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Biomedical subjects

H Shimada

Publications and source records attributed to H Shimada.

At least 703 records · Page 39Linked to original sources
PubMed1990

[Clinical study of preoperative radiotherapy of bladder cancer].

From May 1982 to Nov. 1987, 33 patients with bladder carcinoma were treated with preoperative radiotherapy (20 Gy/5fr) and total cystectomy. The over all 3-year survival rate was 70%. For T1 and T2, 3-year survival rate was 100%, but only 55% and 0% for T3 and T4 respectively. In 23 out of 33 patients, preoperative T-stage was confirmed by TUR-BT. Down-Staging was recognized in 7 out of 23 patients (30%). They were 0 out of 1 patients for Tcis (0%), 2 of 3 for T1 (67%), 3 of 6 for T2 (50%), 2 of 11 for T3 (18%) and 0 of 2 for T4 (0%). This protocol of preoperative radiotherapy is thought to be favorable for T1 and T2 bladder carcinoma, but inadequate for T3 and T4 tumors. Consequently, it is considered that higher dose radiotherapy and postoperative chemotherapy are necessary for T3 and T4 bladder carcinoma.

Adult↗
PubMed1990

Molecular cloning of a cDNA encoding aldosterone synthase cytochrome P-450 in rat adrenal cortex.

Using an oligonucleotide probe designed on the basis of the N-terminal amino acid sequence of purified rat aldosterone synthase cytochrome P-450 [(1989) J. Biol. Chem. 264, 10935] we have isolated from rat adrenal cDNA library a 2687 base pair cDNA that encodes a protein of 500 amino acid residues. The deduced amino acid sequence contained the regions well conserved among all cytochrome P-450s sequenced to date, and also a portion (residues 25-44) which was identical to the N-terminal peptide sequence of rat aldosterone synthase cytochrome P-450. These results indicate that the cDNA encodes a precursor form of rat aldosterone synthase cytochrome P-450.

Adrenal Cortex↗
PubMed1990

Structure of the rat PRPS1 gene encoding phosphoribosylpyrophosphate synthetase subunit I.

Phosphoribosylpyrophosphate (PP-Rib-P) synthetase (EC 2.7.6.1) subunit I gene (PRPS1) is constitutively expressed in various tissues (Taira, M., Iizasa, T., Yamada, K., Shimada, H., and Tatibana, M. (1989) Biochim. Biophys. Acta 1007, 203-208). We report here the exon-intron organization and the transcription promoter sequence of rat PRPS1 gene. This gene has 22 kilobases and is split into 7 exons ranging in size from 99 to 251 base pairs (bp), except for exon 7 (1008 bp). A putative PP-Rib-P binding site is encoded in exon 5. The exon-intron boundaries are similar to the consensus sequences for mammalian introns. S1 nuclease and primer extension assays with the use of RNA from rat Yoshida ascites sarcoma cells led to the identification of four possible transcription start points closely spaced between 126 and 129 bp from the ATG initiation codon. In the upstream region from the transcriptional start sites, we observed a TATA-like sequence (TAATTTAAT) at nucleotides -28, a CCAAT element (AGCCAATC) at nucleotides -80, and three GC boxes (putative Sp1-binding sites) at nucleotides -103, -43, and -10. A comparison of the promoter region for PRPS1 with those of other housekeeping genes revealed a homology resembling that of the beta-actin gene.

Actins↗
PubMed1990

Histopathologic features of composite ganglioneuroblastoma. Immunohistochemical distinction of the stromal component is related to prognosis.

Histopathologic features of 18 cases of composite ganglioneuroblastoma (CGNB) were studied with immunohistochemical staining techniques using antibodies against S-100 protein (S-100), ferritin (FER), and leukocytic common antigen (LCA). Cases of CGNB were divided on the basis of the morphologic features of neuroblastic elements into three prognostic subgroups: "Type A Intermixed," having individual microscopic nests of neuroblasts (N = 4, 100% survival); "Type B Intermixed," having microscopic aggregates of multiple neuroblastic nests (N = 6, 67% survival); and "Nodular," having grossly visible nodule(s) of neuroblastic proliferation (N = 8, 0% survival). Survival rates are significantly different for the prognostic subgroups (P less than 0.025). Each prognostic subgroup demonstrated an immunohistochemically distinct pattern of stromal cell composition in the neuroblastic elements: Type A Intermixed had numerous S-100 cells and no FER cells, Type B Intermixed contained many S-100 cells and a moderate number of FER cells, and Nodular had few S-100 cells with many FER cells. The S-100 and FER scores, determined by counting the positive cells through a line sampling method, differed significantly between these prognostic subgroups. Lymphocytic aggregations in tumor tissue evaluated by volumetric assessment with LCA staining, on the other hand, showed no contribution in predicting the outcome of the patients. There was also an inverse relationship between S-100 and FER score, suggesting a relationship between the relative predominance of these stromal cell types, tumor histopathologic features, and the biologic behavior of CGNB.

Cell Aggregation↗
PubMed1990

Rice chloroplast RNA polymerase genes: the absence of an intron in rpoC1 and the presence of an extra sequence in rpoC2.

The chloroplast genome contains sequences homologous to the Escherichia coli rpoA, rpoB and rpoC genes. The chloroplast rpoC gene is divided into rpoC1 and rpoC2, of which rpoC1 contains an intron. Comparison of the rice rpo genes with those from tobacco, spinach and liverwort revealed unique features of the rice genes; the lack of an intron in rpoC1 and the presence of an extra sequence of 381 bp in rpoC2. The intron in rpoC1 is thus optional, and possible intron boundary sites in split rpoC1 genes can be estimated by comparison with rice rpoC1. The extra sequence is located in the middle of rpoC2 and has repeated structures. The amino acid sequence deduced from this sequence is extremely hydrophilic and anionic. The origin and function of this sequence are discussed.

Amino Acid Sequence↗
PubMed1990

Three-dimensional structure of Alzheimer's neurofibrillary tangles of the aged human brain revealed by the quick-freeze, deep-etch and replica method.

The three-dimensional structure of Alzheimer's neurofibrillary tangles in the pyramidal cells of the hippocampus and in the nerve cells of the parahippocampal gyrus was examined by the quick-freeze, deep-etch and replica method. The tangles consisted of either parallel bundles of or randomly arranged paired helical filaments (PHF), occupying the perikaryotic cytoplasm and extending to the dendritic processes. On the stereophotographs the PHF, measuring 28 to 36 nm in width, had two component filaments of 14 to 18 nm in diameter which were coiled anti-clockwise (left-handed) around each other with periodicity of 70 to 90 nm. The PHF in compact parallel bundles were cross-linked to each other with thin filaments, of about 6 nm in diameter, at relatively regular intervals. Randomly arranged PHF had no cross-bridges or side arms. Straight-type tangles of about 24 nm in diameter were rarely found in the dendritic processes. There were no discernible differences between the PHF of the patients with senile dementia of Alzheimer type and those of nondemented brains.

Aged↗
PubMed1990

Senile dementia of Alzheimer type characterized by laminar neuronal loss exclusively in the hippocampus, parahippocampus and medial occipitotemporal cortex.

Seven cases of senile dementia of Alzheimer type (SDAT) with unusual clinico-pathological findings are reported. The patients showed neuronal loss in laminar pattern, with gliosis exclusively confined to the CA1 of the hippocampus, the area of the hippocampal gyrus (entorhinal cortex) and medial occipitotemporal cortex. This change was more pronounced in the oral region. The subcortical white matter showed more pronounced fibrillary gliosis than loss of myelin. Both Alzheimer's neurofibrillary tangles and senile plaques were less marked than those usually seen in SDAT. The mental disturbance started after the age of 65 in all patients. The main clinical feature was marked character change in addition to disturbance of cognitive function. Cranial computed tomography showed marked dilatation of the oral portion of the inferior horn of the lateral ventricle in the early stage. It was apparent that although the cases in this group could be incorporated within in the spectrum of SDAT, they could also be considered to represent a variant of SDAT. This group could contribute to an understanding of the clinico-pathological spectrum of SDAT as well as indicating ways of managing such patients.

Aged↗
PubMed1990

Loss of nerve fibres in the corpus callosum of progressive subcortical vascular encephalopathy.

The nerve fibres of the corpus callosum were studied by electron microscopy in five elderly patients with progressive subcortical vascular encephalopathy (PSVE) and compared with those in six age-matched controls. The number of nerve fibres per unit area of the corpus callosum was decreased in PSVE by 18-26%. The loss of nerve fibres in the corpus callosum can play a role in inducing the cognitive deficit of PSVE, on the basis of the loss of nerve fibres in the cerebral hemispheres.

Aged↗
PubMed1990

Curly fibers are tau-positive strands in the pre- and post-synaptic neurites, consisting of paired helical filaments: observations by the freeze-etch and replica method.

The ultrastructure of the curly fibers was examined by the transmission and immunoelectron microscopy as well as by the rapid-freeze, deep-etch and replica method. The curly fibers consisted mainly of paired helical filaments (PHF) in the neuropils, both pre- and post-synaptic. On the deep-etch replicas, PHF in the neurites had similar dimensions to those of Alzheimer's neurofibrillary tangles in the nerve cell somata, having the width of 28 to 36 nm. The two component filaments, 14 to 18 nm in width, were twisted left-handedly with about 70- to 90-nm intervals. There were also cross-bridging fibrils of about 6 nm in diameter connecting the neighboring PHF.

Aged↗
PubMed1990

Thrombin stimulates the proliferation of human retinal glial cells.

Retinal glial cells may play a role in most of the proliferative retinopathies. Although glial cell proliferation is a frequent event in retinal pathobiology, no specific mitogens for human retinal glial cells are known. Using cultured retinal glial cells obtained from postmortem adult human eyes, we found that thrombin stimulates glial cell proliferation in a dose-dependent manner with a half-maximal concentration of 100 ng/ml (0.4 U/ml). Thus, thrombin may be a plasma-derived mitogen capable of stimulating retinal glial cells to proliferate when there is a breakdown of the blood-retinal barrier. We also observed that this proliferative response of retinal glia requires more than 6 h of continuous exposure to thrombin. This finding suggests that a thorough wash-out of a thrombin-containing infusate and/or the rapid inactivation of this molecule would prevent thrombin form exacerbating a proliferative disorder of the retina.

Adult↗
PubMed1990

Primary structure of a base non-specific and adenylic acid preferential ribonuclease from Aspergillus saitoi.

The complete primary structure of a base non-specific and adenylic acid preferential RNase (RNase M) from Aspergillus saitoi was determined. The sequence was determined by analysis of the peptides generated by digestion of heat-denatured RNase M with lysylendopeptidase, and the peptides generated from RCM RNase M by digestion with staphylococcal V8 protease or chemical cleavage with BrCN. It consisted of 238 amino acid residues and carbohydrate moiety attached to the 74th asparagine residue. The molecular weight of the protein moiety deduced from the sequence was 26,596. The locations of 10 half cystine residues are almost superimposable on those of RNase Rh from Rhizopus niveus and RNase T2 from Aspergillus oryzae which have similar base specificity. The homology between RNase M and RNase Rh and RNase T2 amounted to 97 and 160 amino acid residues, respectively. The amino acid sequences conserved in the three RNases are concentrated around the three histidine residues, which are supposed to form part of the active sites of these RNases.

Adenosine Monophosphate↗
PubMed1990

Ultrastructural study of the human pineal gland in aged patients including a centenarian.

An ultrastructural study of human pineal glands obtained at autopsy from 7 patients older than 70 years was conducted in order to clarify the functional anatomy of the pineal in the aged. By light microscopy, the pineal glands from aged patients were parenchymatous and almost indistinguishable from those of younger controls. Electron microscopy of the pineal parenchymal cells revealed deep nuclear indentations, synaptic ribbons and ribbon fields, Golgi apparatus, lipofuscin granules and microtubular sheaves in all subjects, cilia with a 9 + 0 pattern in a few, and lamellated structures suggestive of the outer segment of photoreceptor cells very rarely. Microtubules were numerous in the cytoplasmic processes and bulbous endings. Fibrous astrocytes located between the pinealocytes showed long and thin cytoplasmic processes containing numerous glial filaments. Two types of nerve bouton were present in the pineal parenchyma, one of which contained clear vesicles forming synapse-like contacts with pinealocytes. There were no significant age-related changes in these features in a qualitative comparison with pineal glands from 5 adult patients younger than 70 years. These findings indicate that even in advanced age, the human pineal gland maintains some functions, such as intercellular communication and photoreception, in common with the pineal in lower vertebrates.

Adult↗
PubMed1990

[Prevalence of the antibody against human polyoma viruses (JCV and BKV) in aged persons].

JC virus (JCV) and BK virus (BKV) are known as small DNA type tumor viruses belonging to the human polyoma virus. The infectious state of these viruses has not yet been examined extensively in the aged persons; therefore, antibody measurements were made in 349 healthy volunteers from 20 to 90 years old and 383 cases of in-patients from 60 to 100 years old. As controls, measurements were made on the antibody titers to the herpes-type viruses which are known to be reactivated as the immunologic state of hosts decrease. The results obtained were as follows; 1) In the aged cases over 60 years old, the average HI antibody titers for JCV were significantly higher than that for BKV. 2) In the aged persons of the prevalence rate the high antibody titer (1024 less than) for JCV was also higher than that for BKV. 3) In the results with EIA (EIA test human polyoma viruses common antigen), the significant increase in the antibody titer was observed in the aged older than 70. 4) The average antibody titers of HSV and CMV, tended to increase as the age advanced until 60 and to decrease with age over 70. These results indicate that JCV is reactivated in a high rate in the aged (70 less than) persons.

Adult↗
PubMed1990

Inhibitory effect of heparin and/or antithrombin III on intraperitoneal fibrin formation in continuous ambulatory peritoneal dialysis.

The intraperitoneal fibrin formation and its inhibition by intraperitoneal heparin and/or antithrombin III (AT III) were examined in 8 patients on continuous ambulatory peritoneal dialysis (CAPD). With 1,000 and 2,000 U/L of heparin added to inflow dialysate, the concentration of fibrinopeptide A (FPA) in plasma decreased from 39.43 +/- 5.30 (mean +/- SEM) to 8.00 +/- 2.20 and to 0.74 +/- 0.12 ng/ml, respectively. The FPA concentration in outflow dialysate decreased from 34.20 +/- 5.75 to 12.94 +/- 2.10 ng/ml (1,000 U/l of heparin) and to 4.54 +/- 0.79 ng/mg (2,000 U/l of heparin). The AT III concentration was 0.47 +/- 0.07 mg/dl in dialysate and that in plasma was 24.20 +/- 2.76 mg/dl. With 100 U/bag of AT III added to inflow dialysate, the AT III concentration increased from 0.47 +/- 0.07 to 3.36 +/- 0.17 mg/dl in outflow dialysate but did not increase in plasma. The inhibition of fibrin formation of intraperitoneal heparin was increased by addition of AT III without a systemic inhibitory effect on fibrin formation. These data suggest that intraperitoneal administration of heparin without AT III would be sufficient for the purpose of preventing fibrin formation in CAPD patients without any trouble, and additional AT III might increase inhibitory effect of heparin.

Antithrombin III↗
PubMed1990

Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity of inorganic mercury in rats.

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity of inorganic mercury in rats was studied. Rats were injected i.v. with saline or HgCl2 (300 micrograms Hg/kg) and 30 min later they were injected i.p. with saline or BGD (2778 mumol/kg, a quarter of an LD50). Urinary excretion of gamma-glutamyl-transpeptidase (gamma-GTP), which is a brush border enzyme, in rats after mercury treatment significantly increased compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 24 h after the treatment. Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), which is a lysosomal enzyme, also significantly increased after mercury treatment compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 48 h after the treatment. A change in urinary aspartate aminotransferase (AST) activity after mercury treatment followed a pattern similar to that observed with the urinary NAG. BGD treatment did not increase the urinary excretions of gamma-GTP, NAG, and AST. The uptake of p-aminohippuric acid (PAH) by renal cortical slices significantly decreased 24 h after mercury treatment. BGD injection after mercury treatment did not decrease the uptake of PAH by cortical slices. In addition, the microscopic examination of renal tissue from mercury-treated rats revealed necrosis of the proximal tubular cells. However, a photomicrograph of rat renal cortex after BGD treatment showed little abnormality. These results indicated that the mercury-induced renal damage was protected by the injection of BGD 30 min after mercury treatment.

Animals↗
PubMed1990

Protective effect of N-benzyl-D-glucamine dithiocarbamate against cis-diamminedichloroplatinum-induced toxicity in gastrointestinal tract and bone marrow in rats.

The protective effect of N-benzyl-D-glucamine dithiocarbamate (BGD) against gastrointestinal and bone marrow toxicities produced by cis-diamminedichloroplatinum (DDP) injection in rats was studied. Rats were injected i.p. with BGD (2 mmol/kg) immediately after i.v. injection of DDP (20 mumol/kg). A scanning electron micrograph of the jejunum after DDP treatment showed damage in the villi, and that BGD protected the DDP-induced jejunal damage. BGD treatment also had a protective effect against DDP-induced diarrhea. BGD significantly reversed the reduction in maltase and sucrase activities of jejunal mucosa of rats treated with DDP. Platinum (Pt) concentrations in the gastrointestine as well as in the kidney and liver after DDP injection decreased following BGD treatment. The reduction of leukocytes following DDP injection returned to control values after BGD treatment. Biliary and urinary excretions of Pt after DDP injection was remarkably increased by BGD treatment. The results of this study indicated that the injection of BGD to rats treated with DDP can effectively remove Pt from the body through biliary and urinary excretions, resulting in protection of the gastrointestinal and bone marrow toxicities induced by DDP treatment.

Animals↗
PubMed1990

Effects of three dithiocarbamates on tissue distribution and excretion of cadmium in mice.

N-Benzyl-D-glucamine dithiocarbamate (BGD), N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), and N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD) were compared for their relative efficacies in the distribution and excretion of cadmium in mice exposed to cadmium. Mice were injected intraperitoneally with 109CdCl2 (1 mg of Cd/kg and 2 microCi of 109Cd/one animal). Three days later, they were injected with chelating agents (400 mumol/kg) every other day for 2 weeks. After injections of BGD and HBGD, cadmium was excreted mainly in the feces through the bile, and the fecal excretion of cadmium by HBGD was significantly higher than that by BGD or CBGD. These chelating agents increased the urinary excretion of cadmium to a small extent. The hepatic cadmium content was decreased only after HBGD injection. Also, the injection of HBGD caused a much greater decrease in renal cadmium content than did BGD or CBGD. These chelating agents did not result in the redistribution of cadmium to the brain, testes, or heart. The growth of mice was only slightly retarded by injections of these chelating agents. The results of this study indicate that the injection of HBGD to mice pretreated with cadmium can remove cadmium from the body, mainly through fecal excretion, without redistribution of cadmium to other tissues such as the brain, testes, and heart, more effectively than BGD or CBGD.

Animals↗