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Biomedical subjects

M Yano

Publications and source records attributed to M Yano.

At least 253 records · Page 14Linked to original sources
PubMed1999

[An elderly case of giant infected liver cyst that decreased dramatically without percutaneous aspiration].

A 70-year-old woman was referred to our hospital for treatment of cholelithiasis. A giant liver cyst (6 cm in diameter) had been diagnosed three years earlier. On admission, she had low grade fever and hepatomegaly. High values were observed for WBC (9900/microliter), CRP (8.9 mg/dl), GPT (45 IU/l), ALP (1399 IU/l), gamma-GTP (333 IU/l) and LAP (249 IU/l). The diagnosis of infected liver cyst (8 cm in diameter) was made based on contrast-enhanced CT scan. Endoscopic retrograde cholangiopancreaticography showed no communication between the cyst and the intrahepatic bile duct. She was successfully managed with antibiotics and discharged without percutaneous aspiration the cyst. On abdominal CT scan 4 months after the discharge, the liver cyst had decreased dramatically in size (1 cm in diameter). The patient remains healthy without symptoms.

Aged↗
PubMed1999

[Sulfonylureas and daily blood glucose profiles in elderly diabetics].

The aim of this study is to clarify the relationship between the efficacy of sulfonylureas and duration of diabetes in elderly diabetics. Daily blood glucose profiles were measured in 87 Type 2 elderly diabetic patients on sulfonylureas (tolbutamide, gliclazide or glibenclamide). Plasma glucose concentrations were determined at 08.00 (before breakfast), 10.00, 12.00 (before lunch), 14.00, 18.00 (before dinner), 20.00, 24.00, 03.00, 06.00, 08.00 hours. The subjects were divided into 4 sub-groups, according to their duration of the diabetes (< 10, 10-14, 15-19, 20 or more years). Mean plasma glucose values at 08.00, 10.00, 20.00, 03.00 and 06.00 hours were not significantly different among the four groups. However, mean plasma glucose values at 12.00, 14.00, 18.00, 00.00 hours and mean total blood glucose area under the daily profile (total BG) were significantly different among the four groups and the values in patients with a history of diabetes of 15 years or more increased. Duration of diabetes positively correlated with blood glucose values at 12.00, 14.00, 18.00, 00.00, 03.00 hours and total BG, and the dose of sulfonylureas positively correlated with blood glucose values at 12.00, 14.00, 18.00, 00.00 hours and total BG in multiple regression analysis. These results suggest that duration of diabetes and dose of sulfonylureas are important determinants of blood glucose control with sulfonylureas in elderly diabetic patients.

Aged↗
PubMed1999

Close correlation between a p53 or hMSH2 gene mutation in the tumor and survival of hepatocellular carcinoma patients.

We analyzed 42 hepatocellular carcinomas (HCC) (38 patients) for mutations in the DNA mismatch repair gene hMSH2 and the p53 tumor suppressor gene, a possible upregulater of hMSH2. Mutations of the hMSH2 or p53 gene were detected in 13 patients (34%). There were no patients who possessed mutations in both genes. There was a significant correlation between mutation of either gene and pathological indicators of malignancy. The survival rate of patients with hMSH2 or p53 gene mutation-positive tumors was much poorer than that with hMSH2 and p53 gene mutation-negative tumors (p=0.0012). Our results suggest that mutations in the p53 or hMSH2 gene may closely correlate with the survival of hepatocellular carcinoma patients.

Carcinoma, Hepatocellular↗
PubMed1999

[Clinical characteristics and incidence in acute non A-G hepatitis].

We investigated clinical characteristics and incidence of patients with acute non-A-G hepatitis, who were all registered in 17 Japanese National Hospitals. Seven hundreds thirty-one (24.0%) of 3052 patients with sporadic acute hepatitis and 73 (21.2%) of 344 patients with posttransfusion acute hepatitis were diagnosed as acute non-ABC hepatitis. Patients with acute non-ABC hepatitis were older (Mean +/- SD, 44 +/- 15 years) and male/female ratio was 0.70. Although mean levels of liver function abnormality was generally mild, 4(1.8%) of 250 patients with acute non-ABC hepatitis were died of fulminant hepatitis.

Acute Disease↗
PubMed1999

Rare cases of congenital bicuspid aortic valve with an abnormal fibrous band.

Pure aortic regurgitation is usually caused by a congenital bicuspid aortic valve (BAV). In this condition, there are a few cases accompanied by an abnormal fibrous band stretched from the center of the conjoined cusp to the aortic wall. This report describes two cases of congenital bicuspid aortic valve (BAV) with an abnormal fibrous band. The first case of BAV with an abnormal fibrous band developed aortic regurgitation and the second case exhibited aortic stenosis. These two abnormal fibrous bands were confirmed to be congenital by the microscopic findings. According to the literature, the majority of BAV with an abnormal fibrous band were found in the patients with aortic regurgitation. We report here a case study of an elderly female patient with aortic stenosis of BAV with an abnormal fibrous band. To our knowledge, no other case of BAV with an abnormal fibrous band in association with aortic stenosis has ever been reported.

Aortic Valve↗
PubMed1999

[Hepatic arterial infusion of low-dose cisplatin, 5-fluorouracil for hepatocellular carcinoma with tumor thrombi in the portal vein].

Hepatic arterial infusion of low-dose CDDP (10 mg/day), 5-FU (250 mg/day) was performed in 5 unresectable hepatocellular carcinoma (HCC) patients with tumor thrombi in the trunk and/or the first branch of the portal vein. Infusion chemotherapy was continued for five days, then discontinued for the subsequent two days. This procedure was performed repeatedly for at least three weeks. Decrease in the serum levels of the alpha-fetoprotein after the treatment was found in 3 of 4 patients. In one patient, the size of the primary tumor decreased 92%. In two of five patients, the tumor thrombi in the portal vein disappeared, or decreased in size. Side effects of the chemotherapy included liver functional disorder (Grade 3; 1 case), thrombocytopenia (Grade 3; 1 case, Grade 2; 1 case), and leukopenia (Grade 2; 1 case). The present protocol proved to be effective and applicable for patients with advanced HCC associated with severe cirrhosis.

Aged↗
PubMed1999

[Percutaneous microwave coagulation therapy for hepatocellular carcinoma].

We performed percutaneous microwave coagulation therapy (PMCT) for 34 hepatocellular carcinoma (HCC) patients, including 18 primary and 16 recurrent HCC ones. Cumulative 1, 2-, 3- and 4-year survival rates of primary HCC patients were 94, 78, 78% and 62%, respectively, while those of recurrent HCC patients were 100, 79, 62% and 41%, respectively. There were no differences between groups. In both groups, local recurrence was found in about 50% of patients. The mean tumor size (diameter 2.6 +/- 0.6 cm) of patients with local recurrence was relatively larger than that (2.2 +/- 0.6 cm) of patients without local recurrence (p = 0.081). Seventeen of 27 patients with moderately or poorly differentiated HCC had local recurrence, while none of patients with well-differentiated HCC did (p = 0.005). Subsequently, local control failure led some patients to have progressive diseases such as multiple intrahepatic metastasis, tumor thrombi in the portal vein, and distant metastasis. From these findings, PMCT should be performed only for well-differentiated HCC less than 2 cm in diameter. If the patients with moderately or poorly differentiated HCC larger than 2 cm in diameter cannot tolerate hepatic resection because of their poor hepatic functional reserve, PMCT should be performed in combination with other non-surgical treatment modalities.

Aged↗
PubMed1999

[Body surface ultrasonography-guided bronchofiberscopy].

Transbronchial lung biopsies and cytologic studies under ultrasonographic guidance from the body surface were conducted in 39 patients whose lesions were adjacent to the thoracic wall. In 26 patients, biopsy, curettage, or brushing forceps were visualized in the mass or infiltrative lesion by thoracic echogram. Positive findings were obtained in 23 patients, for a conclusive diagnostic rate of 88.5%. Of the 13 patients in whom forceps could not be visualized by echogram, 10 had positive findings, for a diagnostic rate of 76.9%. For visualization by thoracic echogram, abnormal lung lesions must be in direct contact with the thoracic wall. Occasionally, diagnostic procedures may be impeded by anatomical structures such as shoulder joints or scapula. Despite these disadvantages, the ultrasonography-guided bronchofiberscope is quite useful because it facilitates real-time confirmation of the positioning of the forceps relative to the lesions. It is also useful in cases when the peripheral lesions are too small or vague to be demonstrated by fluoroscopy alone, because the echo probe can be the target of the forceps instead of the missing shadows. The diagnostic rate should be higher when the forceps are visualized in the lesions ultrasonographically.

Adult↗
PubMed1999

Brain metastasis from hepatocellular carcinoma after radical hepatectomy.

Brain metastasis from hepatocellular carcinoma (HCC) is a rare, yet perplexing problem in patients with cancer. We report on 5 patients with metastasis of HCC to the brain after radical hepatectomy. Intrahepatic recurrence occurred in 3 patients, and distant metastasis to sites other than the brain was observed in 3 patients (lung, 2; bone, 1). The symptoms for brain metastasis included headache, hemiparesis, and vomiting. Hemorrhage was found in 4 of 5 patients. All patients had a single nodular lesion in the brain. The alpha-fetoprotein levels were more than 10,000 ng/ml in 4 patients. Two patients underwent surgical resection, 1 received cranial irradiation, and 2 were administered corticosteroids. The interval between diagnosis of the primary cancer and detection of brain metastasis ranged from 2 to 54 months. The mean survival period was only 3 months after diagnosis of brain metastasis. All 5 patients died of neurologic causes. Because no effective treatment for brain metastasis from HCC is available, further study is needed.

Adult↗
PubMed1999

[HBV-DNA].

Explore the source record for details and available documents.

DNA, Viral↗
PubMed1999

KEMRI Hep-cell II hepatitis B surface antigen screening kit.

BACKGROUND: Kenya is a high hepatitis B virus (HBV) endemic zone. Prevention of HBV transmission by transfusing safe blood is necessary. Kits for screening hepatitis B surface antigen (HBsAg) are usually imported and are expensive. Hence it has been difficult to screen donated and patient blood samples all over Kenya. OBJECTIVE: To produce a HBsAg screening kit locally in order to be able to screen donated and patient blood samples all over Kenya. DESIGN: A laboratory based study. SETTING: Centre for Virus Research (CVR), Kenya Medical Research Institute (KEMRI), Nairobi. METHOD: Purified HBsAg from plasma of carriers obtained from National Public Health Laboratories Services (NPHLS) was used to minimise guinea pigs to produce antihepatitis B (anti HBs) antibody. The anti HBs was then used to sensitise sheep red blood cells (SRBC). The final product was freeze dried (lyophilised) and its sensitivity and specificity was compared with other commercial kits. RESULTS: The sensitivity and specificity of KEMRI Hep-cell II was found to be 98% and 99%, respectively. The kit was found to be stable and potent for one year whether kept 4 degrees C, 37 degrees C or room temperature. CONCLUSION: KEMRI Hep-cell II was successfully produced locally. The sensitivity and specificity were comparable to other commercial kits. The kit was stable and potent for one year between temperature of 4 degrees C and 37 degrees C. The kit required only simple apparatus to carry out the test hence it can be used anywhere in Kenya. It was also cheap and affordable.

Carrier State↗
PubMed1998

Association between genetic polymorphisms of glutathione S-transferase P1 and N-acetyltransferase 2 and susceptibility to squamous-cell carcinoma of the esophagus.

We examined the effect of genetic polymorphisms of phase-II enzymes, glutathione S-transferase P1 (GSTP1) and N-acetyltransferase2 (NAT2) on susceptibility to esophageal squamous-cell carcinoma To determine the genotypes of the 2 polymorphisms, PCR-based analysis was performed on samples from 66 Japanese patients who had been histologically diagnosed as having esophageal squamous-cell carcinoma, and 164 healthy Japanese controls. The frequency of the AA genotype of GSTP1 was significantly higher in esophageal-cancer patients than in the controls according to logistic-regression analysis (92% of the patients and 68% of the controls; odds ratio (OR), 8.0; p = 0.0013). Also, more patients had the slow and intermediate acetylator genotypes of NAT2 than the controls (15% and 38% vs. 10% and 32% respectively; OR of the slow acetylator genotype, 4.2; p = 0.032; OR of the slow plus intermediate acetylator genotypes, 2.9; p = 0.015). Polymorphisms of GSTP1 and NAT2 may serve as genetic biomarkers for predicting susceptibility to esophageal squamous-cell carcinoma.

Adult↗
PubMed1998

A pathway where polyprenyl diphosphate elongates in prenyltransferase. Insight into a common mechanism of chain length determination of prenyltransferases.

Prenyltransferases catalyze the consecutive condensations of isopentenyl diphosphate to produce linear polyprenyl diphosphates. Each enzyme forms the final product with a specific chain length. The product specificity of an enzyme is thought to be determined by the structure around the unknown path through which the product elongates in the enzyme. To explore the path, we introduced a few mutations at the 5th, the 8th, and/or the 11th positions before the first aspartate-rich motif of geranylgeranyl-diphosphate synthase or farnesyl-diphosphate synthase. The side chains of these amino acids are situated on the same side of an alpha-helix. In geranylgeranyl-diphosphate synthase, a single mutated enzyme (F77S) mainly produces a C25 product (Ohnuma, S.-I., Hirooka, K., Hemmi, H., Ishida, C., Ohto, C., and Nishino, T. (1996) J. Biol. Chem. 271, 18831-18837). A double mutated enzyme (L74G and F77G) mainly produces a C35 compound with significant amounts of C30 and C40. A triple mutated enzyme (I71G, L74G, and F77G) mainly produces a C40 compound with C35 and C45. Mutated farnesyl-diphosphate synthases also show similar patterns. These findings indicate that the elongating product passages on a surface of the side chains of the mutated amino acids, the original bulky amino acids had blocked the elongation, and the path is conserved in prenyltransferases. Moreover, the fact that some double and triple mutated enzymes can also form small amounts of products longer than C50 indicates that the paths in these mutated enzymes can partially access the outer surface of the enzymes.

Alkyl and Aryl Transferases↗
PubMed1998

Functional analysis of human mitochondrial receptor Tom20 for protein import into mitochondria.

The mitochondrial import receptor translocase of the outer membrane of mitochondria (Tom20) consists of five segments, an N-terminal membrane-anchor segment, a linker segment rich in charged amino acids, a tetratricopeptide repeat motif, a glutamine-rich segment, and a C-terminal segment. To assess the role of each segment, four C-terminally truncated mutants of the human receptor (hTom20) were constructed, and the effect of their overexpression in COS-7 cells was analyzed. Expression of a mutant lacking the tetratricopeptide repeat motif inhibited preornithine transcarbamylase (pOTC) import to the same extent as the wild-type receptor. Thus, overexpression of the membrane-anchor and the linker segments is sufficient for the inhibition of import. Expression of either the wild-type receptor or a mutant lacking the C-terminal end of 20 amino acid residues stimulated import of pOTC-green fluorescent protein (GFP), a fusion protein in which the presequene of pOTC was fused to green fluorescent protein. On the other hand, expression of mutants lacking either the glutamine-rich segment or larger deletions inhibited pOTC-GFP import. In vitro import of pOTC was inhibited by the wild-type hTom20 and the mutant lacking the C-terminal end, but much less strongly by the mutant lacking the glutamine-rich segment. On the other hand, import of pOTC-GFP was little affected by any of the forms of hTom20. In binding assays, pOTC binding to hTom20 was only moderately decreased by the deletion of the glutamine-rich segment, whereas pOTC-GFP binding was completely lost by this deletion. Binding of pOTCN-GFP a construct that contains an additional 58 N-terminal residues of mature OTC, resembled that of pOTC. All of these results indicate that the region 106-125 containing the glutamine-rich segment of hTom20 is essential for binding and import stimulation in vivo of pOTC-GFP and for inhibition of in vitro import of pOTC. The results also indicate that this region is important for mitochondrial aggregation. The different behaviors of pOTC and the pOTC-GFP chimera toward hTom20 mutants is explicable on the basis of the conformation of the precursor proteins.

Animals↗
PubMed1998

Differential activation of cardiac c-jun amino-terminal kinase and extracellular signal-regulated kinase in angiotensin II-mediated hypertension.

Two subgroups of mitogen-activated protein kinases, c-jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), are thought to be involved in cultured cardiac myocyte hypertrophy and gene expression. To examine the in vivo activation of these kinases, we measured cardiac JNK and ERK activities in conscious rats subjected to acute or chronic angiotensin II (Ang II) infusion, by using in-gel kinase methods. About 50 mm Hg rise in blood pressure by Ang II (1000 ng . kg-1 . min-1) infusion caused larger activation of left ventricular JNK than ERK, via the AT1 receptor. In spite of short duration (about 30 minutes) of maximal blood pressure elevation by Ang II, JNK sustained the peak value (more than 5-fold increase) from 15 minutes up to at least 3 hours. Similar activation of JNK was seen in the right ventricle. Thus, cardiac JNK activation by Ang II seems to be in part mediated by its direct action via the AT1 receptor. The dose-response relationships for Ang II-induced rises in blood pressure and cardiac JNK and ERK activation indicated that cardiac JNK or ERK was not activated by a mild increase in blood pressure and that cardiac JNK was activated by Ang II-mediated hypertension in a more sensitive manner than ERK. Cardiac hypertrophy, induced by chronic Ang II infusion, was preceded by JNK activation without ERK activation. Furthermore, gel mobility shift analysis showed that cardiac JNK activation was followed by increased activator protein-1 DNA binding activity due to c-Fos and c-Jun. These results provided the first evidence for the preferential activation of cardiac JNK in Ang II-induced hypertension and suggested that JNK might play some role in Ang II-induced cardiac hypertrophic response in vivo. However, further study is needed to elucidate the role of JNK in cardiac hypertrophy in vivo.

Analysis of Variance↗
PubMed1998

The structures of asparagine-linked oligosaccharides of rat liver cathepsin L reflect the substrate specificity of lysosomal alpha-mannosidase.

We have studied the structures of asparagine-linked oligosaccharides of cathepsin L purified from rat liver in detail. The oligosaccharides released from rat liver cathepsin L on glycopeptidase-F treatment were tagged with 2-aminopyridine at their reducing ends. The pyridylamino (PA) derivatives were separated into seven fractions according to molecular size by normal-phase HPLC. The structure of each oligosaccharide thus isolated was analyzed by reversed-phase HPLC and characterized by ion-spray mass spectrometry and high-resolution proton nuclear magnetic resonance (1H-NMR) spectroscopy. Our results indicate that the asparagine-linked oligosaccharides of rat liver cathepsin L are of the oligomannose type, having two to six mannose residues. Among them, the five major ones are Manalpha1-6Manbeta1-4-GlcNAcbeta1-4GlcNAc, Manalpha1 -6Manalpha1-6Manbeta1-4GIcNAcbeta1-4GlcNAc, Manalpha1-6(Manalpha1-3)-Manalpha1-6Manbeta1- 4GlcNAcbeta1-4GlcNAc, Manalpha1-6(Manalpha1-3)Manalpha1-6(Manalpha1-3) Manbeta1-4Glc-NAcbeta1-4GlcNAc, and Manalpha1-6(Manalpha1-3)Manalpha1-6(Manalpha1-++ +2Manalpha1-3)Manbeta1-4GlcNAcbeta1-4Glc-NAc. Their structures are shown to be products of Man6GlcNAc2 hydrolysis with lysosomal alpha-mannosidase.

Animals↗