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Biomedical subjects

H Shimura

Publications and source records attributed to H Shimura.

At least 55 records · Page 3Linked to original sources
PubMed1999

A model of port-site metastases of gallbladder cancer: the influence of peritoneal injury and its repair on abdominal wall metastases.

BACKGROUND: Recent surgical literature contains several reports of wound metastases of unexpected gallbladder cancer after laparoscopic cholecystectomy. We hypothesized that peritoneal injury caused by trocar insertion potentiates wound metastases. This study was designed to determine the effect of peritoneal injury on tumor implantation. METHODS: Cultured human gallbladder cancer cells were injected into the peritoneal cavity of mice immediately after surgical procedures. In a peritoneal injury group muscle and the peritoneum were perforated; in a peritoneal injury and repair group each muscle and peritoneal wound was sutured carefully; in a laparoscopic model group animals underwent peritoneal insufflation with carbon dioxide gas and tumor cell injection and then the abdominal wall was perforated. Some mice (controls) were not subjected to any surgical procedure. All mice (n = 178) were killed 2 weeks after tumor cell injection and were examined for tumor implantation. RESULTS: Although no control mice showed intraperitoneal tumor, all mice in the peritoneal injury group showed tumors at the injured sites. In the laparoscopic model group, 90% of injured sites had tumors. The traumatized site-specific implantation rate in the peritoneal injury and repair group was only 40%, whereas it was 100% in the peritoneal injury group (P < .001). CONCLUSIONS: Peritoneal injury enhances peritoneal implantation of carcinoma cells. Repair of injured peritoneum at trocar sites may reduce the frequency of wound metastases in laparoscopic surgery for unexpected gallbladder carcinoma.

Abdominal Muscles↗
PubMed1999

[Antimicrobial activities of beta-lactam antibiotics against clinically isolated Haemophilus influenzae].

Antimicrobial activities of oral beta-lactam antimicrobial agents against clinically isolated 131 strains of Haemophilus influenzae were studied. The peak of MICs of ampicillin (ABPC) was 0.20 microgram/ml. Those of cefaclor (CCL), cefotiam (CTM), cefteram (CFTM), cefpodoxime (CPDX), cefdinir (CFDN), cefditoren (CDTR), cefcapene (CFPN), and faropenem (FRPM) were 1.56, 0.39, 0.013, 0.05, 0.20, 0.013, 0.013, and 0.39 microgram/ml, respectively. The antimicrobial activities of CFTM, CDTR and CFPN were superior to those of others. There was 74.8% of ABPC-sensitive strains, of which the MICs were below 0.78 microgram/ml. The percentages of beta-lactamase-positive strains and beta-lactamase-negative ABPC-resistant H. influenzae (BLNAR) were 14.5% and 14%, respectively.

Anti-Bacterial Agents↗
PubMed1998

Inhibition of tumor growth and invasion by a four-kringle antagonist (HGF/NK4) for hepatocyte growth factor.

Invasion of various carcinoma cells follows their interaction with stromal cells. Hepatocyte growth factor (HGF), four-kringle-containing growth factor, is a mesenchymal or stromal-derived mediator which affects the growth and the invasiveness of carcinoma cells. We now have evidence that a four-kringle-containing antagonist for HGF, HGF/NK4 inhibits invasion of tumors in vivo, as well as in vitro. HGF/NK4 competitively inhibited the binding of HGF to Met/ HGF receptors on GB-d1 human gallbladder carcinoma cells. HGF induced invasion of the cells through Matrigel basement membrane components and into collagen gels, but HGF-induced invasion was inhibited by HGF/NK4. Invasion of GB-d1 cells was induced by co-cultivation with stromal fibroblasts, which mimics tumor-stromal interaction, but it was almost completely suppressed by HGF/NK4. Likewise, invasive growth induced by HGF in collagen gels in GB-dl cells, HuCC-T1 human cholangiocarcinoma cells, and ME-180 human uterus cervical carcinoma cells was also strongly inhibited by HGF/NK4. When GB-d1 cells were implanted subcutaneously into nude mouse, tumor cells invaded muscular tissue, but the infusion of HGF/NK4 inhibited this invasion. Furthermore, HGF/NK4 increased apoptotic cell death of GB-d1 cells and inhibited tumor growth in vivo. These results indicate that HGF/ NK4 may inhibit growth and invasion of carcinoma cells, as mediated by HGF during tumor-stromal interactions. We propose that there is a unique therapeutic potential for HGF/NK4 to prevent tumor invasion and perhaps even metastasis.

Aged↗
PubMed1998

Laparoscopic treatment of duodenal carcinoid tumor. Wedge resection of the duodenal bulb under endoscopic control.

A 46-year-old man with epigastralgia and slight elevation of urinary 5-hydroxyindole acetic acid (5HIAA) was found to have a well-demarcated carcinoid tumor in the duodenal bulb. The tumor measured 8 mm in size, and showed submucosal involvement but no metastasis to the liver and regional lymph nodes. After laparoscopic exposure and lifting of the duodenal wall around the tumor, wedge resection of the duodenal bulb including the tumor was performed successfully with a laparoscopic endostapler under direct endoscopic control. The postoperative course of the patient was uneventful. Laparoscopic wedge resection of the duodenum would be an appropriate minimally invasive treatment of selected duodenal neoplasms with special preoperative assessments and intraoperative considerations.

Carcinoid Tumor↗
PubMed1998

Laparoscopic treatment of congenital choledochal cyst.

We describe the laparoscopic treatment of a patient presenting with congenital choledochal cyst. Our patient was a 19-year-old man with a complaint of recurrent abdominal pain due to pancreatitis. The choledochal cyst was type I and had a common channel of pancreatobiliary duct, as revealed by endoscopic retrograde cholangiopancreatography. Under laparoscopic guidance, the dilated bile duct and the gallbladder were excised, and a Roux-en-Y anastomosis was constructed with an endo-EEA. Finally, end-to-side anastomosis was carried out by the continuous suture method, aided by an Endostitch between the stump of the hepatic duct and the Roux-en-Y limb. After the operation, slight hyperamylasemia was observed for several days but further treatment was not necessary. Postoperative symptoms were minimal, and the patient was discharged on the 11th day after the procedure. Although it is difficult and time-consuming, laparoscopic operation is highly beneficial for the patient. The use of such instruments as the endostapler and Endostitch may help to simplify this complex intracorporeal procedure involving division and anastomosis of the digestive tract.

Adult↗
PubMed1998

Familial cortical tremor with epilepsy: an under-recognized familial tremor.

The authors report three Japanese families presenting with cortical tremor and epilepsy. The patients showed either tremulous finger movements or seizures as the initial symptoms between 19 and 30 years of the age without progression. Postural tremor resembled essential tremor and responded to the anticonvulsants such as clonazepam, primidone and sodium valproate. Seizures were infrequent. These patients seem to have the same disorder as what the authors have described as 'familial cortical tremor with epilepsy'. Familial cortical tremor must be more common than previously thought and should be taken into consideration in the patients with 'familial essential tremor' who do not respond well to beta-blockers.

Adult↗
PubMed1998

Hepatocyte growth factor stimulates the invasion of gallbladder carcinoma cell lines in vitro.

Human gallbladder cancer is highly malignant and its prognosis is usually poor depending on the extent of surrounding tissue invasion. We examined in vitro the invasive activity of four gallbladder cancer cell lines (GB-d1, GB-h3, GB-d2 and FU-GBC-1) in the absence or presence of hepatocyte growth factor (HGF). In type 1 collagen gel culture, HGF stimulated cell proliferation and induced an invasive phenotype of arborizing structures in GB-d1, GB-h3 and GB-d2. In a Matrigel invasion assay, invasion was also induced in three of these cell lines by HGF but not in FU-GBC-1. Cellular motility was, however, stimulated by HGF in all of the four cell lines to various extents. Zymography for proteolytic enzymes demonstrated high levels of type IV collagenase and urokinase-type plasminogen activator (u-PA) activity in GB-d1, GB-h3 and GB-d2 even in the absence of HGF. In the presence of HGF, the 72 kDa type IV collagenase (MMP-2) activity of GB-h3 and u-PA activities of GB-d1, GB-h3 and GB-d2 were enhanced. In contrast, the MMPs and PAs activities of FU-GBC-1 were faint irrespective of the addition of HGF. A Western blot analysis demonstrated higher levels of 190 kDa c-MET product (HGF receptor) of GB-d1, GB-h3 and GB-d2 than that of FU-GBC-1. The invasion in the Matrigel assay stimulated by HGF was inhibited by protease inhibitors, aprotinin and FOY-305, as well as by anti-HGF antibody. These results thus suggest that, in addition to the importance of the proteolytic activity, the cellular motility induced via the HGF/HGF-receptor system is essential for the invasive progression of gallbladder carcinoma cells.

Adenocarcinoma↗
PubMed1998

Effects of cytokines on expression of thyrotropin receptor mRNA in rat preadipocytes.

Cultured rat preadipocytes express thyrotropin receptor (TSHR) during their differentiation. To evaluate the effects of inflammatory cytokines on the expression of TSHR in cultured rat preadipocytes, we cultured those cells in the presence of recombinant human tumor necrosis factor (rhTNF)-alpha, recombinant human interferon (rhIFN)-gamma, and human transforming growth factor (hTGF)-beta1. The effects on the level of TSHR mRNA and signal transduction were evaluated. Addition to the medium of 1 ng/mL TNF-alpha, 1 ng/mL rhIFN-gamma, and 1 ng/mL hTGF-beta1 during the differentiation of rat preadipocytes inhibited the expression of TSHR mRNA. The decrease in TSHR mRNA was accompanied by a decrease in TSH-stimulated cyclic adenosine monophosphate (cAMP) production. Histochemical analysis showed that these cytokines inhibited the morphological differentiation of the cells. These cytokines also decreased the expression of mRNA for such fat-specific proteins as lipoprotein lipase and aP2. Results indicate that the loss of expression and function of the TSHR is closely related to the inhibition of differentiation. This confirms the close relation between the expression of the TSHR and the differentiation of the rat preadipocytes.

Adaptor Protein Complex 2↗
PubMed1998

Augmentation of mitochondrial reduced glutathione by S-adenosyl-L-methionine administration in ischemia-reperfusion injury of the rat steatotic liver induced by choline-methionine-deficient diet.

We examined whether warm ischemia-reperfusion (I/R) damage of the rat steatotic liver can be reduced by administration of S-adenosyl-L-methionine (SAMe). We examined the effect of SAMe on the mitochondrial reduced-glutathione (GSH) pool. Sixty minutes of partial left lobar vascular clamping followed by 2 h of reperfusion were employed for a model of hepatic warm ischemia. Either 5% dextrose or SAMe was injected intraperitoneally 2 h before I/R in steatotic rats (S-D5% or S-SAMe group). Serum liver enzyme concentrations 2 h after reperfusion were significantly lower in the S-SAMe group than in the S-D5% group. The cytosolic and mitochondrial GSH concentrations after I/R were significantly higher in the S-SAMe group than in the S-D5% group (p < 0.05). The cytosolic and mitochondrial oxidized-glutathione/GSH ratios after I/R were significantly greater in the S-D5% group than in the S-SAMe group (p < 0.01). The adenosine triphosphate concentration was higher in the S-SAMe group than in the S-D5% group (p = 0.0515). These results show that hepatocellular and mitochondrial oxidative stress after I/R in the steatotic liver can be reduced by administration of SAMe. The results also show that mitochondrial function and hepatocellular integrity can be restored by administration of SAMe in steatotic rats.

Animals↗
PubMed1998

Analysis of differentiation-induced expression mechanisms of thyrotropin receptor gene in adipocytes.

Rat adipose tissue, as well as differentiated 3T3-L1 cells, has been shown to express TSH receptor (TSHR) mRNA in amounts approaching those in the thyroid. We investigated the molecular mechanisms of TSHR gene expression in adipose cells. Primer extension and cloned cDNA sequences showed that transcription of the TSHR gene in rat adipose tissue was from multiple start sites clustered between -89 to -68 bp and almost identical to those in FRTL-5 thyroid cells. By transient expression analysis, we localized, between -146 and -90 bp, a positive regulatory element, the activity of which was markedly increased after the differentiation of 3T3-L1 cells. Deoxyribonuclease I protection showed that nuclear extracts from differentiated 3T3-L1 cells strongly protected two sequences, from -146 to -127 bp, including a cAMP response element-like sequence and from -112 to -106 bp containing a putative Ets-binding sequence. In differentiated 3T3-L1 cells, disruption or deletion of either sequence was found to result in the loss of enhancer activity, suggesting both elements may synergistically activate the TSHR promoter. Electrophoretic mobility shift analysis revealed the induction of new protein/DNA complexes formed either with the cAMP response element-like site or with putative Ets elements after the differentiation into adipocytes. In contrast, nuclear proteins, whose binding to DNA was diminished after the differentiation of 3T3-L1 cells, were found to interact with the site contiguous to the 5'-end of the putative Ets-binding sequence. Mutations of this binding site, which reduced the protein/DNA complex formation, increased TSHR promoter activity in undifferentiated cells. These observations suggested that differentiation-induced diminution of suppressor interactions may allow the enhancers to synergistically activate the transcription of TSHR gene in adipocytes.

Adipocytes↗
PubMed1998

Regulation of the rat thyrotropin receptor gene by the methylation-sensitive transcription factor GA-binding protein.

The GA-binding protein (GABP), a transcription factor with a widespread tissue distribution, consists of two subunits, a and beta1, and acts as a potent positive regulator of various genes. The effect of GABP on transcription of the TSH receptor (TSHR) gene in rat FRTL-5 thyroid cells has now been investigated. Both deoxyribonuclease I footprint analysis and gel mobility-shift assays indicated that bacterially expressed glutathione S-transferase fusion proteins of GABP subunits bind to a region spanning nucleotides (nt) -116 to -80 of the TSHR gene. In gel mobility-shift assays, nuclear extracts of FRTL-5 cells and FRT cells yielded several specific bands with a probe comprising nt -116 to -80. Supershift assays with antibodies to GABPalpha and to GABPbeta1 showed that GABP was a component of the probe complexes formed by the nuclear extracts. Immunoblot analysis confirmed the presence of both GABP subunits in the nuclear extracts. A reporter gene construct containing the TSHR gene promoter was activated, in a dose-dependent manner, in FRTL-5 cells by cotransfection with constructs encoding both GABPalpha and GABPbeta1. Both GABP binding to and activation of the TSHR gene promoter were prevented by methylation of CpG sites at nt -93 and -85. These CpG sites were highly methylated (>82%) in FRT cells and completely demethylated in FRTL-5 cells, consistent with expression of the TSHR gene in the latter, but not the former. These results suggest that GABP regulates transcription of the TSHR gene in a methylation-dependent manner and that methylation of specific CpG sites and the methylation sensitivity of GABP contribute to the failure of FRT cells to express the endogenous TSHR gene.

Animals↗
PubMed1998

[Prognosis in the cases with renal cell carcinoma according to clinical parameters].

BACKGROUND: The objects of this study is to evaluate the clinical prognostic factors in renal cell carcinoma. MATERIALS AND METHODS: During a 30-year period from January 1965 to December 1994, 1301 cases with renal cell carcinoma were treated at the Yokohama City University Hospital and its affiliated hospitals. In these cases, cause specific 679 cases from January 1965 to December 1990 were analyzed in a study undertaken to investigate long-term treatment results and clinical prognostic factors. RESULTS: 1. The cause specific 5-, 10-, 15-, and 20-year survival rates were 48.7%, 41.1%, 32.3%, and 26.5% respectively, indicating thus that a great number of cases had an ominous prognosis even 5 years or moreafter surgical treatment. 2. Among patients under 40 years of age (n = 29) none died more than 2 years after receiving operation, the prognosis for this particular group of cases being relatively good. 3. Female, incidentally detected cancer, small tumor size (< or = 4.0 cm), slow growing type and low stage were proven to be favourable prognostic factors in renal cell carcinoma. 4. The cause specific 5-year survival rate for the patients (n = 239) from 1965 to 1981 was 33.8%, while the rate for the patients (n = 440) from 1982 to 1990 was 56.5%. This improvement of survival rate was brought by the increase of the incidentally detected renal cell carcinoma. 5. In the incidentally detected renal cell carcinoma, the incidence of slow growing cases and the cases of less than 4.0 cm tumor size were higher than in the symptomatic renal cell carcinoma. 6. Multivariate analysis using Cox's proportional hazard model showed that stage was the most important prognostic factor. CONCLUSIONS: These results suggested that sex, age, symptom, tumor size, growing type, and stage were important prognostic factors in renal cell carcinoma.

Adolescent↗
PubMed1998

Modulation of cholesterol metabolism affects tumor growth in hamsters.

To investigate the effects of cholesterol and cholesterol-lowering agents on cholesterol metabolism and tumor growth, 0.5% cholesterol, 2% cholestyramine, or 0.01% simvastatin was fed to hamsters with transplanted Simian virus40 transformed tumor cells. Tumor weight, tissue cholesterol and DNA concentrations, and HMG-CoA reductase activities were determined. Cholesterol or cholestyramine feeding did not affect the tumor growth, however, the tumor weight and DNA concentration were decreased and tumor HMG-CoA reductase activity was increased in the simvastatin group. In conclusion, simvastatin may inhibit the DNA synthesis and growth of the Simian virus40 transformed tumor cells possibly through the inhibition of cholesterol and isoprenoids synthesis in the hamster.

Animals↗
PubMed1998

[Thoracoscopic repair of diaphragmatic eventration sustained at knife injury: a case report].

A 46-year-old male taxi driver was stabbed onto the left chest while on duty. On arrival soon after, he was hemodynamically stable. Computed tomography showed omental prolapse into the left thorax through the diaphragm. On the 11th day, he underwent thoracoscopy revealing omental prolapse via a 3-cm rent in the left diaphragm, which was reduced manually. The diaphragmatic orifice was lifted and debrided with suturing using a stapling cutter. The post-operative course was uneventful. Finger palpation through the orifice enabled safe suturing of the left diaphragm facing the omentum, the colon, and the stomach, all of which may suffer iatrogenic injury.

Endoscopy↗