at a dose of 20 mg/kg/day from day 2 did not prolong graft survival time statistically significantly. Induction of prolonged graft survival was not obtained by pretreatment of the prospective donor or recipient; prolonging effects were observed only when the agent was administered after allografting. Thus, the primary effect of the agent is exerted on responder lymphocytes reacting to the donor antigens in the induction phase of long-term graft acceptance. The mechanisms underlying the maintenance of long-term grafts were analyzed by testing the capacity of lymphocytes or serum of long-term graft-bearing rats to inhibit graft rejection in irradiated grafted hosts. Transfer of 2 x 10(8) lymphocytes from FK506-induced long-term F344 graft-bearing WKA rats resulted in indefinite survival of F344 heart allografts, but it did not prolong survival of third-party BN hearts. Transfer of 2.5 ml serum from long-term graft-bearing rats also prolonged graft survival of F344 hearts, but not BN hearts. These results suggest that donor strain-specific suppressor cells and humoral factor(s) are induced by treatment with FK506 in the presence of allografts, and that they play at least partial roles in the maintenance of long-term allograft acceptance.

Administration, Oral↗
PubMed1987

Highly sensitive immunoassay for the alpha subunit of the GTP-binding protein go and its regional distribution in bovine brain.

Antisera were raised in rabbits against the alpha subunit of a GTP-binding protein, Go. Because the antisera cross-reacted weakly with the alpha subunit of inhibitory GTP-binding protein of adenylate cyclase (Gi), they were purified with a Go alpha-coupled Sepharose column. Purified antibodies reacted only with Go alpha and did not cross-react with the Gi alpha subunit or beta gamma subunits in an immunoblot assay. Using these purified antibodies, a highly sensitive enzyme immunoassay method for the quantification of bovine brain Go alpha was developed. The assay system consisted of polystyrene balls with immobilized antibody F(ab')2 fragments and the same antibody Fab' fragments labeled with beta-D-galactosidase from Escherichia coli. The minimal detection limit of the assay was 0.1 fmol, or 4 pg. The assay was specific for Go alpha, and it did not cross-react with Gi alpha or beta gamma. Samples from various regions of bovine brain were solubilized with 2% sodium cholate and 1 M NaCl, and the concentrations of Go alpha were determined. Go alpha was detected in all the regions, and the highest concentration was observed in the cerebral cortex. The immunohistochemical study showed that the neuropil was rich in Go alpha.

Animals↗
PubMed1987

The effect of triiodothyronine (T3) and thyroxine (T4) upon insulin secretion from isolated rat pancreatic islets.

In order to observe the effect of triiodothyronine (T3) or thyroxine (T4) on glucose-induced insulin release from pancreatic islets, isolated pancreatic islets from Wistar male rat were incubated in modified Krebs-Ringer bicarbonate solution (0.2% BSA, pH 7.4) with 3 mM, 5 mM or 10 mM glucose for 60 min with or without exposure to T3 (2.5 micrograms/ml or 7.5 micrograms/ml) or T4 (2.5 micrograms/ml or 7.5 micrograms/ml). Direct exposure of isolated pancreatic islets to T3 or T4 did not have any effect on glucose-induced insulin release from pancreatic islets during 60 min incubation. But, in successive 60 min incubations following 60 min rest periods after exposure to T3 or T4 in the first incubation, glucose-induced insulin release from isolated pancreatic islets previously exposed to T4 was reduced at 5 mM and 10 mM glucose concentrations and previous exposure to T3 had no effect on glucose-induced insulin release. A delayed effect of T4 on the mechanism of insulin secretion from pancreatic islets was suggested.

Animals↗
PubMed1987

Changes in plasma glucose, insulin (IRI), glucagon (IRG) and free fatty acids (FFA) following alanine loading in hyperthyroid patients.

The responses of plasma glucose, insulin (IRI), glucagon (IRG) and free fatty acids (FFA) following alanine loading (0.1 g/kg) were observed in 9 control subjects and 7 hyperthyroid patients, before and after restoration of thyroid function to normal. Despite the persistence of impaired glucose response to alanine, the blunted IRI and IRG responses in the hyperthyroid state were improved with a significant reduction in fasting IRI and IRG after treatment. Markedly increased FFA following alanine loading in hyperthyroid patients was reduced after treatment, but the FFA concentration remained greater than in the control subjects. We tentatively conclude that the impaired alpha and beta-cell responses to alanine were temporarily induced by the direct and/or indirect effects of thyroid hormone excess.

Adult↗
PubMed1987

Reduction and recovery of plasma 1,5-anhydro-D-glucitol level in diabetes mellitus.

The plasma concentration of 1,5-anhydro-D-glucitol (AG) was measured in 135 newly diagnosed patients who were referred for oral glucose tolerance tests. AG concentrations in the nondiabetic patients indicated that the mean value of normal AG concentration was 21.8 micrograms/ml (SD = 5.9 micrograms/ml, range 9.6-38.8 micrograms/ml). This distribution of AG concentration was significantly different from that in patients with impaired glucose tolerance (IGT) (13.3 +/- 5.4 micrograms/ml) and definitely different from that in diabetic patients (2.1 +/- 1.8 micrograms/ml). In a standard glucagon test, it was suggested that the decrease of plasma AG was affected not only by glycemic control of the patients but also by pancreatic cell secretory activity. The reduction of AG concentration was more marked in IDDM patients than in NIDDM patients. In longitudinal studies, AG concentration was shown to be sensitive to glycemic control. However, its recovery showed a tendency toward much delay after the improvement of fasting blood glucose or HbA1 concentrations. On the other hand, AG concentration showed negligible diurnal change and no immediate change as a result of diet, oral glucose load, or acute shift of the insulin level in both normal and diabetic subjects.

Adolescent↗