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T Kiba

Publications and source records attributed to T Kiba.

At least 37 records · Page 2Linked to original sources
PubMed1998

Use of balloon-occluded retrograde transvenous obliteration with ethanolamine oleate for the treatment of hepatic encephalopathy in a cirrhotic patient with a large spontaneous splenorenal shunt.

We describe a technique for the treatment of hepatic encephalopathy in a cirrhotic patient with a large spontaneous splenorenal shunt. This large shunt was successfully occluded without severe complications by retrograde transrenal venous obliteration with ethanolamine oleate after balloon occlusion. This procedure may be an effective method to occlude a large spontaneous splenorenal shunt for the treatment of hepatic encephalopathy.

Aged↗
PubMed1998

Hepatocyte proliferation in rats after ventromedial hypothalamic lesions: immunoreactivity patterns of proliferating cell nuclear antigen (PCNA).

Ventromedial hypothalamic (VMH) lesions result in increased DNA content in the rat liver. However, little information is available concerning the proliferative activity and lobular distribution of different cell populations in VMH-lesioned rat liver. The aim of the present study was to quantitatively assess these parameters in VMH-lesioned rat liver by measuring proliferating cell nuclear antigen (PCNA) reactivity. We investigated to determine whether this mitotic response involves acinar zones 1, 2, or 3. Changes in immunohistochemical labeling indices in rat liver were measured with an antibody against PCNA until 7 days after VMH lesioning. The effects of hepatic vagotomy on proliferation were also examined. Proliferation of hepatocytes in acinar zones 1-3 began to increase on day 1, and reached a maximum at 3 days. The area of most intense proliferation progressively shifted from acinar zone 1 to zone 3 in several days. The proliferation was completely inhibited by hepatic vagotomy, indicating that VMH lesions induce cell proliferation in rat liver via hepatic vagus nerve activity. This study implicates the information available on neural factors which initiate hepatocyte proliferation.

Animals↗
PubMed1998

Ocular arterial flow hemodynamics in patients with diabetes mellitus.

The purpose of this study was to investigate ocular blood flow hemodynamics in patients with diabetes mellitus. We used color Doppler sonography, in 22 normal subjects and 52 patients with (n = 25) or without (n = 27) diabetic retinopathy, to determine blood flow velocities and the resistive index of the central retinal artery. The resistive index of the central retinal artery in patients with diabetic retinopathy (0.85 +/- 0.09) was significantly greater (P < 0.01) than that in normal subjects (0.72 +/- 0.08) and in patients without diabetic retinopathy (0.81 +/- 0.09). The resistive index of the central retinal artery in the patients without diabetic retinopathy was also significantly greater than that of normal subjects (P < 0.01). The resistive index of ocular arterial flow was increased in the patients with diabetes mellitus and further increased in the presence of retinopathy. Increased resistance in the peripheral ocular vascular bed contributes to diabetic retinopathy, and this change is present before the appearance of overt diabetic retinopathy.

Blood Flow Velocity↗
PubMed1998

[SMANCS-TAE combined with PEI in the treatment for hepatocellular carcinoma].

From January 1996 to August 1997, 24 patients with advanced hepatocellular carcinoma (HCC) equal to or more than 2 cm (mean +/- SD; 4.1 +/- 3.0 cm) in main tumor diameter were treated by SMANCS-TAE (20 cases) or SMANCS-TAI (4 cases) combined with PEI. Six cases had solitary lesion, 16 cases had multiple lesions, and 2 cases had massive lesions. After this combination therapy, 21 of 24 cases had complete tumor necrosis. During 3 to 19 months follow up period, 12 cases had cancer-free survival (SMANCS-TAI; 3 cases), and 9 cases had tumor recurrences (3 cases were local recurrences and 6 cases involved new lesions). Two cases died of hepatic infarction and cancer death, however, the remaining 22 cases were surviving. SMANCS-TAE combined with PEI is useful treatment for advanced large or multiple HCC lesions in patients who are poor surgical risks.

Aged↗
PubMed1997

Plus- and minus-stranded hepatitis G virus RNA in liver tissue and in peripheral blood mononuclear cells.

Hepatitis G virus (HGV), which was recently identified, is a single, plus-stranded RNA virus that is thought to replicate via minus-stranded RNA, but no information is available about the distribution of either plus- (genomic) or minus- (replicative) stranded HGV RNAs in HGV infected patients. We, therefore, tested the serum, liver tissue, and peripheral blood mononuclear cells (PBMCs) of six hepatitis patients with HGV infection for the presence of plus- and minus-stranded HGV RNA. The RT-nested PCR was used with primers derived from 5'-noncoding region of the genome. Before RT-PCR analysis, the 3'-termini of RNA specimens were chemically modified to discriminate between plus- and minus-stranded HGV RNA. Plus-stranded HGV RNA was detected in the serum and liver tissue of all six patients and in the PBMCs of five patients. Minus-stranded RNA was detected in the liver tissue of all six patients, in the serum of two patients, and in the PBMCs of one patient. In summary, the detection of minus-stranded HGV RNA in liver tissue may indicate that HGV replicates in the liver.

Flaviviridae↗
PubMed1997

Use of hepatic tumor index on color Doppler sonography for differentiating large hepatic tumors.

OBJECTIVE: Color flow patterns on Doppler sonography are nonspecific for differentiating various hepatic tumors. We previously reported that a tumoral peak systolic flow velocity of 0.40 m/sec or greater suggested a malignant hepatic tumor rather than a hemangioma. However, tumoral peak systolic flow velocity failed to differentiate hepatocellular carcinomas and metastatic tumors. In this study, we attempted to assess the value of the hepatic tumor index for differentiating hepatocellular carcinomas and other hepatic tumors. MATERIALS AND METHODS: Color Doppler sonography was performed in 80 patients with 108 hepatic lesions larger than 2.0 cm in diameter. The hepatic tumor index was calculated as the ratio of the tumoral peak systolic velocity to the peak systolic velocity of the right or left hepatic artery. RESULTS: Pulsatile color flow images were obtained in 42 of 48 hepatocellular carcinomas, 25 of 32 hepatic metastases, and 13 of 28 hemangiomas. The mean hepatic tumor indexes obtained from hepatocellular carcinomas, metastases, and hemangiomas were 1.14 +/- 0.37 (+/-SD), 0.63 +/- 0.22, and 0.60 +/- 0.17, respectively. The hepatic tumor indexes of hepatocellular carcinomas significantly exceeded those of metastases and hemangiomas (p < .01 in both cases). A hepatic tumor index equal to or greater than 1.0 was associated with 76% sensitivity, 92% specificity, and 82% accuracy in distinguishing hepatocellular carcinomas from hepatic metastases. In lesions with a tumoral peak systolic velocity of 0.40 m/sec or greater, a hepatic tumor index equal to or greater than 1.0 was associated with 91% sensitivity, 83% specificity, and 89% accuracy in distinguishing hepatocellular carcinomas from hepatic metastases. CONCLUSION: The hepatic tumor index on color Doppler sonography was useful in differentiating large hepatocellular carcinomas from hepatic metastases.

Adult↗
PubMed1996

Ventromedial hypothalamic lesion-induced vagal hyperactivity stimulates rat pancreatic cell proliferation.

BACKGROUND & AIMS: Ventromedial hypothalamic (VMH) lesions cause an increase in DNA content in the rat pancreas. This study examined the role of cell proliferation in the mitotic response of the rat pancreas after VMH lesion formation. METHODS: Alterations in rat pancreatic DNA content, DNA synthesis, and labeling indices using antiproliferation cell nuclear antigen molecular antibody were measured 0,1,3, and 7 days after VMH lesion formation. Additionally, the effects of vagotomy, atropine, or anti-insulin antibody on VMH lesion-induced alterations in DNA synthesis were examined. Pancreatic samples were also treated with double immunostaining: first for PCNA and then for insulin, glucagon, and somatostatin. RESULTS: Pancreatic weight, DNA content, and DNA synthesis increased in animals receiving VMH lesions. Proliferation was primarily observed in islet B and acinar cells beginning 1 day after VMH lesion formation, reaching a maximum rate after 3 days. VMH lesion-induced stimulation of DNA synthesis was completely inhibited by vagotomy or atropine administration but not by anti-insulin antibody. CONCLUSIONS: Vagal hyperactivity produced by VMH lesions stimulated cell proliferation of rat pancreatic islet B and acinar cells primarily through a cholinergic receptor mechanism.

Analysis of Variance↗
PubMed1995

Lateral hypothalamic lesions facilitate hepatic regeneration after partial hepatectomy in rats.

It has been reported that ventromedial hypothalamic lesions facilitate hepatic regeneration through the hepatic vagal nerve after partial hepatectomy. However, whether the lateral area of the hypothalamus is involved in liver regeneration after partial hepatectomy is unknown. To determine the role of the lateral hypothalamic area in this phenomenon, we studied hepatic DNA synthesis during liver regeneration after partial hepatectomy with bilateral lesions of the area. Lesioning of the lateral hypothalamus accelerated the increase in hepatic DNA synthesis and raised the peak level of [methyl-3H]thymidine incorporation after partial hepatectomy. These effects of hypothalamic lesioning were inhibited by combined hepatic vagotomy and sympathectomy. Our results demonstrate that lesioning of the lateral hypothalamus promotes hepatic regeneration through the autonomic nervous system after partial hepatectomy and suggest that the lateral hypothalamic area is involved in liver regeneration through neural mediation.

Animals↗
PubMed1995

Ventromedial hypothalamic lesions induce the proliferation of gastrointestinal mucosal cells in the rat.

We reported recently that ventromedial hypothalamic (VMH) lesions increased the synthesis of DNA in the gastrointestinal tract of rats by the firing of vagus nerve activity, mainly via cholinergic receptor mechanisms. In the present study, we examined whether the mitotic response is due to proliferation of a cell population--mucosal, submucosal, or muscular layer. A monoclonal antibody to proliferating cell nuclear antigen (PCNA) has previously been shown to be capable of identifying proliferating cells. Samples of formalin-fixed gastrointestinal epithelium, taken before and after VMH lesioning, were immunostained with the anti-PCNA monoclonal antibody, and the labeling index (LI) was determined. To discriminate the effect of hyperphagia in VMH lesioned rats, we utilized the method of pair-feeding. Cell proliferation was examined by the PCNA-labeling technique 0, 1, 3, and 7 days after VMH lesioning. The increase in proliferation was confined to cells in the mucosa and did not involve the muscularis and serosa. Studies in control animals showed that the LI was higher in the small intestine than in other gut segments, and higher in the large intestine than in the stomach. The mean PCNA-LI began to increase at 1 day and continued to increase for 3 days, then decreased 7 days following the lesioning. Results indicate that the gastrointestinal mucosa is in a state of hyperproliferation after VMH lesioning.

Animals↗
PubMed1994

Facilitation of liver regeneration after partial hepatectomy by ventromedial hypothalamic lesions in rats.

Whether or not the hypothalamus is involved in initiating hepatic DNA synthesis after partial hepatectomy is unclear. To determine the role of the ventromedial hypothalamic nuclei in liver regeneration after partial hepatectomy, we studied hepatic DNA synthesis during liver regeneration in rats with bilateral lesions of these nuclei. Lesions of the ventromedial hypothalamus accelerated the increase in hepatic DNA synthesis and raised the peak level of thymidine incorporation after partial hepatectomy. These effects of hypothalamic lesions were completely inhibited by hepatic vagotomy. Thus, lesions of the ventromedial hypothalamus appear to promote hepatic regeneration by increasing vagal stimulation of the liver.

Animals↗
PubMed1993

Mutations of the p53 tumor suppressor gene and the ras gene family in intrahepatic cholangiocellular carcinomas in Japan and Thailand.

The incidence and pattern of mutations of the ras oncogenes and the p53 tumor suppressor gene have been shown to differ among different cancer types and even among the same cancer types with different etiological backgrounds. For example, in a previous study we showed that not only the etiology but also the incidence of point mutation of the c-Ki-ras oncogene in cholangiocellular carcinomas (CCCs) differ between Japanese and Thai patients. In the study presented here, we examined the incidence of mutations in the ras gene family and the p53 gene in CCCs of both Japanese and Thai patients by single-strand conformation polymorphism and direct sequencing analyses and compared the pattern of p53 mutation between these two CCC groups. Although the incidence of ras mutation differed markedly between Japanese (seven of 12, 58%) and Thai (two of 26, 8%) cases, the incidence of p53 mutation was similar: four of 12 (33%) and nine of 26 (35%), respectively. Except for one case in which deletion-insertion was detected in the second exon of the N-ras gene, all ras mutations occurred at codon 12 or 13 of the c-Ki-ras gene. All p53 mutations but one were detected in a highly conserved region, and the predominant form of the mutations was G:C-->A:T transition at CpG sites in both Japanese and Thai cases, similar to that reported for colorectal cancers. Therefore, in contrast to the ras oncogenes, mutation of the p53 gene was frequently involved in the development of CCCs in both Japanese and Thai patients, irrespective of any difference in etiology.

Adult↗
PubMed1993

Comparison of DNA synthesis in white and brown adipose tissue in rats with ventromedial hypothalamic lesions.

Ventromedial hypothalamic (VMH) lesions cause excessive fat accumulation in white adipose tissue (WAT), and brown adipose tissue (BAT); however, little information is available on whether or not cell proliferation occurs in WAT and BAT after VMH lesioning. In this study, we determined the DNA content and thymidine incorporation in unilateral parametrial WAT and interscapular BAT 0, 1, 3, and 7 days after VMH lesioning, and examined the mechanism of increased DNA content in WAT. In rats with VMH lesions, the weight of WAT and BAT had increased significantly at 7 days, and the DNA content and thymidine incorporation of WAT had increased significantly at 3 days and continued to increase for up to 7 days, while those of BAT did not increase for as long as 7 days after VMH lesioning. Restricted food intake according to the pair-feeding method partially inhibited the increased DNA content in WAT. The increased DNA content in WAT was mostly restored but not completely by the administration of anti-insulin antibody, and by administration of propranolol, a beta-adrenergic blocker. The results demonstrated that VMH lesions induced DNA synthesis in WAT early after VMH lesioning, but did not induce DNA synthesis in BAT, and suggested that either hyperinsulinemia or a beta-adrenergic receptor mechanism or both may be responsible for the increased DNA content in WAT.

Adipose Tissue↗
PubMed1993

Ventromedial hypothalamic lesions increase gastrointestinal DNA synthesis through vagus nerve in rats.

BACKGROUND: It was recently reported that ventromedial hypothalamic (VMH) lesions produced an increase in gastrointestinal DNA content in rats. In the present study, the mechanism of this alteration was examined. METHODS: The DNA content and synthesis after VMH lesioning in rat gastrointestinal tracts were determined. RESULTS: Total content of DNA in stomach and small intestine began to increase at 3 days and continued to increase for 7 days, whereas DNA content in the large intestine began to increase at 3 days and maintained the same level until 7 days after VMH lesioning. DNA synthesis of these organs increased and reached maximum at 3 days and then decreased to the initial level 7 days following the lesions. This increase in DNA content and synthesis in these organs was largely inhibited by bilateral subdiaphragmatic vagotomy or the administration of atropine, a cholinergic blocker, but not by the administration of anti-insulin antibody. CONCLUSIONS: VMH lesions induce cell proliferation in the rat gastrointestinal tract by the firing of vagus nerve activity mainly through the cholinergic receptor mechanism.

Animals↗
PubMed1992

Role of vagus nerve in increased DNA synthesis after hypothalamic ventromedial lesions in rat liver.

We recently reported that ventromedial hypothalamic (VMH) lesions produced an increase in DNA content in rat liver. In the present study, we examined the mechanism of increased hepatic DNA content produced by VMH lesions. Hepatic DNA content began to increase 3 days after VMH lesioning and continued to increase until 7 days after the lesioning. Hepatic DNA synthesis increased and reached maximum 3 days after the lesioning and then decreased to the initial level 7 days after lesioning. The increased DNA content and synthesis after VMH lesioning were completely inhibited by vagotomy (hepatic vagotomy or bilateral subdiaphragmatic vagotomy) and largely inhibited by the administration of atropine but not by administration of anti-insulin antibody. These results suggest that vagus firing produced by VMH lesions stimulates DNA synthesis in rat liver mainly through cholinergic receptor mechanisms.

Animals↗
PubMed1991

Comparison of DNA contents of visceral organs in rats with ventromedial hypothalamic lesions and fed a high fat diet.

Bilateral lesions of ventromedial hypothalamus are followed by a number of changes including vagal hyperactivity and hyperinsulinemia. To investigate if cell proliferation occurs in visceral organs in rats with ventromedial hypothalamic (VMH) lesions and fed a high fat diet, we determined DNA contents of visceral organs (liver, pancreas, small and large intestines, spleen, kidney and heart) 1 and 4 week after VMH lesions or start of high fat diet. In rats with VMH lesions, DNA contents increased significantly in liver, pancreas, and small and large intestines at 1 week, and maintained the same levels until the 4th week. DNA contents increased most in the pancreas, followed by small and large intestines, and liver. DNA content did not change in spleen, kidney, or heart. In rats fed a high fat diet, there was no increase in the DNA content of these organs, except in the small intestine at 4 weeks. The results suggest that VMH lesions produce excessive DNA synthesis in visceral organs, whereas a high fat diet does not. VMH lesions may induce cell proliferation in visceral organs through vagal hyperactivity and/or changes of humoral growth factors.

Animals↗