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S Baba

Publications and source records attributed to S Baba.

At least 163 records · Page 9Linked to original sources
PubMed1998

Pathophysiological appraisal of a rat model of total hepatic ischemia with an extracorporeal portosystemic shunt.

BACKGROUND: Animal models of total hepatic ischemia (THI) and reperfusion injury are restricted by concomitant splanchnic congestion. This study was performed to determine the requirement suitable for an extracorporeal portosystemic shunt (PSS) to maintain the intestinal integrity in a rat model of THI. MATERIALS AND METHODS: Using a polyethylene tube (0.86 or 1 mm i.d.), PSS was placed between the mesenteric and jugular veins. Comparison was done between THI models with or without PSS and a partial ischemia model with hepatectomy of the nonischemic lobes. Well-tolerated hepatic ischemic period, portal pressure after 10 min of hepatic ischemia, portal endotoxin levels at 1 h after reperfusion, histological features of the small bowel just before reperfusion, and local jejunal and ileal blood hemoglobin oxygen saturation index (ISO2) were compared among the models. RESULTS: Animals without PSS poorly tolerated 30 min of THI. Animals receiving THI with PSS or partial hepatic ischemia tolerated a longer ischemic period (60 min) with a significantly higher small bowel ISO2, lower portal pressure and endotoxin levels (P < 0.01), and less histological damage of the small bowel when compared to those receiving THI without PSS. Portal endotoxin levels after THI with PSS using a 1-mm i.d. tube as well as partial hepatic ischemia were significantly lower than those after THI with PSS using a 0.86-mm i.d. tube. CONCLUSIONS: THI with PSS using a 1-mm i.d. tube was strikingly similar to partial hepatic ischemia in the pathophysiological profile during hepatic ischemia. PSS with a tube 1 mm or more in inner diameter offers pathophysiological advantages in experiments on THI and reperfusion.

Animals↗
PubMed1998

Primary dissection of the hepatic artery: report of a case.

Dissecting aneurysms of the hepatic artery are extremely rare. We report herein the case of a 51-year-old man with massive hepatic metastases from rectal carcinoma, who was found incidentally to have a left hepatic artery aneurysm by a preoperative angiography. After replacing the left hepatic artery with a 2-cm segment of long saphenous vein, an extended right lobectomy with partial resection of the left lateral segment for multiple metastases was successfully performed. To prevent thrombus formation at the anastomosis, the Pringle maneuver was not used during dissection of the hepatic parenchyma. Histological examination of the resected specimen showed a dissecting aneurysm of the left hepatic artery, but there were no findings to suggest the etiology of this disease. The patient is currently alive 13 months after his operation without any evidence of further recurrence of the carcinoma. To the best our knowledge, 12 case reports of this anomaly have been documented, but only one of these describes a successful operation. The clinical features and etiology of the hepatic artery aneurysm that develops independent of other vascular diseases are discussed following this case report.

Aortic Dissection↗
PubMed1998

Murine cytomegalovirus induces apoptosis in non-infected cells of the developing mouse brain and blocks apoptosis in primary neuronal culture.

Cytomegalovirus (CMV) is the most common cause of congenital infection, resulting in birth defects such as microcephaly. In this study, we found that apoptosis is induced in the developing mouse brain infected with murine cytomegalovirus (MCMV) in an association with neuronal cell loss. With the combination of the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) technique and immunohistochemical staining, 3.8% of the TUNEL-positive cells were double-stained with the antibody to neuron-specific enolase, while none of the TUNEL-positive cells were stained with antibodies to the immediate early and early viral antigens of MCMV. Furthermore, distribution pattern of the TUNEL-positive cells was different from that of viral DNA-positive cells detected by the in situ DNA-DNA hybridization. More than 30% of the TUNEL-positive cells were double-stained with the F4/80 antibody specific for microglia/macrophages, which were sometimes swollen, presumably the consequence of engulfment of the neuronal apoptotic cells. In the primary neuronal cultures, MCMV infection inhibited the induction of apoptosis either by serum deprivation or by glutamate treatment. It was also confirmed by the double-staining method that apoptosis was not induced in the viral-infected neuronal cultures. These results suggest that MCMV infection induces apoptosis in non-infected neuronal cells, presumably by indirect mechanisms, and that apoptotic cells are engulfed by microglia/macrophages. The induction and blocking of neuronal apoptosis by viral infection may be important for morphological and functional brain disorders in the congenital CMV infection.

Animals↗
PubMed1998

Localization of the gene responsible for Peutz-Jeghers syndrome within a 6-cM region of chromosome 19p13.3.

Patients with Peutz-Jeghers syndrome (PJS), an autosomal dominant disease characterized by hamartomatous polyposis of the gastrointestinal tract, are thought to be predisposed to malignancies of the digestive tract, genital tract, and other organs. Using microsatellite markers on chromosome 19p, we have closely defined the region containing the gene responsible for this disorder through linkage analysis in seven affected families. The lack of obligate recombinants at two of these loci, D19S883 and D19S878, with maximum LOD scores of 2.88 and 3.75, confirmed the localization of the PJS locus to chromosome 19. Furthermore, haplotype analysis placed the PJS locus within a 6-cM telomeric region of chromosome 19p, between D19S886 and D19S565.

Centromere↗
PubMed1998

Nine novel germline mutations of STK11 in ten families with Peutz-Jeghers syndrome.

Peutz-Jeghers Syndrome (PJS) is an autosomal dominant hereditary disease characterized by hamartomatous polyposis involving the entire bowel. Recently STK11, a gene bearing a mutation responsible for PJS, was isolated. We investigated the entire coding region of STK11 in 15 unrelated PJS families by the PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) method and PCR-direct sequence analysis, and found nine different, novel mutations among ten of those families. One nonsense mutation and five different frameshift mutations (two families carried the same mutation), all of which would cause truncation of the gene product, were found in seven families; mutations found in five families were clustered within exon 6. Among these five mutations, three occurred at the mononucleotide-repeat region (CCCCCC) of codons 279-281, suggesting that this region is likely to be a mutational hotspot of this gene. One of the remaining three families carried a 3-bp in-frame deletion that would eliminate an asparagine residue within a kinase domain of the product; the other two carried intronic mutations at or adjacent to the consensus dinucleotide sequences of splice-acceptor or -donor sites, which were likely to lead to aberrant splicing.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

Surgical management for a malignancy of the digestive organs accompanied with an abdominal aortic aneurysm.

Surgical management of patients with simultaneous coexisting malignancy of the digestive organs and an abdominal aortic aneurysm (AAA) remains controversial. In the five patients who underwent the aneurysmectomy first, no complications developed after an aneurysmectomy and a resection of malignancy could be performed within 4 weeks, whereas postoperative complications after the resection of malignancy developed in two of them. Two patients underwent a one-stage operation, in which one was unable to tolerate the two procedures, and no postoperative complications were seen; however, one patient with cardiac dysfunction who first underwent an aneurysmectomy died 3 months after operation due to cardiac and renal failure. These results indicate that the aneurysmectomy first is preferred, when such patients do not have absolute indications of malignancy or AAA; however, a one-stage operation should be chosen when the patients show a disturbance of key organs.

Adult↗
PubMed1998

Development of approximate formula for LDL-chol, LDL-apo B and LDL-chol/LDL-apo B as indices of hyperapobetalipoproteinemia and small dense LDL.

Estimation of LDL-chol and LDL-apo B is useful for the diagnosis of hyperapobetalipoproteinemia (normal LDL-chol with increased LDL-apo B), which is one of the most commonly occurring lipoprotein disorders associated with atherosclerotic cardiovascular diseases. The LDL-chol/LDL-apo B ratio reflects the level of small dense LDL, which is an important risk factor for IHD, CVD and ASO. In order to estimate LDL-apo B and LDL-chol/LDL-apo B ratio from blood chol, TG, HDL-chol and apo B values, we developed a formula for LDL-chol ¿0.94Chol- 0.94HDL-chol - 0.19TG¿, LDL-apo B ¿apo B - 0.09Chol + 0.09HDL-chol-0.08TG¿, and LDL-chol/LDL-apo B [¿0.94Chol-0.94HDL-chol - 0.19TG¿/¿apo B - 0.09Chol + 0.09HDL-chol-0.08TG¿] using ultracentrifugal data from 2179 subjects. These were calculated by the least squares method on the assumption that a certain compositional relationship exists between Chol, TG and apo B in VLDL, IDL and LDL. Friedewald's formula for LDL-chol (Chol - HDL-chol - 0.2TG) includes IDL-chol, but the present new formula theoretically excludes IDL-chol. It suggests a better estimation for the correct LDL-chol. Estimated LDL-apo B is useful for the diagnosis of hyperapobetalipoproteinemia and detection of small dense LDL. Without performing ultracentrifuge, additional information is obtained for the quantitative and qualitative alteration of LDL, such as small dense LDL. The above formulae and a new classification of lipoproteinemia including apo B were applied to the analyses of lipoprotein profiles of subjects with cardiovascular diseases, which were compared with those in the general population. Hyperapobetalipoproteinemia with high TG was observed 2-3 times more frequently in subjects with CAD, MI and ASO than in the Suita population. Lower ratios of LDL-chol/LDL-apo B, reflecting preponderance of small dense LDL, were observed in the above three groups. Type IIb and combined low HDL-chol were also frequent phenotypes in CAD, A-Th and ASO. The present formulae are useful for the detailed analyses of lipoprotein disorders in both qualitative as well as quantitative aspects.

Apolipoproteins B↗
PubMed1998

Development of vanadate sensitive human erythrocytes insulin receptor tyrosine phosphatase assay.

The aim of this study was to investigate the effect of sodium orthovanadate on the alterations of human erythrocytes insulin receptor autophosphorylation. Human erythrocytes were incubated with insulin in a cell system and then lysed. The autophosphorylated insulin receptors were measured with the aid of a two-site immunofluorometric assay and using a monoclonal anti-insulin receptor antibody to label the insulin receptors and a monoclonal anti-phosphotyrosine antibody to assess tyrosine phosphorylation. When the erythrocytes were treated with insulin and then reincubated in insulin-free medium, vanadate completely inhibited insulin receptor dephosphorylation, although it had no effect on in vitro receptor autophosphorylation. Thus insulin receptor tyrosine phosphatase activity is postulated to be [% (autophosphorylated insulin receptors with vanadate - autophosphorylated insulin receptors without vanadate)/total insulin receptors] under overall steady conditions in a cell system. Using this assay, the insulin receptor tyrosine phosphatase activities of 25 control and 32 diabetic subjects were studied. There was no significant difference in insulin receptor tyrosine phosphatase activity between control subjects and diabetic subjects (0.173 +/- 0.062 vs 0.209 - +/- 0.057 autophosphorylated insulin receptors units/insulin receptors units). The assay used in this study requires only 0.6 ml of whole blood, and so should be a useful tool for detecting patients who are insulin-resistant due to abnormal insulin receptor tyrosine phosphatase activity.

Animals↗
PubMed1998

Neuropeptide Y produces anxiety via Y2-type receptors.

In the present study, the effects of intracerebroventricular (ICV) NPY, [Leu31, Pro34]NPY and NPY13-36 have been evaluated with respect to anxiety in mice in the elevated plus maze. NPY had opposing effects on behavior, depending on the doses used. NPY decreased the normal preference for the closed arms of the maze at 0.7 nmol, indicating an anxiolytic effect; however, at 7 pmol NPY further increased the preference for the closed arm, indicating an anxiogenic effect. [Leu31, Pro34]NPY, a Y1-type receptor agonist, significantly reduced the preference for the closed arms at 70 pmol. NPY13-36, a Y2-type receptor agonist, significantly intensified the preference at 20 pmol. It has been demonstrated that NPY produces not only an anxiolytic effect via Y1-type receptors, but also an anxiogenic effect via Y2-type receptors. The time course of these NPY actions are quite different and the anxiogenic effect was observed only shortly after ICV NPY injection.

Animals↗
PubMed1998

Two-dimensional configuration of the myoneural junctions of human masticatory muscle detected with matrix electrode.

Motor unit action potentials (MUAPs) propagate bidirectionally from the myoneural junction along the muscle fibre. The propagation of excitation within single motor units can be detected during sustained isometric contraction using a surface electrode array. Electromyographic (EMG) signals from an adjacent pair of contacts along the muscle fibres show a very similar wave form with a time shift. In the present study, EMG signals of the masseter and the temporal muscles were obtained from two male adults during clenching in the intercuspal position using the multichannel surface electrode with 17 x 11 contacts. The two-dimensional location of the myoneural junction for each column from the source of the propagation was estimated. Each of the myoneural junctions was located in the lower portion of the masseter muscle and in the upper portion of the temporal muscle. However, the junction was distributed within 10 mm along the muscle fibres at different contraction levels in each muscle. This noninvasive technique of multiple surface electrodes enabled us to add to knowledge of the anatomical structure of the masticatory muscles examined.

Action Potentials↗
PubMed1998

Effect of Helicobacter pylori infection on gastric juice pH.

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion is still unclear. METHODS: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls. RESULTS: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed. CONCLUSIONS: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Acquired reactive perforating collagenosis with IgA nephropathy.

A 25-year-old Japanese man developed numerous discrete umbilicated papules on his face, trunk, and both forearms at the onset of IgA nephropathy. The newest lesion was a nonumbilicated skin-colored papule. On histopathologic examination, alteration of capillaries was observed in both newer and umbilicated papules. In our case, a primary cause of the reactive perforating collagenosis could be an alteration of the capillaries.

Adrenal Cortex Hormones↗
PubMed1998

Genetic alterations of mixed hyperplastic adenomatous polyps in the colon and rectum.

Some mixed hyperplastic adenomatous polyps (MHAPs) contain dysplastic lesions or even carcinomas. These polyps are considered to be different from ordinary hyperplastic polyps and may have a preneoplastic potential. We investigated APC and K-ras mutations in MHAPs of the colon and rectum, and also in colorectal adenomas and hyperplastic polyps to identify molecular differences between MHAPs, adenomas and hyperplastic polyps, using direct sequencing of mutation cluster regions (MCR) in APC and K-ras. No APC mutations were identified in 12 MHAPs and 8 hyperplastic polyps, whereas 10 of 27 (37.0%) adenomas showed somatic mutations. K-ras mutations were identified in one of 12 (8.3%) MHAPs, one of 8 (12.5%) hyperplastic polyps, and 10 of 27 (37.0%) adenomas. p53 mutation was found in a carcinoma arising in an MHAP. Mutations other than APC mutations may play a role in the development of MHAPs.

Adenoma↗
PubMed1998

Piroxicam and acarbose as chemopreventive agents for spontaneous intestinal adenomas in APC gene 1309 knockout mice.

The use of nonsteroidal anti-inflammatory drugs has been suggested to have a chemopreventive effect against colon carcinoma, through the inhibition of cyclooxygenases 1 and 2, in patients with familial adenomatous polyposis and in animal models. Acarbose, an alpha-glycosidase inhibitor, may also be chemopreventive. In order to examine the effects of these drugs we employed APC gene knockout mice randomized into 3 groups, one for treatment with piroxicam (0.05% concentration in drinking water), one for acarbose (0.04% concentration in food) and another for the control. After 14 weeks of treatment, mice were killed for quantitation of gastric and intestinal adenomas. Tumor multiplicity in the whole gastrointestinal tract decreased from 33.89 +/- 13.07 tumors/mouse in the control group to 17.05 +/- 7 tumors/mouse in the piroxicam-treated group (P < 0.001). The decrease in the acarbose-treated group (29.68 +/- 12.86 tumors/mouse) was not significant (P < 0.05). The number of tumors > or = 3 mm in diameter was also quantified in all gastrointestinal segments. The number of such tumors in the piroxicam group was decreased to 0.56 +/- 1.2 tumors/mouse from the control value of 3.78 +/- 1.17 tumors/mouse (P < 0.001), while in the acarbose-treated group the number decreased to 2.36 +/- 1.7 tumors/mouse (P < 0.01). Thus, piroxicam decreases the size and number of gastrointestinal adenomas in APC 1309 knockout mice, while acarbose decreases only the size.

Acarbose↗
PubMed1998

Antitumor effect of a neutralizing antibody to vascular endothelial growth factor on liver metastasis of endocrine neoplasm.

Distant metastasis of gastrointestinal endocrine neoplasm is resistant to currently available treatments. Because hematogenic metastasis is dominant, anti-angiogenic drugs are expected to be a novel therapy for this neoplasm. In the present study, the therapeutic effect of vascular endothelial growth factor neutralizing antibody (VEGFAb) on liver metastasis of an endocrine neoplasm was investigated experimentally. Cecal transplantation into nude mice of small pieces of EN-1, a xenotransplanted human intestinal endocrine neoplasm, resulted in liver metastasis. A treated group (n = 19) received 100 micrograms/mouse of VEGFAb intraperitoneally on alternate days from day 10 after tumor transplantation, and the control group (n = 19) received saline. Five of the 19 control mice died of tumor progression, of which 2 could not be evaluated. The cecal tumor weighed 6316 +/- 2333 mg (n = 17) in the control group and 1209 +/- 837 mg (n = 19) in the treated group (P < 0.01) 6 weeks after transplantation. Liver metastasis developed in 16 of 17 control mice and in 2 of 19 treated mice (P < 0.01). The VEGF level of the whole cecal tumor in the control group was significantly higher than that in the treated group (305.1 +/- 174.1 vs. 54.7 +/- 41.2 mg; P < 0.001). VEGFAb did not cause any body weight loss (28.52 +/- 1.63 in the control vs. 28.44 +/- 1.71 g in the treated group). These results indicate that VEGFAb may be a novel therapeutic agent for endocrine neoplasm with distant metastasis.

Aged↗
PubMed1998

Collagen and elastin synthesis by desmoid tumor in vitro.

In order to characterize human desmoid tumors in vitro, the production of collagen and elastin and the expression of collagen types alpha1(I), alpha1(III) and transforming growth factor (TGF)-beta1 mRNA were investigated in six desmoid tumors; five derived from familial adenomatous polyposis patients and one from a sporadic case. The proportion of collagen production to total protein production was determined by 3H-imino acid incorporation, an indicator of collagen synthesis, using high-performance liquid chromatography (HPLC). The proportion of collagen production to total protein production was much higher in all six desmoid tumors compared with human skin fibroblasts (HSF). Quantitatively, the rate of elastin synthesis in desmoid tumor cells monitored by valine-proline peptide was also significantly higher than in HSF. Pro-alpha1(I) collagen mRNA was highly expressed in both desmoid tumors and HSF at approximately the same level, whereas pro-alpha1(III) collagen mRNA was more abundant in some of the desmoid tumors than the normal skin fibroblastic cell lines. Tumor growth factor-beta1 mRNA, which is believed to stimulate collagen synthesis, was expressed in both desmoid tumors and HSF to the same extent. These results demonstrate the increased formation of collagen and elastin in desmoid tumors in vitro and suggest that the increased synthesis of elastin rather than of collagen and TGF-beta1 may be involved in increased fibrogenesis by desmoid tumors.

Adenomatous Polyposis Coli↗