T Kamada

Fukushima Medical University, Hukusima, Fukushima, Japan

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Publications (896)4083.37 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: The heterogeneity of the hepatitis C virus (HCV) genome has been reported to be associated with the effectiveness of interferon therapy. We investigated the correlation of the viral and host factors, including the degree of sequence complexity of the HCV genome for responses to interferon-α in patients with chronic hepatitis C. Methods: Ninety-seven patients received a 26-week course of recombinant interferon-α2a therapy. The sequence complexity of the envelope 1–2 region was evaluated by polymerase chain reaction-mediated single-strand conformation polymorphism (PCR-SSCP) analysis. Results: Of the 85 patients who completed the treatment, 31 (36%) achieved a sustained response, and 28 (33%) showed a sustained loss of HCV RNA. A low HCV RNA level, determined by the branched DNA probe assay, and serotype group 2 HCV correlated with a sustained response. In patients with serotype group 1 HCV of more than the threshold of the branched DNA probe assay, a band number on PCR-SSCP analysis of more than 2 could be associated with inefficacy of interferon therapy. Multivariate analysis in the 50 patients whose sera were available for all the virologic tests showed that only the HCV RNA level is independently predictive of a sustained response. Conclusions: Determination of the HCV RNA level is most important for predicting the response before interferon therapy. PCR-SSCP analysis may be useful as an additional test for patients with a high HCV RNA level of serotype group 1 HCV.
    Scandinavian Journal of Gastroenterology 07/2009; 31(10):1021-1026. DOI:10.3109/00365529609003123 · 2.33 Impact Factor
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    ABSTRACT: Ischaemic preconditioning (IP) protects the myocardium against irreversible ischaemic injury by activating protein kinase C (PKC). The mechanism by which PKC protects the myocardium is unknown. We have shown that PKC increases the activity of ecto-5′-nucleotidase (ecto-5′-N) and thereby the production of adenosine in cardiomyocytes which may protect the myocardium against ischaemia-reperfusion injury in vivo.The objective of this study was to elucidate the possible role of PKC-induced activation of ecto-5′-N in the cardioprotection associated with IP in the canine heart.IP increased the activities of both ecto-5′-N and PKC, and minimized ischaemic damage (infarct size: 7.5±1.8 vs. 42.3±2.8%, P<0.01 vs. the control group). Treatment with the PKC activator (4β-phorbol 12-myristate-13-acetate) also reduced infarct size (13.5±2.9%, P<0.01 vs. the control group). 8-Sulfophenyltheophylline (an antagonist of adenosine receptors) or α,β-methyleneadenosine 5′-diphosphate (an inhibitor of ecto-5′-N) eliminated the cardioprotective effect of the PKC activator (infarct size: 36.6±3.9 and 34.7±4.2%, respectively), suggesting that PMA limits infarct size by increasing the activity of ecto-5′-N and the adenosine level.The PMA-induced cardioprotection was blunted by GF109203X (an inhibitor of PKC, infarct size: 36.2±3.1%), but not by pretreatment with dexamethasone (infarct size, 14.2±2.6%).We conclude that the PMA- and IP-induced cardioprotection is attributable to phosphorylation and activation of ecto-5′-N.British Journal of Pharmacology (1997) 120, 273–281; doi:10.1038/sj.bjp.0700890
    British Journal of Pharmacology 02/2009; 120(2):273 - 281. DOI:10.1038/sj.bjp.0700890 · 4.99 Impact Factor
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    ABSTRACT: To investigate the astrocyte response to hypoxia/reoxygenation, as a model relevant to the pathogenesis of ischemic injury, cultured rat astrocytes were exposed to hypoxia. On restoration of astrocytes to normoxia, there was a dramatic increase in protein synthesis within 3 h, and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of metabolically labeled astrocyte lysates showed multiple induced bands on fluorograms. Levels of cellular ATP declined during the first 3 h of reoxygenation and the concentration of AMP increased to ± 3.6 nmol/mg of protein within 1 h of reoxygenation. Reoxygenated astrocytes generated oxygen free radicals early after replacement into ambient air, and addition of diphenyliodonium, an NADPH oxidase inhibitor, diminished the generation of free radicals as well as the induction of several bands on fluorogram. Although addition of cycloheximide on reoxygenation resulted in inhibition of both astrocyte protein synthesis and accumulation of cellular AMP, it caused cell death within 6 h, suggesting the importance of protein synthesis in adaptation of hypoxic astrocytes to reoxygenation. Potential physiologic significance of biosynthetic products of astrocytes in hypoxia/reoxygenation was suggested by the recovery of glutamate uptake. These results indicate that the astrocyte response to hypoxia/reoxygenation includes generation of oxygen free radicals and de novo synthesis of products that influence cell viability and function in ischemia.
    Journal of Neurochemistry 06/2008; 62(4):1489 - 1495. DOI:10.1046/j.1471-4159.1994.62041489.x · 4.24 Impact Factor
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    ABSTRACT: Kupffer cells (KC) become activated in response to lipopolysaccharide (LPS) and produce a variety of mediators. Among them, TNFα is known to injure the liver. Here we report that TNFα mediates apoptosis in KC and sinusoidal endothelial cells. After stimulation for 24 h with LPS (0-10 μg/mL), apoptosis in KC detected by TUNEL TdT-mediated dUTP-biotin nick end labelling (TUNEL) increased in a concentration-dependent manner (0 μg/mL, 12 ± 4%; 0.1 μg/mL, 36 ± 11%; 1.0 μg/mL, 65 ± 9%; 10 μg/mL, 78 ± 15%). In contrast, co-incubation of endothelial cells with LPS-stimulated KC resulted in a marked increase in TUNEL-positive endothelial cells. TNFα antibody blocked apoptosis in both KC and endothelial cells. Apoptosis was observed in cells adjacent to or in contact with KC. Reducing transmembrane TNFα expressed on KC also led to a decrease in endothelial cell apoptosis, suggesting that transmembrane TNFα is implicated in the cell-to-cell contact mechanism of induction of apoptosis. Thus, TNFα mediates apoptosis in KC and endothelial cells.
    Journal of Gastroenterology and Hepatology 06/2008; 10(S1):S65 - S67. DOI:10.1111/j.1440-1746.1995.tb01802.x · 3.63 Impact Factor
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    ABSTRACT: Biopsy samples from patients with liver cirrhosis were investigated for changes in gastric mucosal energy metabolism and intracellular mucin content using high performance liquid chromatography and an image analysing system. The test group consisted of eight non-cirrhotic patients with endoscopically normal mucosa (controls) and eight cirrhotic patients with oesophageal varices. The amount of ATP, energy charge level and intracellular mucin content were all significantly decreased in cirrhotic patients when compared with those of the controls. The decrease in energy charge also correlated well with the decrease in intracellular mucin content in the gastric mucosa. The results indicate that gastric mucosal energy metabolism is impaired in cirrhotic patients concomitantly with a decrease in the intracellular mucin content in the gastric mucosa. These changes may weaken defensive mechanisms against acid and NSAID, resulting in gastric mucosal injury in cirrhotic patients.
    Journal of Gastroenterology and Hepatology 06/2008; 11(4):380 - 384. DOI:10.1111/j.1440-1746.1996.tb01387.x · 3.63 Impact Factor
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    ABSTRACT: Although interleukin (IL)-8 is well known as a chemotactic agent for neutrophil migration in vitro, the relationship between IL-8 activity and the degree of neutrophil infiltration in gastric mucosa is still unclear. In the present study, we investigated IL-8 and myeloperoxidase activity, a marker of neutrophil infiltration, in gastric antral mucosa using biopsy samples in 23 patients with no gastric lesions. The results indicate that there is a good correlation between IL-8 and myeloperoxidase activity (y = 0.173x + 13.9; r = 0.49, P<0.01). Furthermore, IL-8 and myeloperoxidase activity are significantly higher in Helicobacter pylori-positive patients than in H. pylori-negative patients. In conclusion, an increase of IL-8 activity in the gastric mucosa causes increased neutrophil infiltration in human gastric mucosa and H. pylori infection acclerates these reactions in the mucosa.
    Journal of Gastroenterology and Hepatology 06/2008; 12(2):104 - 108. DOI:10.1111/j.1440-1746.1997.tb00392.x · 3.63 Impact Factor
  • NOBUHIRO SATO · SUNAO KAWANO · MASUKI FUKUDA · TAKENOBU KAMADA
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    ABSTRACT: A double-blind placebo-controlled parallel design study was conducted in 12 healthy male volunteers to examine the effects of misoprostol, a newly synthesized prostaglandin E1 analogue, on gastric mucosal haemodynamics in human. The indices of mucosal blood volume (expressed as ΔEr) and mucosal blood haemoglobin oxygenation (Hb-SO2) were measured at 20 locations in the stomach prior to and after administration of misoprostol or its placebo using reflectance spectrophotometry during endoscopy. It was found that after misoprostol administration, mucosal blood volume was increased by approximately 10–25% throughout the stomach without any significant change in mucosal blood Hb-SO2. Administration of placebo produced no significant change in these parameters. The results suggest that misoprostol has the potential to accelerate healing of gastric ulcers by increasing the gastric mucosal blood volume and oxygenation in addition to its gastric acid antisecretory activity.
    Journal of Gastroenterology and Hepatology 03/2008; 2(6):499 - 505. DOI:10.1111/j.1440-1746.1987.tb00197.x · 3.63 Impact Factor
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    ABSTRACT: Abstract Changes in gastric mucosal haemoglobin concentration (mucosal blood volume), mucosal haemoglobin oxygenation, mucosal blood flow and gastric arterial blood flow caused by indomethacin, an ulcerogenic agent, and anti-ulcer agents were investigated in the stomach flap of anesthetized dogs. Indices of mucosal haemoglobin concentration and haemoglobin oxygenation, mucosal blood flow and arterial blood flow to the stomach flap were measured simultaneously. The intravenous injection of indomethacin (10 mg/kg) caused an immediate decrease in mucosal haemoglobin concentration with a gradual decrease in mucosal and arterial blood flow, and a slight decrease in mucosal haemoglobin oxygenation. The topical application of prostaglandin E2 (10 μg/ml) and spizofurone (a new anti-ulcer agent, 1 mg/ml) to the mucosa significantly increased these parameters, and remedied the decreases of these parameters caused by indomethacin. Cimetidine (20 mg/ml), pirenzepine (10 mg/ml) and proglumide (40 mg/ml) given topically did not significantly increase these parameters in the resting state or the indomethacin-induced ischaemic state. This study indicates that: indomethacin decreases gastric haemodynamics, and that improvement occurred with application of mucosal protective agents (i.e. prostaglandin E2 and spizofurone) and changes in mucosal blood concentration were closely correlated with those in mucosal blood flow and arterial blood flow, but correlated less well with those in the case of haemoglobin oxygenation.
    Journal of Gastroenterology and Hepatology 03/2008; 1(2):87 - 96. DOI:10.1111/j.1440-1746.1986.tb00103.x · 3.63 Impact Factor
  • Nippon rinsho. Japanese journal of clinical medicine 12/2005; 63 Suppl 11:512-5.
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    ABSTRACT: Little is known about the clinical efficacy of co-therapy of enprostil, a prostaglandin E2 analogue, with a histamine H2-receptor antagonist. We aimed to assess the additive benefit of enprostil in combination with cimetidine for treating gastric ulcer in a prospective multicenter randomized controlled trial. In 43 hospitals 171 intention-to-treat (ITT) patients, diagnosed as having gastric ulcer by endoscopy, were randomly allocated to receive either enprostil 25microg b.i.d. and cimetidine 400mg b.i.d. (Group E=85), or cimetidine 400mg b.i.d. alone (Group C=86) for 8 weeks. Healing was examined by endoscopy at 4 and 8 weeks. Per protocol (PP) analysis comprised 166 patients (E=82, C=84). Despite no significant advantage at 4 weeks (E=55.3%, C=42.2%), the combination yielded higher healing rates at 8 weeks by ITT (E=89.4%, C=68.6%; p<0.001) and PP analysis (E=92.7%, C=70.2%; p<0.001). Symptom relief rates [E, C] at 2, 4, and 8 weeks were [80.2%, 68.3%] (not significant), [97.4%, 88.3%] (p<0.05), and [95.6%, 87.0%] (p<0.05), respectively. Significant advantage was observed in the patients aged 40 or older, with solitary ulcer (>5mm in diameter), and without smoking or drinking habits. No adverse effects were critical. Enprostil safely and significantly augmented gastric ulcer healing and symptom relief by cimetidine.
    Hepato-gastroenterology 01/2005; 52(66):1925-9. · 0.91 Impact Factor
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    ABSTRACT: Little is known about the clinical efficacy of co-therapy of ecabet sodium, a mucoprotective agent, and a histamine H2-receptor antagonist. The aim of the present study was to assess its additive benefit in combination with cimetidine for gastric ulcer. In this prospective randomized study, after gastric ulcer was confirmed by endoscopy, 200 patients in 47 hospitals received either ecabet sodium 1 g b.i.d and cimetidine 400 mg b.i.d. (EC), or cimetidine 400 mg b.i.d. alone (C) for 8 weeks. Healing was examined by endoscopy at 4 and 8 weeks. Of the intention-to-treat (ITT) population (EC, 103; C, 97), 181 patients comprised the per protocol (PP) analysis (EC, 93; C, 88). At 4 weeks, healing rates were significantly higher in the EC group (60%) than in the C group (36%) ( p < 0.01). At 8 weeks, those by the ITT and PP analyses were 82% (EC) versus 58% (C), and 90% (EC) versus 64% (C), respectively ( p < 0.01 and p < 0.001). Symptom relief rates (EC vs C) at 2, 4 and 8 weeks were 73%versus 47% ( p < 0.01), 89%versus 66% ( p < 0.001), and 97%versus 73% ( p < 0.001), respectively. Significant additive effects of ecabet sodium were observed in patients aged 60 years or older, with solitary and medium to large ulcer, and without smoking or drinking habits. No adverse effects were critical. Ecabet sodium significantly augmented gastric ulcer healing and symptom relief by cimetidine, especially in the elderly.
    Journal of Gastroenterology and Hepatology 09/2003; 18(9):1029-33. DOI:10.1046/j.1440-1746.2003.03093.x · 3.63 Impact Factor
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    ABSTRACT: Predicting the effect of beta-blockade therapy on the clinical outcome of patients with dilated cardiomyopathy (DCM) is difficult prior to the initiation of therapy. Myocardial fatty acid metabolism has been shown to be impaired in patients with DCM. We examined whether the extent of myocardial injury, as assessed by iodine-123 15-( p-iodophenyl)-3- R, S-methylpentadecanoic acid (BMIPP) myocardial scintigraphy, is related to the response of patients with DCM to beta-blockade therapy. Thirty-seven patients with DCM were examined using BMIPP myocardial scintigraphy before and after 6 months of treatment with metoprolol. Myocardial BMIPP uptake (%BM uptake) was estimated quantitatively as a percentage of the total injected count ratio. The left ventricular end-diastolic and end-systolic dimensions (LVDd, LVDs) and ejection fraction (LVEF) were also evaluated. The patients were divided into two groups according to their functional improvement (>10% elevation of LVEF) after 6 months of metoprolol therapy. Twenty-eight patients responded to the therapy, while nine did not. Prior to the therapy, no significant differences in LVDd, LVDs or LVEF were observed between the responders and non-responders. However, the %BM uptake was significantly lower in the non-responders than in the responders (1.0%+/-0.2% vs 2.1%+/-0.5%, P<0.001). The %BM uptake could be used to distinguish the responders from the non-responders with a sensitivity of 0.93 and a specificity of 1.00 at a threshold value of 1.4. After the metoprolol therapy, the %BM uptake improved significantly in the responders (2.5%+/-0.5%, P<0.01) but did not change in the non-responders. These results indicate that myocardial BMIPP uptake could predict the response of DCM patients to beta-blockade therapy.
    European Journal of Nuclear Medicine 12/2001; 28(12):1811-6. DOI:10.1007/s00259-001-0668-2 · 5.38 Impact Factor
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    ABSTRACT: The aim of this study was to clarify the immunological and virological responses to pre-administration of interferon-gamma prior to initiation of interferon-alpha treatment in patients with refractory chronic hepatitis C. Twenty-two nonresponders to 6-months of IFN-alpha treatment were enrolled. The hepatitis C virus (HCV) genotype was Ib in all. Natural IFN-gamma (1 MIU/day) was administered daily for 14 days followed by natural IFN-alpha (5 MIU/day) daily for 14 days and then three times weekly for 22 weeks. Serum immunological parameters (IL-10, neopterin, BMG, sCD8, sCD4, IL-6, IL-12) were measured as were the levels of several cytokines (IFN-gamma, TNF-alpha, IL-2, IL-4, IL-5, IL-6, IL-10). Three patients dropped out; two because of the occurrence of other diseases and one because of an adverse effect. At the end of the period of IFN-alpha treatment, HCV-RNA had become negative in six of 19 patients (end-of treatment response; ETR). Six months after the completion of IFN administration, a virological sustained response (SR) was seen in two of 19 patients. The mean serum levels of IL-10 were significantly decreased 6 weeks after the start of treatment. Other immunological parameter levels increased significantly during the period of IFN-gamma administration, and tended to return to the pretreatment level after the start of IFN-alpha administration. Univariate logistic regression analysis showed that the initial change in the levels of these parameters or the change in the ratios of Th1/Th2 parameter levels are useful factors indicative of the end of the treatment response. These findings suggest that priming with IFN-gamma prior to the initiation of IFN-alpha treatment in patients with refractory chronic hepatitis C can modulate the host immune response and this might contribute to viral clearance.
    Journal of Viral Hepatitis 06/2001; 8(3):180-5. DOI:10.1046/j.1365-2893.2001.00274.x · 3.31 Impact Factor
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    ABSTRACT: Angiotensin-converting enzyme (ACE) inhibitors are effective in the secondary prevention of ischemic heart disease, but they do not reduce the rate of restenosis. Vascular ACE activity in the culprit coronary lesions of these patients, however, has never been quantified. We measured the ACE activity of vascular tissue obtained by directional coronary atherectomy in patients with acute coronary syndrome (n=17) and in patients with stable ischemic heart disease (n=36), with and without restenosis. The ACE activity of the culprit coronary lesions was significantly increased in patients with acute coronary syndrome (0.87+/-0.12 nmol. min(-1). mg protein(-1); P:<0.01) but not in patients with ischemic heart disease with restenosis (n=11, 0.19+/-0.05 nmol. min(-1). mg protein(-1)) when compared with those patients with ischemic heart disease without restenosis (n=25, 0.20+/-0.05 nmol. min(-1). mg protein(-1)). There was no difference between the ACE activity of the coronary tissue of the in-stent (n=5) and stent-unrelated (n=6) restenosis patients (0.24+/-0.10 versus 0.15+/-0.04 nmol. min(-1). mg protein(-1)). Serum ACE activity did not differ significantly among the patients. The present study demonstrates increased ACE activity in culprit lesions in acute coronary syndrome, indicating that enhanced ACE activity is related to the causative mechanism of active coronary lesions.
    Circulation 02/2001; 103(5):630-3. DOI:10.1161/01.CIR.103.5.630 · 14.95 Impact Factor
  • Kanzo 01/2001; 42(10):528-535. DOI:10.2957/kanzo.42.528
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    ABSTRACT: The effect of interferon on the long-term clinical outcome of patients with chronic hepatitis C remains unclear. This study included 594 patients with chronic hepatitis C who received interferon-alpha therapy (Interferon group) and 144 patients with chronic hepatitis C who did not receive interferon (Control group). The patients in the Interferon group were classified into the following three groups based on the response of the serum aminotransaminase level of the patient during and after completion of the therapy protocol: sustained responders (n = 175), transient responders (n = 165), and non-responders (n = 254). The age, sex, serum aminotransaminase level, platelet count, histological staging, hepatitis C virus (HCV) subtype, and HCV concentration at baseline were adjusted with the Cox proportional hazards model. The length of follow-up for assessment of the risk for developing hepatocellular carcinoma (HCC) was 57.2 +/- 13.9 months in the Interferon group and 67.7 +/- 28.7 months in the Control group. Multivariate analysis showed that interferon therapy decreased the risk for developing HCC by 48% compared with that in the Control group (P = 0.064). The older the age, being male, having a low platelet count, and higher histological stage were independent factors associated with the development of HCC. The hazard rate ratio for development of HCC in the sustained responders, transient responders, and non-responders was 0.16 (95% confidence interval [CI]: 0.04-0.62), 0.27 (95% CI: 0. 09-0.79), and 0.74 (95% CI: 0.37-1.48), respectively. During follow-up, 18 patients in the Interferon group died (10 from liver-related diseases) and 17 patients in the Control group died (10 from liver-related diseases). No sustained responder or transient responder in the Interferon group died of liver-related disease. The cumulative survival rates of the Interferon and Control groups were nearly identical during the first 5 years following diagnosis. Thereafter, the cumulative survival rate of the Control group declined, resulting in an 8-year survival rate in the Interferon and Control groups of 97% and 81%, respectively (P = 0. 061). Similar trends were seen in the survival analysis of those who had died of liver disease: the 8-year survival rates of the Interferon and Control groups were 98% and 88%, respectively (P = 0. 32). Our study demonstrated that interferon therapy significantly lowered the incidence of HCC among patients with chronic hepatitis C who showed sustained normalization and among patients who showed transient normalization of the serum aminotransferase level after completion of interferon therapy. The survival analyses and determination of cause of death suggested that interferon therapy improves the long-term survival of chronic hepatitis C patients who respond to this therapy, possibly by decreasing mortality from liver-related diseases.
    International Journal of Cancer 10/2000; 87(5):741-9. · 5.01 Impact Factor
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    ABSTRACT: The effect of interferon on the long-term clinical outcome of patients with chronic hepatitis C remains unclear. This study included 594 patients with chronic hepatitis C who received interferon-α therapy (Interferon group) and 144 patients with chronic hepatitis C who did not receive interferon (Control group). The patients in the Interferon group were classified into the following three groups based on the response of the serum aminotransaminase level of the patient during and after completion of the therapy protocol: sustained responders (n = 175), transient responders (n = 165), and non-responders (n = 254). The age, sex, serum aminotransaminase level, platelet count, histological staging, hepatitis C virus (HCV) subtype, and HCV concentration at baseline were adjusted with the Cox proportional hazards model. The length of follow-up for assessment of the risk for developing hepatocellular carcinoma (HCC) was 57.2 ± 13.9 months in the Interferon group and 67.7 ± 28.7 months in the Control group. Multivariate analysis showed that interferon therapy decreased the risk for developing HCC by 48% compared with that in the Control group (P = 0.064). The older the age, being male, having a low platelet count, and higher histological stage were independent factors associated with the development of HCC. The hazard rate ratio for development of HCC in the sustained responders, transient responders, and non-responders was 0.16 (95% confidence interval [CI]: 0.04–0.62), 0.27 (95% CI: 0.09–0.79), and 0.74 (95% CI: 0.37–1.48), respectively. During follow-up, 18 patients in the Interferon group died (10 from liver-related diseases) and 17 patients in the Control group died (10 from liver-related diseases). No sustained responder or transient responder in the Interferon group died of liver-related disease. The cumulative survival rates of the Interferon and Control groups were nearly identical during the first 5 years following diagnosis. Thereafter, the cumulative survival rate of the Control group declined, resulting in an 8-year survival rate in the Interferon and Control groups of 97% and 81%, respectively (P = 0.061). Similar trends were seen in the survival analysis of those who had died of liver disease: the 8-year survival rates of the Interferon and Control groups were 98% and 88%, respectively (P = 0.32). Our study demonstrated that interferon therapy significantly lowered the incidence of HCC among patients with chronic hepatitis C who showed sustained normalization and among patients who showed transient normalization of the serum aminotransferase level after completion of interferon therapy. The survival analyses and determination of cause of death suggested that interferon therapy improves the long-term survival of chronic hepatitis C patients who respond to this therapy, possibly by decreasing mortality from liver-related diseases. Int. J. Cancer 87:741–749, 2000. © 2000 Wiley-Liss, Inc.
    International Journal of Cancer 09/2000; 87(5):741 - 749. DOI:10.1002/1097-0215(20000901)87:5<741::AID-IJC18>3.0.CO;2-B · 5.01 Impact Factor
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    ABSTRACT: Although transient atrial dysfunction has been reported after electrical cardioversion of atrial fibrillation (AF), the difference in the time to recover from the atrial hormonal, mechanical, and electrical dysfunction has not been described. Thus, we evaluated the time course of recovery from atrial hormonal, mechanical, and electrical dysfunction after cardioversion in patients with nonvalvular AF. We attempted electrical cardioversion in 87 consecutive patients with nonvalvular AF that had persisted for > or =6 months, and in 24 patients (28%) with maintained sinus rhythm for > or =6 months. To evaluate atrial hormonal, mechanical, and electrical dysfunction in these 24 patients, we measured plasma concentration of atrial natriuretic peptide, the atrial peak velocity in transmitral flow, and the ratio of peak systolic-to-diastolic pulmonary venous flow (S/D ratio) using echocardiography, and the duration and the root mean voltage for the terminal 20 ms (LP20) of the filtered P wave using P-wave signal-averaged electrocardiography. Atrial natriuretic peptide rapidly returned to baseline within 1 day after cardioversion, and maintained these levels for 6 months. Atrial peak velocity in transmitral flow and S/D ratio were significantly increased at 2 weeks, and continued to increase until 1 month, and then reached a plateau. The duration and LP20 began to recover only 6 months after cardioversion. One to 3 years after conversion, the duration and LP20 had nearly reached a plateau, but the latter value remained below normal. In patients with nonvalvular AF of prolonged duration, recovery from atrial electrical dysfunction after sinus conversion took much longer than that from either atrial hormonal or mechanical dysfunction.
    The American Journal of Cardiology 06/2000; 85(12):1451-4. DOI:10.1016/S0002-9149(00)00793-1 · 3.43 Impact Factor
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    ABSTRACT: Background: The selection of hepatitis C virus (HCV)-related cirrhotic patients for interferon treatment is necessary to improve the efficacy of this treatment. Currently, it is impossible to predict which cirrhotic patients will ultimately respond to this treatment with viral clearance. Moreover, the dose and duration of this therapy for cirrhotic patients remain controversial. Aims: The aims of this study were to determine a useful regimen of interferon treatment for such patients, to identify the predictors of the response to interferon and to assess the clinical outcome after interferon therapy. Methods: Forty-seven patients were treated with 6 million units of natural interferon alpha for either 26 weeks (19 cases) or 52 weeks (28 cases). Results: Sustained virological response with HCV eradication was not observed in patients treated for 26 weeks but it was found in five cases (18%) treated for 52 weeks (P=0.14), suggesting that prolonged interferon treatment would be more useful for cirrhotic patients. However, no clearance of HCV RNA was found for patients with a high viral load (serum HCV RNA level≥107 copies/ml serum), even when the 52-week course of interferon treatment was carried out. HCV eradication was achieved in patients with HCV RNA level of less than 106 copies/ml, when prolonged interferon therapy was performed. In multivariate regression analysis, the pretreatment level of HCV RNA correlated independently with HCV eradication (P=0.01). The 4-year appearance rates of hepatocellular carcinoma in the 26- and 52-week courses of interferon therapy were predicted to be 45.4 and 26.0%, respectively. Thus, the cumulative probability without hepatocellular carcinoma appeared to be higher for the 52-week group than the 26-week group, partly because the frequency of HCV eradication was higher in the 52-week group. Conclusions: The use of a 12-month course of interferon treatment for HCV-related cirrhotic patients may be beneficial for eradicating HCV, with the benefits being greater for patients with a low viral load. Such cirrhotic patients should be treated with a 12-month course of interferon in expectation of HCV eradication. However, its usefulness needs to be studied further in a large number of patients.
    Hepatology Research 01/2000; 16(2):124-138. DOI:10.1016/S1386-6346(99)00045-5 · 2.22 Impact Factor
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    ABSTRACT: The aim of the present study was to evaluate a new endoscope disinfector (WM-1) that uses acidic electrolytic water (AEW). AEW was produced by electrolysis of a 0.05% NaCl-water mixture, with a redox potential greater than 1000 mV and a pH lower than 2.7. In the first study, an endoscope artificially contaminated with 15 species of bacteria and four strains of viruses was treated using the WM-1. In the second study, endoscopic contamination after clinical use was examined by culture for Helicobacter pylori and other bacteria, and by polymerase chain reaction for the H. pylori urease gene and hepatitis C virus. The extent of contamination was then examined after exposing the WM-1 to AEW. The safety of AEW was examined using both in vivo and in vitro studies. All of the bacteria and viruses were destroyed or inactivated after the instrument had been exposed to AEW. Clinical contamination was detected from the instrument in 19 of 30 endoscopic procedures, whereas no bacteria or viruses were detected after five minutes' exposure to AEW. AEW was found to be nonirritant, nontoxic to cells, and nonmutagenic. The WM-1 successfully and safely disinfected the endoscopes. With running costs of yen 24 per day ($0.21 per day), the WM-1 provides an effective and inexpensive alternative to conventional disinfection equipment.
    Endoscopy 10/1999; 31(7):528-35. DOI:10.1055/s-1999-55 · 5.20 Impact Factor

Publication Stats

19k Citations
4,083.37 Total Impact Points

Institutions

  • 1977–2008
    • Fukushima Medical University
      • Division of Medicine
      Hukusima, Fukushima, Japan
  • 1968–2008
    • Osaka City University
      • • Graduate School of Medicine
      • • First Department of Internal Medicine
      • • Division of Nuclear Medicine
      Ōsaka, Ōsaka, Japan
  • 1993–2003
    • Osaka Rosai Hospital
      Ōsaka, Ōsaka, Japan
    • Xi'an Medical University
      Ch’ang-an, Shaanxi, China
  • 1986–2001
    • Osaka University
      • • Graduate School of Medicine
      • • Department of Internal Medicine
      • • School of Medicine
      • • Division of Physiopathology
      Suika, Ōsaka, Japan
    • University of London
      Londinium, England, United Kingdom
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 2000
    • Osaka Medical Center for Cancer and Cardiovascular Diseases
      Ōsaka, Ōsaka, Japan
  • 1992–1997
    • Juntendo University
      • • Division of Metabolism and Endocrinology
      • • Division of Gastroenterology
      Edo, Tōkyō, Japan
  • 1996
    • Emory University
      • School of Medicine
      Atlanta, Georgia, United States
  • 1995
    • Kobe Gakuin University
      Kōbe, Hyōgo, Japan
  • 1987–1995
    • Osaka National Hospital
      Ōsaka, Ōsaka, Japan
  • 1994
    • Universität des Saarlandes
      Saarbrücken, Saarland, Germany
    • Osaka Red Cross Hospital
      Ōsaka, Ōsaka, Japan
    • Osaka Kosei Nenkin Hospital
      Ōsaka, Ōsaka, Japan
    • University of Toronto
      • Faculty of Medicine
      Toronto, Ontario, Canada
    • Hokkaido University
      • Department of Cardiovascular Medicine
      Sapporo, Hokkaidō, Japan
  • 1981–1993
    • Kagoshima University
      • • Department of Laboratory Medicine
      • • School of Medicine
      Kagosima, Kagoshima, Japan
  • 1989–1992
    • Osaka Police Hospital
      Ōsaka, Ōsaka, Japan
  • 1991
    • Johns Hopkins University
      • Department of Medicine
      Baltimore, Maryland, United States
  • 1988–1991
    • Sakurabashi Watanabe Hospital
      Ōsaka, Ōsaka, Japan
    • Kanazawa Medical University
      Kanazawa, Ishikawa, Japan