Heterogeneity of antigens related to 7S domain of type IV collagen in serum: application to patients with chronic liver disease.
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Biomedical subjects
Publications and source records attributed to S Yamada.
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Dynorphin (1-100 nM) dose dependently inhibited both spontaneous and electrically evoked endogenous dopamine (DA) release from slices of the nucleus accumbens of untreated rats. When this inhibitory effect was compared, it was significantly reduced in rats pretreated (for 9 days) with methamphetamine (6 mg/kg per day i.p.) relative to rats treated with saline. These findings indicate that dynorphin inhibits DA release from the nucleus accumbens, and that treatment with methamphetamine reduces the modulatory action of dynorphin on DA release. It is possible that repeated administration of methamphetamine leads to attenuation of the inhibition of DA release from the nucleus accumbens via presynaptic dynorphin-sensitive receptors.
The first practical fluorometric assay of plasma 25-hydroxyvitamin D3 (25-OH-D3) and 24R,25-dihydroxyvitamin D3 (24,25-(OH)2D3) is described. The method uses a highly fluorescent dienophile, 4-[2-(6,7-dimethoxy-4-methyl-3-oxo-3,4-dihydroquinoxalyl)ethyl]-1, 2,4- triazoline-3,5-dione (DMEQ-TAD), to fluorescence-label vitamin D. Vitamin D metabolites were roughly purified with a short cartridge column followed by HPLC, labeled with DMEQ-TAD, and the product was analyzed on HPLC. In the assay of 25-OH-D3 the new fluorometric method was compared with the HPLC-uv method and was confirmed to be as accurate and reliable (CV, 4-5%) as the HPLC-uv method. Plasma 24,25-(OH)2D3 was accurately assayed by the HPLC-FL method, where the standard addition method was successfully used to calculate the overall recovery.
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Recently we purified to homogeneity hyaluronidase from stonefish (Synanceja horrida) venom, for the first time from a marine source [Poh, Yuen, Chung & Khoo (1992) Comp. Biochem. Physiol., in the press]. In the present study the reaction products of the hyaluronidase purified from stonefish venom were analysed. It produced tetra-, hexa-, octa- and deca-saccharides as major end products, but not disaccharides. The structure of the tetrasaccharide product was determined by enzymic analysis, in conjunction with h.p.l.c. and by 1H n.m.r., as GlcA beta 1-3GlcNAc beta 1-4GlcA beta 1-3GlcNAc. Chemical shifts of the structural-reporter-group protons of the constituent monosaccharides for the tetrasaccharide have been assigned. The enzyme did not act on chondroitin sulphate or dermatan sulphate. The results indicate that the stonefish hyaluronidase is an endo-beta-N-acetylglucosaminidase specific for hyaluronate.
The results of treating 54 esophageal carcinomas with low-dose rate telecobalt therapy (LDRT) as a boost were compared with those of treating 97 esophageal carcinomas with conventionally fractionated irradiation alone (CFI). The LDRT (100 cGy/hr, 500 to 700 cGy/day, a total dose of 1400 to 2000 cGy) was boosted at 10 days after 6000 cGy of the CFI dose. Although the LDRT group included more advanced cases than the CFI group, local effects and survival rates in the former group were slightly better than in the latter group. Late complications were more severe in the LDRT group. However, they were acceptable when the total dose administered to this group was less than 8000 cGy. Using LDRT as a boost against esophageal carcinomas was found to be satisfactory therapeutically.
A preparation of porcine stage 14 intestinal heparin, which contains Ser as a predominant amino acid, was used for isolation of the carbohydrate-protein linkage region of heparin. Two glycoserines were isolated in a molar ratio of 96:4 after an exhaustive digestion with a mixture of bacterial heparinase and heparitinases. Their structures were determined by composition analysis, heparitinase digestion, co-chromatography with an authentic glycoserine on high performance liquid chromatography, and by 500-MHz one- and two-dimensional 1H NMR spectroscopy. The structure of the major one is delta GlcA beta 1-3Gal beta 1-3Gal beta 1-4Xyl beta 1-O-Ser and that of the minor is delta GlcA beta 1-4GlcNAc(6-O-sulfate) alpha 1-4GlcA beta 1-3Gal beta 1-3Gal beta 1-4Xyl beta 1-O-Ser. The novel 6-O-sulfated GlcNAc residue was demonstrated to occur in the vicinity of the carbohydrate-protein linkage region. The Gal residues were nonsulfated, in contrast to the sulfated Gal structures recently discovered in the carbohydrate-protein linkage region of chondroitin sulfate proteoglycans. The structural features are discussed in relation to biosynthetic mechanisms of the heparin glycosaminoglycans.
Localization of hepatitis C virus (HCV) RNA was investigated by non-radioactive in situ hybridization in human liver specimens of chronic non-A, non-B (NANB) hepatitis patients who were seropositive for antibodies to HCV (anti-HCV). For in situ hybridization, T-T dimerized synthetic oligodeoxynucleotide probes were used and DNAs hybridized in situ were detected immunohistochemically using specific antibodies against T-T dimer. The data demonstrates that HCV-RNA was localized in the cytoplasm of hepatocytes in human liver biopsies obtained from the patients with chronic NANB hepatitis seropositive for anti-HCV.
The gene expression of human type I procollagen was investigated in cirrhotic human liver by using in situ hybridization with nonradioactive DNA probes. Using in situ hybridization can provide direct evidence for the cell type capable for type I collagen synthesis in tissues. T-T dimerized DNA probes were used and DNAs hybridized in situ were detected immunohistochemically using specific antibodies against T-T dimer. The data demonstrated that type I collagen is synthesized in hepatocytes and stellate cells in pseudolobules and in fibroblasts in Glissons capsules in cirrhotic human livers. We indicated hepatocytes morphologically and functionally by using immunohistochemical localization of albumin, which was used as a marker of hepatocyte, since albumin is synthesized exclusively by hepatocytes.
A system for the evaluation of antifungal activity of volatile compounds has been developed that is based on dynamic growth of a single hypha. The newly developed system is composed of a reaction vessel under a microscope, automatic stage, charge coupled device (CCD) camera, TV monitor, video tape recorder (VTR), and a microcomputer. A fungus was inoculated in the reaction vessel containing agar medium and then was treated with an antifungal reagent in the gas phase either in batch or flow reaction manner. The apex of a growing hypha displayed on a TV monitor was followed automatically. From the ratio of the growth rate under exposure of a reagent (UEXPO) to the growth rate before the exposure (UPRE), the antifungal activity was expressed quantitatively.
To evaluate abnormal secretion of growth hormone (GH) in cases of liver diseases, the authors performed a loading test of growth hormone-releasing factor (GRF) and approximately one week later, a loading test of thyrotropin-releasing hormone (TRH), and measured serum GH in 15 cases of liver cirrhosis (LC), 5 with chronic active hepatitis (CAH), and 5 controls. In the TRH test, 8 of 15 LC patients showed a peak GH value of 6 ng/ml or more and were classified as the TRH-responder group (LC-R). Seven other LC patients showing a peak GH value of less than 6 ng/ml were classified as the TRH-non-responder group (LC-NR). None of the CAH cases or controls showed a peak GH value of 6 ng/ml or more. In GRF test, the response of GH was poor in all 8 in the LC-R group. The responses in the LC-NR group were significantly greater than those in the LC-R group from 15 to 90 minutes after the GRF loading. In the LC-R group, greater impairment of liver function was indicated by total bilirubin, serum protein and cholinesterase values compared to the LC-NR group. Fischer's ratio was significantly lower in the LC-R group. In cases of liver diseases, Fischer's ratios negatively correlated with the peak GH values in the TRH test (r = -0.679, P less than 0.01). These results suggest that in LC cases showing a paradoxical GH response to TRH, the GH response to GRF which is a GH stimulatory hormone, is decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum type IV collagen fragment (7S collagen domain) was measured in 30 controls and 152 liver disease patients with a radioimmunoassay using a polyclonal antibody to human placenta 7S collagen. The serum concentrations of 7S collagen (mean +/- SD) were 4.2 +/- 0.9 ng/mL in controls, 5.1 +/- 2.0 ng/mL in acute hepatitis, 6.5 +/- 2.5 ng/mL in chronic inactive hepatitis, 9.5 +/- 3.8 ng/mL in chronic active hepatitis, 14.4 +/- 7.5 ng/mL in liver cirrhosis, and 14.4 +/- 6.9 ng/mL in hepatocellular carcinoma. In acute hepatitis, 7S collagen was slightly increased, whereas type III procollagen N-peptide and prolyl hydroxylase were markedly increased. In chronic liver disease, 7S collagen concentrations increased with the severity of the disease, and also reflected the degree of fibrosis. The serum 7S collagen concentrations were significantly correlated with those of type III procollagen N-peptide and prolyl hydroxylase in all subjects. These results suggest that serum 7S collagen concentration is a useful diagnostic aid for determining hepatic collagen metabolism in liver diseases.
When prostaglandin (PG) E1 was continuously administered to rats from 24 hours before giving a dose of carbon tetrachloride, deranged serum glutamic pyruvic transaminase levels and prothrombin time were significantly reduced 12 hours after intoxication compared with controls. A similar effect of PGE1 was seen at 24 hours in D-galactosamine-intoxicated rats. Liver histology showed a comparable attenuation of injury in these rats. These results were consistent with reported effects of PGE2, suggesting that both prostaglandins may share a common pathway in protection against liver injury. When PGE1 or 16,16'-dimethyl PGE2 was added to the medium of primary cultured rat hepatocytes, lipid peroxidation-dependent killing of the cells by tert-butyl hydroperoxide was significantly attenuated without affecting the extent of malondialdehyde accumulation compared with controls. Both prostaglandins significantly reduced the extent of increased plasma membrane microviscosity of these cells assessed by 1-[4-(trimethyl-ammonio)phenyl]-6-phenyl-1,3,5-hexatriene. PGE1 and PGE2 may possess cytoprotective effects on liver parenchymal cells through stabilization of membrane microviscosity, which may contribute to protection against liver injury.
Serum hepatocyte growth factor levels were measured in hepatectomized and nonhepatectomized surgical patients. The levels were significantly increased and reached a maximum within 7 days after surgery in both groups, returning to preoperative levels 28 days after partial hepatectomy and 7 days after other operations. Multiple regression analysis showed that such maximal hepatocyte growth factor levels were significantly related to having liver cirrhosis and postoperative maximal serum total bilirubin and alanine aminotransferase levels and peripheral white blood cell counts in the hepatectomized group and to postoperative maximal peripheral white blood cell counts and serum C-reactive protein levels in the nonhepatectomized group. However, the levels showed no relation to the resected liver volume and increment of the remaining liver volume 28 days after partial hepatectomy. It is concluded that serum hepatocyte growth factor levels were increased after partial hepatectomy in association with hepatocellular dysfunction and necrosis and systemic inflammation. It is unlikely that the increase was related to liver regeneration.
The complexity of cranioplasty increases with increased defect size. It is difficult to produce a symmetric, accurate implant presurgically or at the time of surgery when the defect is greater than 50 cm2. The procedure is also more difficult to perform when the defect is located in the temporal, infratemporal, or frontal areas. A new procedure generates a three-dimensional cast of the skull through computed tomography and computer-aided design reformation. This article describes the process of model generation and the production of a preprocessed cranial implant. To date, six cranial implants have been made with this technique. The whole head models are accurate and help the neurosurgeon-prosthodontist team in the creation of a symmetric, anatomically correct restoration. It is the technique of choice for large implants or where the cranial bones are thin. It is not necessary to augment or alter the implant during surgery. The technique reduces surgical time, and postsurgical complications have been minimal.
Binding properties of naftopidil and alpha 1-adrenoceptor antagonists to alpha-adrenoceptors in prostates from benign prostatic hypertrophy (BPH) were characterized by radioreceptor assays using [3H]prazosin and [3H]rauwolscine. Specific binding of [3H]prazosin and [3H]rauwolscine in human prostatic membranes was saturable and of high affinity, and it showed a pharmacological specificity which characterized alpha 1 and alpha 2-adrenoceptors, respectively. Naftopidil and several alpha 1 antagonists competed for prostatic [3H]prazosin binding in order: R-(-)-YM-12617 greater than prazosin greater than bunazosin greater than terazosin greater than naftopidil greater than urapidil, and the inhibitory effect (Ki = 11.6 nM) of naftopidil was 10 to 45 times less potent than quinazoline derivatives such as prazosin, bunazosin and terazosin. The potencies of these antagonists in competing for [3H]prazosin binding sites in human prostates correlated well with their pharmacological potencies (pA2). Scatchard analysis indicated that the decrease of prostatic [3H]prazosin binding by naftopidil was due to a marked increase in the Kd value without a change in the Bmax value. The inhibition of prostatic [3H]prazosin binding by naftopidil was reversible. Naftopidil also inhibited prostatic [3H]rauwolscine binding (Ki = 70.0 nM). Thus, it is suggested that naftopidil antagonizes alpha 1-adrenoceptors in human prostates in a competitive and reversible manner.
This study was undertaken to investigate changes in feeding behavior and ambulatory activity, in rats with D-galactosamine (D-GAL)-induced hepatic failure. D-GAL was administered (1000 mg/kg) IP at 1800, just before the dark phase. The first significant decrease of ambulatory activity in rats with hepatic failure was observed between 0000 and 0300 h. A significant increase in drinking behavior was observed between 1800 and 2100 h, and a significant decrease was observed between 2100 and 0300 h. A significant decrease in food intake occurred between 1800 and 2400 h. Thereafter, there was no difference in food intake. In conclusion, we demonstrated significant changes in ambulatory activity, drinking behavior and food intake produced by D-GAL. A wide variation in systems, including monoamine turnover, and amino acid disturbance could be expected in these animals, and such changes might also have contributed to the results observed.
Using a neural network, we have developed a program for fast and precise detection of action potentials (AP) in raw multi-channel optical recording data. The AP detection was performed in two steps: first, peaks were detected in raw optical data, and, second, the peaks were classified by the neural network into APs, noise and undecided peaks. The network was optimized and trained by the backpropagation learning algorithm, employing some thousands of manually classified peaks. The performance of the optimized network was found to be not completely satisfactory, although it was better than the classification by template matching and nearest-neighbor rules. The addition of a signal-to-noise ratio (SNR) of a peak to the network classification improved the classification performance: in comparison with the manual classification results, 96% of manually classified APs were detected. The causes of classification errors were discussed. In spite of the fact that the program required a slight amount of human intervention for undecided peaks, the program could allow mostly automatic AP detection.