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Biomedical subjects

F Marumo

Publications and source records attributed to F Marumo.

At least 235 records · Page 13Linked to original sources
PubMed1996

Fibrinogen, coagulation factor VII, tissue plasminogen activator, plasminogen activator inhibitor-1, and lipid as cardiovascular risk factors in chronic hemodialysis and continuous ambulatory peritoneal dialysis patients.

Mortality rates associated with cardiovascular disease (CVD) are high in long-term dialysis patients. Increased levels of plasma fibrinogen (FBG), coagulation factor VII (FVII), tissue plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1) as well as hyperlipidemia are regarded as important risk factors for CVD. To investigate whether there are differences in the risk of CVD between chronic hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) patients, serum lipid levels and plasma FBG, FVII, t-PA, and PAI-1 levels were measured in 17 patients on HD and 17 patients on CAPD. FBG was measured by the thrombin time method, FVII activity (FVIIc) by the chromogenic prothrombin time method, and t-PA and PAI-1 activity by the chromogenic substrate assay. No difference was found in body mass index (BMI) between HD and CAPD patients. Total cholesterol (TC), TC/high-density lipoprotein (HDL)-C ratio, low-density lipoprotein (LDL)-C, and triglycerides (TG) were significantly increased, and HDL-C was significantly decreased in CAPD patients compared with HD patients. FBG and FVIIc were significantly elevated in CAPD patients compared with controls or HD patients. T-PA activities were significantly higher in HD and CAPD patients than in controls. CAPD patients showed significantly higher PAI-1 activities than controls or HD patients. Significant positive correlations were found between FBG or FVIIc and TC, between FBG and LDL-C or TG, and between FVIIc and LDL-C in these patients. T-PA showed significant negative correlations with FBG, PAI-1, TC, LDL-C, and TG. There was a significant positive correlation between PAI-1 and TG and a significant negative correlation between PAI-1 and HDL-C. We conclude that CAPD patients may have a greater risk of CVD than do HD patients, and that coagulation and fibrinolytic activity are correlated with lipid disorders in these patients.

Adult↗
PubMed1996

Does appropriate endurance exercise training improve cardiac function in patients with prior myocardial infarction?

OBJECTIVE: The objective of the present study was to determine whether appropriate endurance exercise training improves cardiac function in patients with prior myocardial infarction. METHODS: Twenty-nine patients with prior myocardial infarction were divided into three groups (Group 1: control, Group 2: low-intensity training, Group 3: high-intensity training). Low and high training intensities were determined according to the gas exchange threshold of each patient. The patients in Groups 2 and 3 performed 15 min of home-based physical training safely, twice a day, 5 days a week for 2 months. Prior to and following this training, each patient performed two constant work rate tests (moderate and heavy intensity) and a symptom-limited incremental exercise test. RESULTS: Heart rates at rest and during exercise were decreased significantly after 2 months in all three groups. Stroke volume at rest increased significantly after 2 months only in Group 3. Stroke volume after 6 min of heavy-intensity exercise increased significantly in Groups 2 and 3. However, the ejection fraction at 6 min of heavy-intensity exercise increased significantly only in Group 3. The maximal work rate attained during incremental exercise testing increased significantly in Groups 2 and 3. This parameter did not significantly change in the control group. CONCLUSIONS: Effects of physical training on maximal exercise capacity were noted in both exercise training groups. However, improvement in cardiac function (such as stroke volume), both at rest and during exercise, was noted only in the high-intensity training group. Our results suggest that relatively high-intensity training may improve exercise capacity and cardiac function of patients with prior myocardial infarction.

Adult↗
PubMed1996

Role of urinary arginine vasopressin in the sodium excretion in patients with chronic renal failure.

Patients with chronic renal failure show almost equal levels of sodium excreted in the urine as healthy subjects through an increase of the fractional excretion sodium (FE(Na)). The mechanisms of this adaptation, however, are unknown. Recently, urinary arginine vasopressin (AVP) has been shown to inhibit the antidiuretic action of plasma AVP in the collecting ducts of rabbits and rats. In this article, the roles of plasma and urinary AVP are examined with other hormones in the sodium excretion of 57 patients with chronic renal disease. The fractional excretion of AVP, plasma atrial natriuretic peptide (ANP) and endothelin-1 (ET-1), urinary ET-1, and FE(ET-1) correlated with the decrease of creatinine clearance (Ccr). Multiple and stepwise regression analyses showed that FE(AVP) is the major dependent determinant for FE(Na) (adjusted r2 = 0.78). These results suggest that the increase of AVP excretion per remaining nephron could be a cause of the increase of FE(Na) in patients with renal failure. Although plasma AVP works as an antidiuretic hormone, urinary AVP serves as an intrinsic diuretic, especially in patients with chronic renal failure.

Adolescent↗
PubMed1996

Ischemic hepatitis in cirrhosis. clinical features and prognostic implications.

To characterize liver dysfunction in patients with cirrhosis after variceal bleeding, we analyzed 50 cirrhotic patients who had bleeding esophageal varices with or without shock. Increases in serum total bilirubin levels by 1.5 times were observed within 24 h in 11 of 12 patients with shock who died > 4 days after hemorrhage but in only one of eight patients with shock who survived (p < 0.01). Increases in serum aspartate aminotransferase and alanine aminotransferase by 2.5 times were observed in six patients in the former group but in none of the latter (p < 0.05). In postmortem livers, hepatocellular degeneration with minimal inflammatory cell infiltration was observed. Ischemic hepatitis is frequently noted in cirrhotic patients with ruptured esophageal varices. Patients with increases in the serum level of total bilirubin and/or aminotransferases within 24 h from onset of hemorrhage should be carefully treated even if hemorrhage is controlled.

Adult↗
PubMed1996

Improvement of peripheral blood lymphocyte subsets in primary biliary cirrhosis after ursodeoxycholic acid therapy.

Immunological abnormalities frequently observed in patients with primary biliary cirrhosis are considered to be related to the pathogenesis of this disease. We performed a prospective trial to evaluate whether immune mechanisms play a role in the effectiveness of ursodeoxycholic acid (UDCA) therapy. Fifteen female patients with primary biliary cirrhosis were followed for 1 year and were then treated with UDCA (600 mg/day) for another year. Laboratory tests, including peripheral blood lymphocyte subsets assessed by dual colour fluorescence analysis using monoclonal antibodies against respective T cell markers, were evaluated at the beginning of the study, at the start of therapy and at the end of therapy. In primary biliary cirrhosis, the proportion of cytotoxic T cells, suppressor inducer T cells and alpha beta-receptor bearing T cells were significantly lower than in healthy controls. No significant changes were observed in the proportions during the year before the therapy. These reductions, however, recovered to normal ranges after 1 year of UDCA therapy. These changes were associated with an improvement in the serum levels of aspartate aminotransferase, alkaline phosphatase, gamma-globulin and IgM. The close correlation between the improvement in the imbalance of lymphocyte subsets after the therapy and the clinical status suggests that an immunological process may play a role in the effectiveness of therapy in primary biliary cirrhosis.

Aged↗
PubMed1996

Roles of alcohol, hepatitis virus infection, and gender in the development of hepatocellular carcinoma in patients with liver cirrhosis.

To assess the interaction of alcohol, hepatitis C virus (HCV), and hepatitis B virus (HBV) infection in hepatocarcinogenesis, we prospectively observed 449 patients with liver cirrhosis (LC) who presented to our outpatient clinics in 1 month; 164 patients with habitual drinking [alcoholic liver-liver cirrhosis (AL-LC)] who had taken > 72 g alcohol/day (HCV-positive 81 cases: HCV + AL; HCV-negative 83 cases: AL); 176 patients with HCV infection, but without alcohol intake: 34 patients with HBV infection: 6 patients with HCV and HBV coinfection; and 82 patients with liver diseases from other etiologies, such as primary biliary cirrhosis. In the HCV group, the cumulative occurrence rate of hepatocellular carcinoma (HCC) was 9%, 18%, and 23% in the first, second, and third years, respectively. In the HCV + AL group, that was 13%, 17%, and 28%, respectively. There was no difference in the HCC occurrence rate between the two groups. In the AL group, the cumulative HCC occurrence rate was only 1% during the observation period of 3 years. The occurrence rate was significantly lower in the AL group, compared with the HCV and the HCV + AL groups. In the HBV group, the cumulative occurrence rate of HCC during the observation period of 3 years was 17%, which was similar to that of the HBV + AL group, 14%. We also examined some other variables that might be related to the development of HCC. The cumulative occurrence rate of HCC in male patients was 31%, whereas that was 18% in female patients. In the HCV group, there was a significant increase of HCC occurrence rate in male patients. In contrast, no difference was observed in the HCC occurrence rate between male and female patients in the HBV group. The present study suggests that alcohol alone may not be an independent risk factor for HCC, nor does it accelerate HCC development in LC patients with HCV and HBV infection during the prospective observation of 3 years.

Adult↗
PubMed1996

Distribution of hepatitis C virus RNA in the liver and its relation to histopathological changes.

To investigate a cellular mode of HCV-infection in the liver and its pathological implications in relation to histopathological changes or clinical data, we studied the distribution of HCV-RNA in the livers of 21 patients with HCV-related chronic liver disease (chronic active hepatitis, 14 cases; cirrhosis, 7 cases) using the in situ hybridization technique. In situ hybridization was performed on 4% paraformaldehyde-fixed frozen sections with digoxigenin-labeled DNA probe deduced from the core region of HC-J4. In situ hybridization showed positive signals in the liver specimens of 20/21 cases. The signals were localized in the cytoplasm of hepatocytes. The distribution pattern of positive cells was individually different, whereas the pattern was identical in the right and left lobes. There were no correlations of the HCV-positive cell number with serum aminotransferase levels at biopsy or with genotypes of HCV. The positive hepatocytes were occasionally associated with infiltrating mononuclear cells, and they were sparsely distributed in the area of piecemeal necrosis. These findings suggest that factors such as host immunoreaction to the virus may be more important than its direct cytopathy in the pathogenesis of chronic hepatitis C virus infection.

Alanine Transaminase↗
PubMed1996

Natural history of polypoid lesions in the gall bladder.

BACKGROUND: Although polypoid lesions of the gall bladder are frequently observed in asymptomatic subjects, the natural history of these lesions has never been studied using ultrasonography. AIM: The natural history of polypoid lesions of the gall bladder was investigated using ultrasonography. SUBJECTS: Among 4343 patients who presented to the outpatient clinic of Tsuchiura Kyodo General Hospital in 1988, 111 subjects were diagnosed as having polypoid lesions of the gall bladder by ultrasonography. Among these patients, two had gall bladder carcinoma. The remaining 109 subjects (58 female; age: median 54, range 25-89) were enrolled in this study. METHODS: The subjects were followed up by ultrasonography once or twice a year until 1994. RESULTS: Four patients received cholecystectomy and two patients died of other causes during the observation period. In one patient, gall bladder carcinoma was found, but its location was different from that of the pre-existing polyp. The size of the lesions did not change in 88.3% of the other 130 patients during this period, even among those in whom the initial size of the lesion exceeded 10 mm. There was no apparent correlation between the change in the diameter of the polypoid lesions and patients' sex or age. CONCLUSION: Most polypoid lesions of the gall bladder detected by ultrasonography are benign.

Aged↗
PubMed1996

Functional activity of H-K-ATPase in individual cells of OMCD: localization and effect of K+ depletion.

Recent studies have indicated the presence of hydrogen-potassium-adenosinetriphosphatase (H-K-ATPase) in the collecting duct. We examined the localization of functional H-K-ATPase activity in individual cells of the outer and inner stripes of outer medullary collecting ducts (OMCDo and OMCDi). Tubules were isolated from control and K(+)-depleted rabbits and perfused in vitro. Intracellular pH (pHi) of principal cells, intercalated cells, and OMCDi cells was monitored by fluorescence ratio imaging using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). An intracellular acid load was induced by NH3/NH4 prepulse in extracellular Na(+)-, K(+)-, and HCO3(-)-free condition, and then 5 mM K+ was added to the lumen or the bath in the presence of Ba2+. Functional activity of H-K-ATPase was estimated by the difference in the rates of pHi recovery before and after K+ addition. In the control condition, luminal addition of K+ significantly increased the pHi recovery rate by 1.6 +/- 0.4 and 1.9 +/- 0.4 x 10(-3) pH units/s in intercalated calls and OMCDi cells, respectively, but not in principal cells. This K(+)-dependent pHi recovery was inhibited by 63% in intercalated cells and 74% in OMCDi cells in the presence of luminal Sch-28080 (10 microM) but was not affected in the presence of luminal bafilomycin-A1 (10 nM). K+ depletion increased the K(+)-dependent pHi recovery to 2.3-fold in intercalated cells and 2.6-fold in OMCDi cells. By contrast, K(+)-dependent pHi recovery was not detected in the basolateral membrane of any cell types in either the control or the K(+)-depleted condition. These results provide functional evidence that H-K-ATPase is distributed in the luminal membrane of intercalated cells and OMCDi cells and that this ATPase is activated by K+ depletion, suggesting the contribution of intercalated cells and OMCDi cells to K+ conservation in rabbit OMCD.

Animals↗
PubMed1996

Repressive regulation of the aquaporin-2 gene.

Expression of aquaporin-2 (AQP2) is exclusively limited to kidney collecting duct cells, and this strictly limited expression could be mediated by transcription of the gene. We first examined AQP2 mRNA expression in many cultured epithelial cells derived from kidney. Northern blot using OK, LLC-PK1, Madin-Darby canine kidney, and outer medullary collecting duct (OMCD) cells and primary culture of inner medullary collecting duct (IMCD) cells did not reveal any significant signal. A more sensitive method, ribonuclease protection assay, could detect a faint signal in OMCD cells when they were bathed in a hypertonic medium. Reverse-transcribed polymerase chain reaction applied to primary culture of IMCD cells showed a rapid dissipation of AQP2 mRNA within 4 days after culture. A reporter gene assay performed in the 1st day of primary culture of IMCD cells showed that the 5' region up to -2.9 kb worked as a promoter. Deletion experiments showed that at least two regions, from -434 to -364 and from -153 to -84, contain negatively acting cis-elements. When connected to a heterologous promoter, these regions repressed the activity in an orientation-dependent manner. These results suggest that transcription of AQP2 gene is strictly regulated and its ability is rapidly depressed in culture condition. This cell differentiation-specific expression of the gene may be, at least in part, mediated by the repressors present in its 5'-flanking region.

Animals↗
PubMed1996

One-compartment urea kinetic modeling is not acceptable for quantifying the adequacy of hemodialysis: comparison of a one-compartment model with a two-compartment model.

We can quantify the adequacy of hemodialysis (HD) as the dialysis dose using urea kinetic modeling (UKM). Though the one-compartment model (1CM) has frequently been applied, there are some studies which have successfully applied the two-compartment model (2CM) including urea rebound. To clarify whether 1CM or 2CM is more acceptable, we analyzed 100 patients using UKM, applying each model. The dialysis dose was defined as the logarithm of pre-/post-HD urea volume in the body. In about half the patients analyzed, 1CM estimation of the dialysis dose exceeded 2CM estimation by more than 10%, and the 1CM was not considered to be acceptable.

Adult↗
PubMed1996

Role of vasopressin V2 receptor in acute regulation of aquaporin-2.

Aquaporin-2 (AQP-2) has been shown to be a vasopressin-sensitive water channel in collecting duct (CD) cells of the kidney. To prove the role of the vasopressin V2 receptor (V2R) in the regulation of intracellular AQP-2 shuttling, we examined the acute effects of vasopressin and V2R antagonist on the distribution of AQP-2 in the cells. Normal Wistar rats were given continuous infusions of vasopressin, vasopressin V2R antagonist (OPC31260), or both. The kidneys were then processed for immunofluorescent studies with an affinity-purified specific antibody to AQP-2. One hour after the infusion of the V2R antagonist, AQP-2 staining was diffusely distributed in the CD cells from the cortex to the inner medulla. This tendency was not changed by the concomitant infusion with vasopressin. Vasopressin infusion without antagonist, however, induced intensified AQP-2 staining of the apical membrane in the CD cells. The ratio of the fluorescence intensity of the apical to subapical region was determined by confocal laser microscopy. In the inner medulla, this ratio was significantly increased in the vasopressin treatment group (2.26 +/- 0.76) as compared to the V2R antagonist group (1.03 +/- 0.34) and the combined treatment group (0.84 +/- 0.43). The increase in the ratio was also demonstrated in the cortex and the outer medulla in the vasopressin-treated group. In addition, Northern blotting studies clearly revealed that mRNA of AQP-2 in the vasopressin-treated group was increased when compared to the combined treatment animals. Our present results reveal that localization and gene expressions of AQP-2 are acutely regulated via vasopressin V2R.

Animals↗
PubMed1996

Characteristics of anti-HCV antibody-positive patients with hepatocellular carcinoma on chronic hemodialysis: recommendation of periodic ultrasonography for early detection.

We analyzed 10 patients (male:female 9:1, mean age 64.2 years) who developed hepatocellular carcinoma during the observation period of 2 years among 2,164 chronic hemodialysis patients in 23 dialysis centers. Among them, 409 patients were positive for serum anti-HCV antibodies (19%). They were all positive for serum anti-HCV antibodies but negative for HBs antigen. None of the anti-HCV antibody-negative patients developed hepatocellular carcinoma during this period. Although liver function tests of the patients were almost normal, pathological examination of the liver revealed chronic active hepatitis or cirrhosis. Periodic ultrasonographic examination is necessary for early detection of hepatocellular carcinoma in chronic hemodialysis patients with positive anti-HCV antibodies even if liver function tests are within normal ranges.

Aged↗
PubMed1996

Shared amino acid motifs in T-cell receptor beta junctional regions of bronchoalveolar T cells in patients with pulmonary sarcoidosis.

To clarify the nature of the accumulated lung T cells of pulmonary sarcoidosis, we studied bronchoalveolar and peripheral blood (PB) lymphocytes from Japanese patients for expressed T-cell receptor beta-chain variable (TCR V beta) gene usage. Quantitative polymerase chain reaction technique revealed that the V beta repertoires of bronchoalveolar and PB T cells were heterogeneous. However, the bronchoalveolar lymphocytes from five out of 10 patients showed overrepresentation of T cells, with a few TCR V beta families, which varied among individuals, possibly reflecting a difference in the human leukocyte antigen (HLA) backgrounds. Nucleotide sequence analysis of third complementarity determining region (CDR3) segments in overrepresented V beta families demonstrated limited diversity of the transcripts. Two HLA-DR 12(5)+ individuals with overrepresented V beta 6 gene transcripts in the lungs shared a common amino acid motif within their CDR3. By contrast, non-overrepresented TCR V beta transcripts did not show clonal expansion, and the oligoclonal clones in the lung were not found in PB of the corresponding patient. These results showed that, at least in subsets of Japanese patients with pulmonary sarcoidosis, a limited number of T-cell clones are accumulated in the lung in response to a specific antigen. They may mediate an immune response to shape pathology of the disease.

Adult↗
PubMed1996

Specific binding sites for proadrenomedullin N-terminal 20 peptide (PAMP) in the rat.

Adrenomedullin (AM), a potent and novel vasodilator 52-residue peptide originally isolated from pheochromocytoma, is processed from a precursor molecule (preproAM) in which another unique 20-residue sequence, termed proadrenomedullin N-terminal 20 peptide (PAMP), exists. Using [125I Tyr0] rat PAMP as a radioligand, we have examined PAMP binding sites in various rat tissues and cultured vascular smooth muscle cells (VSMC) from rat aorta. Specific binding sites for rat PAMP, although very low, were widely distributed in various rat tissues examined. The relatively more abundant sites were present in aorta and adrenal glands, followed by lung, kidney, brain, spleen, and heart. An equilibrium binding study using cultured rat VSMC revealed the presence of a single class of high-affinity [dissociation constant (Kd): 3.5 x 10(-8) M] binding sites for rat PAMP with a maximal binding capacity of 4.5 x 10(6) sites per cell. Binding studies revealed that synthetic rat PAMP(1-19)-NH2 was about 10-fold less potent, and rat PAMP(1-20)-OH and human PAMP were about 20-fold less potent than rat PAMP(1-20)-NH2. SDS-polyacylamide gel electrophoresis after affinity-labeling of membranes from various rat tissues (aorta, adrenal glands, lung) and VSMC revealed a distinct labeled band with the apparent molecular mass of 90 kDa, which was diminished by excess unlabeled rat PAMP. A nonhydrolyzable GTP analog (GTP-gammaS) dose-dependently reduced binding of [125I] rat PAMP to VSMC membranes, while ATP-gammaS had no effect. Neither cyclic AMP nor inositol-1,4,5-triphosphate formation was affected by rat PAMP in rat VSMC. The present study demonstrates for the first time that PAMP receptors are widely distributed in various rat tissues, among which aorta and adrenal glands have the most abundant sites. Our data suggest that PAMP receptors are functionally coupled to G-proteins, although its signal transduction remains obscure. The present study also shows that amidation of C-terminal residue of PAMP is critical for receptor binding. The physiological function of PAMP remains undetermined.

Adenosine Triphosphate↗