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M Moriyama

Publications and source records attributed to M Moriyama.

At least 73 records · Page 4Linked to original sources

[Characteristics of functional training and effects on physical activities of daily living].

PURPOSE: The effects of functional training on physical Activities of Daily Living (ADL) based on the Health and Medical Service Law for the Elderly have been controversial. The aim of the present study was to explore its characteristics and influence with a large sample. SUBJECTS AND METHODS: 669 participants and 1,110 non-participants in functional training were recruited from 54 cities and villages in 1998. The effects of functional training on physical ADL were evaluated by comparing the baseline ADL and 1-year follow-up ADL in the "index of Activities of Daily Living for bedridden elderly (1993)". RESULTS: 1. The change in physical ADL in participants was significantly better than that in non-participants after adjusting for age. 2. Significant effects of functional training were observed in both sexes, in all three age groups, and in ranks J, A and B. 3. There was no significant difference between the sexes in terms of the influence of functional training. Functional training was more effective in the younger group, in stroke subjects, and individuals suffering from any disease within one year prior to the baseline. 4. A total of 16.4% of the participants demonstrated increased physical ADL, while 7.2% of the participants also had increased mobility. CONCLUSION: Functional training has a significant positive effect on increase of physical ADL. Functional training based on the Health and Medical Service Law for the Elderly is an effective program especially for homebound and/or frail people who are at risk of becoming bedridden. Further longitudinal studies are now needed to improve functional training for increasing ADL and QOL.

Activities of Daily Living↗

Serum concentration of interferon-alpha: a comparison between once-a-day and twice-a-day administration.

The aim of this study was to determine the possible mechanism of the antiviral activity of twice daily administration of interferon (IFN)-alpha for active hepatitis C and to evaluate serum concentrations of IFN-alpha with enzyme-linked immunosorbent assay (ELISA). Forty-seven patients with active hepatitis C received IFN-alpha intramuscularly for 24 weeks. They were divided into once-a-day and twice-a-day groups. Changes in serum IFN-alpha levels were assessed during the treatment period. Compared with twice-a-day treatment, the once-a-day group showed no increase in serum IFN-alpha at the end of daily treatment (p < 0.03). In contrast, one-third of the twice-a-day group showed increased IFN-alpha at the end of daily treatment (p < 0.02). In conclusion, measured with ELISA, twice-daily administration of IFN-alpha manifested prolonged elevation in serum levels when compared with once daily administration.

Adult↗

Identification of heterologous translocation partner genes fused to the BCL6 gene in diffuse large B-cell lymphomas: 5'-RACE and LA - PCR analyses of biopsy samples.

In order to elucidate the molecular mechanism(s) for BCL6 translocation, we identified translocational partner genes by subjecting clinical biopsy samples from patients with non-Hodgkin's lymphoma to 5'-rapid amplification of cDNA ends (5'-RACE). Sequence analysis of the 5'-RACE product revealed that the BCL6 gene was fused to the J segment of the immunoglobulin heavy chain (IgH) gene in about half of the cases, but in the other half, it was fused to heterologous partners, including the MHC class II transactivator (CIITA), pim-1, eukaryotic initiation factor 4AII (eif4AII), transferrin receptor (TFRR) and ikaros genes. Since analyses using genomic long and accurate (LA) - PCR revealed that the breakpoints in the partner gene were confined to the first intron or the second exon in all cases, the promoter and the first exon of the BCL6 gene were replaced by the promoter and the first or both the first and second exon of the partner gene. The breakpoint flanking sequences had no recombination signal sequences (RSSs) or chi sequences and were homologous with the switch region only when the BCL6 gene was fused to the IgH gene, suggesting that BCL6 translocation cannot be explained solely by mistakes of V(D)J, or chi-mediated or class-switch recombination, but rather another mechanism may also be required to explain the molecular mechanism for the promiscuous BCL6 translocation.

5' Untranslated Regions↗

Changes in fructose-induced production of glucose in the rat liver following partial hepatectomy.

The fructose-induced production of glucose in the liver after partial hepatectomy (PH) was evaluated by using the liver-perfusion system. There was no significant difference in plasma glucose level between hepatectomized (HX) and sham-operated (SO) rats at 24 h after surgery, and, thereafter, almost similar levels were obtained in both groups. However, the level of serum free fatty acids (FFA) was significantly higher in HX rats than that in SO rats at 24 and 48 h after surgery. When both groups of rats were given fructose by gavage, the increment of plasma glucose was significantly larger in HX rats than in SO rats. Lactate infusion failed to increase the rate of glucose production in perfused livers of both HX and SO rats and there was no significant difference in the activity of hepatic phosphoenolpyruvate carboxykinase. By contrast, fructose infusion elicited a large increase in glucose production in the perfused livers of HX rats at 24 and 48 h after PH. The increase was closely associated with not the change in fructose 2,6-bisphosphate levels but the increment of the intracellular levels of citrate. Treatment of octanoate or oleate, which supplies acetyl-CoA via fatty acid oxidation, mimicked the fructose-induced increase in glucose production in SO rats with a concomitant increase in hepatic levels of citrate. These results suggest that the oxidation of FFA may play an important role in glucose production induced by fructose administration during the early phase of liver regeneration.

Acetyl Coenzyme A↗

Hepatoprotective action of adenovirus-transferred HNF-3gamma gene in acute liver injury caused by CCl(4).

Hepatocyte nuclear factor-3gamma (HNF-3gamma) is an important regulator of liver-specific genes and the expression of this factor is reduced in the liver injured by carbon tetrachloride (CCl(4)). Wistar rats were infected with a recombinant adenovirus carrying the cDNA for HNF-3gamma (AxCAHNF3gamma) via the tail vein and were treated with CCl(4) by intraperitoneal injection. Liver damage, such as swelling of the hepatocytes and increases in serum marker enzymes were markedly alleviated by AxCAHNF3gamma infection. Interestingly, hepatocyte growth factor (HGF) was strongly induced in the AxCAHNF3gamma-infected liver. Likewise, HNF-1alpha and HNF-1beta levels were increased, but HNF-3alpha and HNF-3beta levels were depressed in the liver. Our results suggest that the transduced HNF-3gamma gene leads to a hepatoprotective effect via the induction of HGF by the combined actions of liver-enriched transcription factors.

Acute Disease↗

Interferon therapy reduces the risk for hepatocellular carcinoma: national surveillance program of cirrhotic and noncirrhotic patients with chronic hepatitis C in Japan. IHIT Study Group. Inhibition of Hepatocarcinogenesis by Interferon Therapy.

BACKGROUND: Previous studies on the effect of interferon therapy on the incidence of hepatocellular carcinoma have not sufficiently assessed degree of liver fibrosis, a major risk factor for hepatocellular carcinoma. OBJECTIVE: To evaluate the effect of interferon therapy on incidence of hepatocellular carcinoma, adjusting for risk factors, including the degree of liver fibrosis. DESIGN: Retrospective cohort study. SETTING: Seven university hospitals and one regional core hospital in Japan. PATIENTS: 2890 patients with chronic hepatitis C who had undergone liver biopsy since 1986. Of these patients, 2400 received interferon and 490 were untreated. MEASUREMENTS: The degree of liver fibrosis was assessed from stage F0 (no fibrosis) to stage F4 (cirrhosis). Response to interferon was determined virologically and biochemically. Screening for development of hepatocellular carcinoma was performed periodically during an average follow-up of 4.3 years. Effect of interferon therapy on the risk for hepatocellular carcinoma was analyzed by using Cox proportional hazards regression. RESULTS: Hepatocellular carcinoma developed in 89 interferon-treated patients and in 59 untreated patients. Among untreated patients, the annual incidence of hepatocellular carcinoma increased with the degree of liver fibrosis, from 0.5% among patients with stage F0 or F1 fibrosis to 7.9% among patients with stage F4 fibrosis. The cumulative incidence in treated and untreated patients differed significantly for patients with stage F2 fibrosis (P = 0.0128) and for those with stage F3 fibrosis (P = 0.0011). In multivariate analysis, interferon therapy was associated with a reduced risk for hepatocellular carcinoma (adjusted risk ratio, 0.516 [95% CI, 0.358 to 0.742]; P < 0.001), especially among patients with sustained virologic response (risk ratio, 0.197 [CI, 0.099 to 0.392]), among those with persistently normal serum alanine aminotransferase levels (risk ratio, 0.197 [CI, 0.104 to 0.375]), and among those with alanine aminotransferase levels less than two times the upper limit of normal (risk ratio, 0.358 [CI, 0.206 to 0.622]). CONCLUSIONS: Interferon therapy significantly reducesthe risk for hepatocellular carcinoma, especially among virologic or biochemical responders.

Alanine Transaminase↗

Changes in hepatic nitrogen metabolism in isolated perfused liver during the development of thioacetamide-induced cirrhosis in rats.

Changes in hepatic nitrogen metabolism in isolated perfused liver were studied during the induction of experimental cirrhosis by thioacetamide in female Sprague-Dawley rats. Cirrhosis of the micronodular type developed during 12-week administration of thioacetamide. Despite an increase in food consumption for 4 weeks after the end of administration, the physiological changes characteristic of cirrhosis were maintained. The rate of urea excretion per unit liver weight was significantly decreased compared with pair-fed control rats both during and after thioacetamide treatment. During 4 weeks of thioacetamide treatment, the rate of urea production in perfused liver from a combination of 0.25 mM NH4Cl and 1 mM glutamine decreased slightly, without a decrease in the maximum rate of urea production from 10 mM NH4Cl. In cirrhotic rats, the rate of urea production in perfused liver from NH4Cl and/or glutamine decreased, with a decrease in the maximum rate of urea production. The Km of ureagenesis for NH3 was unchanged in cirrhotic livers. During 4 weeks of thioacetamide treatment, glutamate dehydrogenase activity decreased, but the thioacetamide-induced cirrhotic state had no effect on glutamate dehydrogenase or glutaminase activity. Glutamine synthetase activity was decreased in rats treated with thioacetamide for 4 or 12 weeks. These results are consistent with the hypothesis that the capacity for urea production from NH3 and amino acids is decreased in the development of cirrhosis.

Alanine Transaminase↗

Multiple sequence-reactive antibodies induced by a single peptide immunization with hypervariable region 1 of hepatitis C virus.

Hypervariable region 1 (HVR1) of hepatitis C virus (HCV) is known to contain neutralizing epitopes. We previously found that murine antibodies against HVR1-#6 captured a different isolate, HCV-#7, and cross-reacted with the HVR1 peptide of HCV-#7. We investigated the inducibility and generality of cross-reaction of animal anti-HVR1 antibody responses in this study. Anti-HVR1-#7 antibodies, which were induced in mice and a chimpanzee by immunization, were found to be cross-reactive to HVR1-#6 peptide. Antibody responses against HVR1-#6-1 and HVR1-#7 peptides were detected in 11/165 (6.7%) and 26/165 (15.8%) HCV-infected individuals, respectively. Nine HVR1 sequences from six individuals, who were strongly positive for anti-HVR1-#7 antibodies, were only 50-64.5% identical to that of HVR1-#7. All nine of these HVR1 peptides were reactive to sera from the six patients and/or to antisera against HVR1-#6 and HVR1-#7 produced in mice and chimpanzees. Cross-inhibition tests of chimpanzee antisera indicated that a given species of anti-HVR1 antibodies was reactive to multiple HVR1 sequences. Fine epitope mapping of polyclonal and monoclonal anti-HVR1 antibodies showed that conserved subregions in HVR1 sequences determined the observed immunological cross-reactivity. Our data demonstrate that cross-reacting anti-HVR1 antibodies are inducible by a single peptide immunization.

Amino Acid Sequence↗

Determination of plasma phenobarbital concentration by high-performance liquid chromatography in rat offspring.

Plasma phenobarbital (PB) concentrations in rat offspring were determined using a 9 microl capillary by high-performance liquid chromatography (HPLC). Capillary plasma which was put into a Bond Elut cartridge column by using 1 ml of 0.01 M KH2PO4 was applied to the column with 50 microl of 2 microg/ml of acetanilide (internal standard, I.S.). After washing the column, PB and I.S. were eluted with methanol and injected into the HPLC system. There were excellent linear correlation between the amount of PB and length of the capillary at three different concentrations. Calibration for PB was linear in the range of 0-50 microg/ml. The coefficients of variation were 3.4-5.0% and 5.9-7.5% in the within-day and between-day assays, respectively. The extraction recovery rates were 87.5-105.4%. By this method, it was possible to measure plasma PB concentrations in rat offspring without killing. These results suggested that this method is very useful to determine the plasma PB concentration derived from mother's milk in newborn rats.

Animals↗

Characteristics of nitrogen metabolism in rats with thioacetamide-induced liver cirrhosis.

Female Sprague-Dawley rats were given 0.03% thioacetamide (TAA) in their drinking water daily for 4 or 12 weeks, and were then given normal water for 4 weeks after the end of a 12-week TAA treatment to investigate amino acid metabolism. In the malnourished precirrhotic stage (stage 1) and the malnourished cirrhotic stage (stage 2), the aromatic amino acids (AAA), Glu, Asp, Orn, Arg and Cit increased, and the branched-chain amino acids (BCAA) decreased slightly. Because these changes normalized in the well-nourished cirrhotic stage (stage 3), they might have resulted from impairment of hepatocytes and malnutrition. The net uptake of BCAA into the liver increased in stage 2, but the AAA uptake did not exceed that in normal controls. Portal venous plasma AAA increased to the same level as arterial plasma AAA. These results suggest that the decrease in BCAA was partially due to liver uptake and that the increase in AAA was induced by reduction of liver uptake and overproduction in extrahepatic tissues. The liver contents of BCAA and AAA were unchanged in all stages, so were fully utilized in the impaired liver. The increases in Glu, Asp, Orn and Cit might have resulted from overproduction in the liver, because these contents of the liver increased in stage 2. In conclusion, the changes in amino acid metabolism in rats with cirrhosis induced by TAA closely resemble those seen in human liver cirrhosis.

Amino Acids↗

Adenovirus-mediated high expression of BCL-6 in CV-1 cells induces apoptotic cell death accompanied by down-regulation of BCL-2 and BCL-X(L).

The BCL-6 proto-oncogene encodes a 92- to 98-kDa transcriptional repressor containing the BTB/POZ domain at its N-terminal region and the zinc finger domain at its C-terminal region, respectively. In the present study, we examined the function of BCL-6 by using a recombinant adenovirus expressing BCL-6 (Ax1CA-BCL-6) and the lacZ reporter gene (Ax1CA-lacZ). Viability of CV-1 and HeLa cells infected with Ax1CA-BCL-6 was markedly reduced due to apoptosis, suggesting that BCL-6-overexpression induces apoptosis in CV-1 and HeLa cells. FACS analysis revealed that BCL-6-overexpressing cells are accumulated not only at the sub-G1 but also at G2/M phase. Induction of apoptosis by BCL-6 was preceded by down-regulation of apoptosis repressors BCL-2 and BCL-X(L). These results suggest that BCL-6 induces apoptosis by regulating the expression of these apoptosis-regulating genes.

Adenoviridae↗

Expression of functional CD40 in human hepatocellular carcinoma.

CD40, a member of the tumor necrosis factor receptor (TNFR) family, plays a crucial role in the survival, proliferation, and differentiation in B cells. However, the expression of CD40 other than in B cells has not been well studied. Therefore, we investigated the expression and function of CD40 in hepatocellular carcinomas (HCCs). Expression of CD40 mRNA in 6 established HCC cell lines was analyzed by reverse-transcription polymerase chain reaction (RT-PCR) and CD40 expression on cell surface was examined by flow cytometrical analysis. We also examined the expression of CD40 in human HCC tissues (45 cases) and nontumor liver tissues (30 cases) by immunohistochemistry. To examine the function of CD40 in HCC cells, we investigated the effect of CD40 signaling on anti-Fas antibody and TNF-alpha-induced apoptosis in HepG2 cells. In addition, intracellular levels of cysteine protease P32 (CPP32) protein in HepG2 cells were also determined by Western blotting. We have shown that 6 HCC cell lines constitutively expressed CD40 mRNA and membrane-bound CD40 antigen, which was slightly up-regulated by interferon gamma (IFN-gamma). In addition, 60% of human HCC tissues demonstrated positive staining for CD40, whereas nontumor tissues showed little detectable staining. In HepG2 cells, CD40 stimulation does not affect cell viability, but significantly inhibited Fas and TNFR-mediated apoptosis in a dose-dependent manner by blocking the activation of CPP32. From these results, we conclude that CD40 expression in HCCs plays an important role in tumor biology, especially the resistance against Fas and TNFR-mediated apoptosis.

Apoptosis↗

Development of diffuse invasive (grade 4D) human oral squamous cell carcinoma model in severe combined immunodeficiency mice: microangioarchitectural analysis and immunohistochemical study.

Among oral squamous cell carcinomas (OSCCs), the diffuse invasive (grade 4D) tumour exhibits the highest degree of malignancy. The TSU cell line, which has been established from a grade 4D OSCC, has not been successfully grown even in immuno-suppressed hosts. Here, invasive cells were selected by the repeated inoculation of TSU cells with Matrigel and gelatin sponge into the subcutaneous tissue of nude mice. The selected cells formed oral tumours temporarily in nude mice and produced lethal tumourgenicity in severe combined immunodeficiency (SCID) mice without the addition of other materials. The microangioarchitecture of the tumours in SCID mice showed neovascularization and the formation of a vascular network. An immunohistochemical study demonstrated that the expressions of vascular endothelial growth factor and matrix metalloproteinase-2 were strong, whereas desmoglein-1 and type-IV collagen were absent. These findings suggested that the loss of intercellular junctions and dissolution of basement membranes may underlie the pathogenesis of diffuse invasive growth in grade 4D tumours.

Animals↗

Ossifying fibromyxoid tumor of soft parts: clinicopathologic, immunohistochemical and ultrastructural study of four cases.

Four cases of uncommon soft tissue tumors were investigated histopathologically. All of them consisted of fibrous and myxoid components, and mature bone showed shell-like characteristics. Histological features revealed these tumors were well circumscribed by a thick collagenous fibrous capsule and composed of uniform-sized fusiform cells with eosinophilic cytoplasm and a round or oval nucleus in the myxoid matrix. An incomplete shell of mature bone with lamellar structure was also observed at the periphery. Immunohistochemical and ultrastructural studies were performed. The major component of the proliferating cells in the tumors had positive staining for vimentin, S-100 protein, neuron-specific enolase and synaptophysin. The myxoid matrix was stained by alcian blue and was digested completely by pretreatment with hyaluronidase. Electron microscopy showed the cytoplasm contained dense-core granules measuring 100-200 nm and abundant filaments of an intermediate size. It is suggested that these uncommon tumors might be diagnosed as the 'ossifying fibromyxoid tumor of soft parts' previously described by Enzinger et al., which were derived from peripheral nerve sheath tumors such as neurofibroma and myxoid neurofibroma.

Adult↗

Blinded, prospective, and serial evaluation by quantitative-EEG in interferon-alpha-treated hepatitis-C.

OBJECTIVES: To estimate the effect of brain function due to IFN-alpha in chronic hepatitis C patients by the quantitative EEG. METHODS: 56 chronic hepatitis C patients were administered IFN-alpha intramuscularly at 9x10(6) IU daily for the first 4 weeks and then 3 times/week for the next 20 weeks. Serial EEGs were obtained in each subject before, at 2 and 4 weeks, and after completing the treatment. Resting EEG without artifacts was selected for quantitative EEG analysis, which was performed blindly. The frequency range was divided into delta to beta. The absolute and relative powers of each frequency band in each subject were calculated and the differences of these powers at different stages were analyzed statistically. RESULTS: The absolute powers of slow waves (delta, theta 1, and theta 2) increased while alpha 2 and fast wave (beta) decreased significantly at all locations during IFN-alpha administration. The total power and alpha 1 values revealed no significant alterations. The relative power revealed the same alteration during treatment. These changes disappeared following the treatment. Such diffuse slowing in the EEG was revealed by the total change in the whole subjects. CONCLUSIONS: Diffuse slowing in the EEG was induced by IFN-alpha, was reversible, and was evident as the total change in the subjects. These findings suggested mild IFN-alpha-induced encephalopathy.

Analysis of Variance↗

[Serum leptin level among non-obese students: relationship to body fat, blood pressure, serum lipids, physical activity, and eating habits].

Leptin, a product of the ob gene, is thought to play a key role in the regulation of adiposity. However, it is unclear in humans as to whether or not leptin influences the blood pressure, serum lipids, physical activity level, or eating behavior in relation to obesity. Recent reports have indicated both gender-based differences in the leptin levels and a correlation of the percentage of body fat with leptin levels has been observed among obese subjects. As far as we know, these relationships among non-obese young adults have yet to be studied. Therefore, the serum leptin concentrations among 107 non-obese students (72 males and 35 females) were measured by a radioimmunoassay(RIA). Fasting leptin levels ranging between 1.2 and 23.4 ng/mL were observed in all subjects, and the levels among females were 2.6 times higher than in males (7.64 vs 2.95 ng/mL; p < 0.001). A close correlation was observed regarding the log-transformed leptin levels with the percentage of body fat as determined by the bioelectrical impedance analysis method(r = 0.734, p < 0.001 in males and r = 0.579, p < 0.001 in females). In conclusion, these data thus suggest the serum leptin levels among non-obese students show significant gender-based differences while, in addition, the leptin levels also correlate positively with the percentage of body fat. However, it remains unclear as to whether or not the leptin levels are independently related to the blood pressure, serum lipids, physical activity level (sports activity and leisure-time activity), and eating behavior (eating breakfast, mid-day snacking and nighttime snacking).

Adipose Tissue↗

Temporal changes in mRNA expression for bikunin in the kidneys of rats during calcium oxalate nephrolithiasis.

Inter-alpha-inhibitor and other bikunin-containing proteins are synthesized in relatively large quantities by the liver. These proteins function as Kunitz-type serine protease inhibitors and appear capable of inhibiting calcium oxalate (CaOx) crystallization in vitro. Preliminary studies have shown that renal tubular epithelial cells synthesize bikunin in response to CaOx challenge. To examine this response in vivo, a sensitive reverse transcription-quantitative competitive template-PCR was developed to detect and quantify poly(A)+ -tailed bikunin mRNA expression in kidney tissue from normal rats and rats developing CaOx nephrolithiasis after challenge with ethylene glycol. Bikunin mRNA expression in rat liver tissue was assessed as a positive control. The expression of bikunin mRNA in liver did not differ significantly between normal control rats and experimental rats with induced hyperoxaluria and renal CaOx crystallization. In contrast, there were significant temporal increases in the levels of bikunin mRNA expression in rat kidneys during CaOx nephrolithiasis after challenge with ethylene glycol. Urinary excretion of bikunin-containing proteins seemed to increase concomitantly. These findings indicate an association between the induction of hyperoxaluria/CaOx nephrolithiasis and the expression of the bikunin gene in rat kidneys.

Alpha-Globulins↗

[Report of two rare cases of fungal sinusitis].

Two cases of aspergillosis of the paranasal sinuses are reported. The first case was a 30-year-old man who had a 5-month history of bilateral proptosis. Physical examination revealed nasal polyps in both middle meatus. A skin test for Aspergillus was positive. Laboratory study showed levels of serum IgE and IgE specific for Aspergillus level to be elevated significantly. Computed tomography (CT) and magnetic resonance imaging (MRI) showed pansinusitis with some bone erosion. The patient underwent bilateral Caldwell-Luc procedures and external sinus surgery (frontal, ethmoid and sphenoid sinuses). Histopathological examination showed thin septate hyphae in allergic mucin. The patient is now being treated with sinus irrigation and oral administration of fluconazole and suplatast tosilate. The second case was a 78-year-old man who had a 2-month history of nasal obstruction and a 3-week history of headaches. He also had a history of diabetes mellitus. Physical examination showed swelling of the nasal septum due to abscess. CT showed an abscess in the nasal septum and opacification of the left sphenoid sinus. There was no bone destruction. The patient underwent left sphenoid sinus surgery, and histopathological examination revealed aspergillosis of the sphenoid sinus. He presented with left visual disturbance and blepharoptosis 2 months after surgery. Ocoulusion of the internal carotid artery was revealed by MR angiography and it was thought to be caused by intracranial invasion of aspergillus. Loss of consciousness and right hemiplegia ensued despite antifungal chemotherapy. The patient died about 1 year after the onset of symptoms. Case 1 was thought to involve allergic aspergillus sinusitis, and Case 2 invasive aspergillus sinusitis. We emphasize the significance of headache, diabetes mellitus and lesion in the sphenoid sinus as a sigh of intracranial aspergillus invasion, based on our experience as well as findings reported by other clinicians in the Japanese literature.

Adult↗