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M Kako

Publications and source records attributed to M Kako.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Changes of serum GBV-C RNA levels under administration of interferon and cyclosporine for patients with GBV infected hepatitis].

We describe here interferon(IFN) and cyclosporine(CyA) therapy for GBV/HGV hepatitis. Up to the present, reported cases with IFN therapy in Japan were all most co-infected with chronic hepatitis C virus by retrospective studies. According to these results, IFN induced a transient decrease of serum GBV-C RNA levels during the administration, but, after the administration, these returned to levels at the pretreatment. We summarized in this review these therapeutic effects of previous reports in Japan. And, we reported our experienced case of GBV-C RNA-positive fulminant hepatitis treated with IFN and CyA. These observations induced that IFN was effective for decreasing serum levels of GBV-C RNA, and CyA was effective for increasing these levels. However, effects of IFN were transient. Therefore, we are planning re-treatment of IFN for this patient in near feature. Further study about the epidemical analysis of GBV-C/HGV hepatitis and therapeutic analysis of IFN for this disease are needed.

Adult↗
PubMed1997

[Establishment of the optimal conditions for detecting anti-M2 by western blotting in primary biliary cirrhosis].

Anti-mitochondrial antibodies(AMA) are serodiagnostic markers for primary biliary cirrhosis(PBC) but heterogenous in antigen molecules which they recognize. A disease-specific AMA for PBC is anti-M2. The conventional examination methods are indirect immunofluorescence and ELISA. However, there are some problems in specificity, because the antigen preparations used are crude. Thus, analysis with Western-blotting(W-B) is needed, because it allows the identification of a molecule which the antibody reacts with. In this report, we established the optimal conditions for detecting anti-M2 with W-B in PBC. As antigen, we used mitochondrial fractions derived from beef hearts. Because a positive band at 74 kDa became negative after absorbing sera with PDH purified from porcine hearts, this band corresponded to major antigeneity of anti-M2. Titration experiments with SDS-PAGE showed that the optimal concentration of this antigen preparation for loading is 0.04 mg/ml. We also performed titration experiments to determine the optimal dilutions for second antibodies and serum samples. The results showed that the optimal dilution for second antibodies, anti-IgG and anti-IgM, were 1:3000 and 1:1000, respectively. The optimal dilution for serum samples was shown to be 1:10(2). Moreover, the W-B technique gave a positive result even for sera from AMA-negative PBC patients which had tested negative with conventional methods, if undiluted sera were examined or if anti-IgG or anti-IgM was used as a second antibody. Thus, the W-B technique is more sensitive than conventional methods of analysis. Based on these results, we will be able to detect anti-M2 with maximum efficiency, thus improving our ability to study the relationship between anti-M2 and the pathological conditions in PBC.

Autoantibodies↗
PubMed1997

[Western blot analysis of anti-M2 antibodies in anti-mitochondrial antibody-negative primary biliary cirrhosis].

One variety of anti-mitochondrial antibody(AMA) is characteristically found in sera from patients with primary biliary cirrhosis(PBC). The major target antigens of this type of AMA are M2s. It is well known, however, that AMA-negative PBC also exists. An alternative disease concept, called autoimmune cholangiopathy, recently has been advocated. This new concept is defined by the following criteria: 1)the failure to detect AMA and anti-M2, 2)the detection of a diffuse type of anti-nuclear antibody and anti-smooth muscle antibody, 3)pathological findings compatible with PBC, and 4)the effectiveness of prednisolone. However, the difference between AMA-negative PBC and autoimmune cholangiopathy is controversial. Therefore, we analyzed antibodies to four major M2 proteins with Western blotting in 34 cases of immunofluorescent AMA-negative PBC. In 31(91.2%) of these 34 AMA-negative sera, antibodies to at least one of these four major M2 proteins was detected. In serum samples from 34 control patients with AMA-positive PBC, antibodies to at least one of these four proteins were detected in all cases. In addition, we studied the frequency of cases which satisfied the serological criteria of autoimmune cholangiopathy. In only one(0.7%) of 141 cases was the serological criteria met. We conclude that to clarify the serological differences between autoimmune cholangiopathy and AMA-negative PBC, the analysis of M2 proteins by Western blotting is essential.

Adult↗
PubMed1997

[Efficacy and safety of sulbactam/cefoperazone for hepato-biliary infections].

We studied efficacy and safety of sulbactam/cefoperazone (SBT/CPT) in the treatment of biliary tract infections in hospitalized patients at 26 hospitals from February 1993 to March 1995. Secondary to dropout, 273 out of 338 patients entered in the study were evaluated, 127 patients with cholecystitis, 132 patients with cholangitis, and 14 patients with liver abscesses. Of these, 93 patients (34.1% had malignancy as an underlying disease. SBT/CPZ had an efficacy of 79.9% (218 patients; excellent: 52, good: 166), with the efficacy in patients with cholecystitis, cholangitis and liver abscess at 89.0% (113 patients), 77.3% (102 patients and 21.4% (3 patients), respectively. A significant difference (p < 0.05) was observed in the efficacy rates of patients with (59 patients [63.4%]) and without malignancy (159 patients [88.3%]). A total of 84 strains were isolated from bile specimens of 53 patients, and the major isolates were Escherichia coli, Pseudomonas aeruginosa and Enterococcus spp. Two or more bacterial strains were isolated simultaneously in 20 patients. Mild or moderate side effect (allergic reaction including rash etc.) were noted in 4 patients (1.18%), and laboratory abnormalities (increased GOT, etc.) were in 16 patients (4.71%) out of the total 338 patients. This study clearly demonstrated that SBT/CPZ retains its excellent clinical efficacy and safety profile, throughout its use over the past decade.

Adolescent↗
PubMed1996

Hypoglycemic effect of the rhizomes of Polygala senega in normal and diabetic mice and its main component, the triterpenoid glycoside senegin-II.

The hypoglycemic effect of the rhizomes of Polygala senega L. var. latifolia Torrey et Gray (Polygalaceae) was investigated in normal and KK-Ay mice, one of the model animals of non-insulin dependent diabetes mellitus (NIDDM). The n-butanol extract of senega rhizomes (SN) (5 mg/kg) reduced the blood glucose of normal mice from 191 +/- 3 to 120 +/- 3 mg/dl 4 hours after intraperitoneal administration (P < 0.001), and also showed a significant decrease in the glucose level of KK-Ay mice from 469 +/- 38 to 244 +/- 14 mg/dl under similar conditions (P < 0.001). But streptozotocin-induced diabetic mice did not experience a change in the blood glucose after administration of SN. We propose that the hypoglycemic effect of SN occurs without altering the insulin concentration. Moreover, SN needs the presence of insulin in order to act. In addition, one of the active components of the hypoglycemic effect was identified as a triterpenoid glycoside, senegin-II.

Animals↗
PubMed1996

Determination of hemoglobin A1C in normal and diabetic mice: neonatal streptozotocin-induced diabetic mice and KK-Ay mice.

We have determined Hemoglobin A1C (HbA1C) in normal, neonatal streptozotocin-induced diabetic animals (NSZ), a model of lean-type non-insulin-dependent diabetes mellitus (NIDDM) with hypoinsulinaemia, and KK-Ay mice, a model of obese-type NIDDM with hyperinsulinaemia. The HbA1C of NSZ mice was slightly increased from 5 to 20 weeks while the HbA1C of KK-Ay mice was markedly increased from 5 to 10 weeks. Our findings showed a difference between experimentally-induced (NSZ) and genetically (KK-Ay) diabetic animals.

Animals↗
PubMed1996

Effect of ginseng radix on GLUT2 protein content in mouse liver in normal and epinephrine-induced hyperglycemic mice.

The oral administration of the water extract of Ginseng Radix (GR) to normal and epinephrine-induced hyperglycemic mice caused a significant decrease in the blood glucose level 4 h after its administration. The hepatic content of facilitative glucose transporter isoform 2, liver type glucose transporter (GLUT2) protein content from mouse liver significantly increased in the orally GR-treated normal and epinephrine-induced hyperglycemic mice compared to that in the controls. These results suggest that the hypoglycemic activity of GR is presumably due, at least in part, to the increment of GLUT2 protein content.

Animals↗
PubMed1996

Intraperitoneal administration of Senegae Radix extract and its main component, senegin-II, affects lipid metabolism in normal and hyperlipidemic mice.

The hypolipidemic effect of Senegae Radix, i.e. "Senega," was investigated in normal and hyperlipidemic mice. The n-butanol fraction of the methanol extract of Senegae Radix (SN) (5 mg/kg) significantly reduced the blood triglyceride level of normal mice 7 h after intraperitoneal administration (p < 0.05) and also significantly reduced the blood triglyceride level of cholesterol-fed mice under similar conditions (p < 0.05). SN (5 mg/kg) also reduced the blood triglyceride and cholesterol levels after repeated administration to cholesterol-fed mice. SN also decreased the blood triglyceride level in Triton-induced hyperlipidemia. It is suggested that this fraction contains one or more hypolipidemic components including the main triterpenoid glycoside, senegin-II, which significantly reduces the levels of blood triglycerides in normal mice.

Animals↗
PubMed1996

[Measurement of portal and splenic venous flow volume (PV and SV), congestion index (CI) and SV/PV% in various liver diseases using by Doppler echo-sonography].

We measured the portal and splenic venous flow volume (PV and SV), congestion index (CI) and SV/PV% in various stages of the liver diseases chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis without esophageal varices (LCvarix(-)), and liver cirrhosis with esophageal varices (LCvarix(+))¿, and normal volunteers (NC). The results were as follows: PV was 869.4 +/- 184.0 ml/min in NC, 920.4 +/- 242.5ml/min in CIH, 900.0 +/- 216.9ml/min in CAH, 841.8 +/- 253.0 ml/min in LCvarix(-) and 909.7 +/- 430.7ml/min in LCvarix(+). SV was 241.0 +/- 80.0 ml/min in NC, 289.4 +/- 131.6 ml/min CIH, 286.4 +/- 108.8 ml/min CAH, 272.7 +/- 135.7 ml/min in LCvarix(-), 398.0 +/- 280.5 ml/min in LCvarix(+). SV/PV% was 28.1 +/- 10.1 in NC, 31.4 +/- 14.0 CIH, 32.1 +/- 9.6 in CAH, 32.4 +/- 16.0 in LCvarix(-), 43.1 +/- 23.7 in LCvarix(+). CI was 0.06 +/- 0.019 in NC, 0.07 +/- 0.028 in CIH, 0.09 +/- 0.05 in CAH, 0.11 +/- 0.03 in LCvarix(-), 0.145 +/- 0.047 in LCvarix(+). These results suggested that: (1) From the measurement of CI, portal venous pressure is begun to increase at the stage of chronic active hepatitis. (2) Increasing of splenic venous flow volume is begun at the stage of chronic hepatitis and it effects to the portal hypertension of liver cirrhosis. (3) The change of component of intrahepatic portal venous blood flow and decreasing of liver function tests was affected by increasing of splenic venous flow volume. (4) SV/PV% may be useful parameter to evaluate the decreasing of liver function tests and to estimate the complication of esophageal varices at the liver cirrhosis.

Blood Volume↗
PubMed1996

Core promoter mutations of hepatitis B virus for the response to interferon in e antigen-positive chronic hepatitis B.

OBJECTIVES: Mutations in the precore region are not always detected in hepatitis B virus (HBV) from patients with chronic hepatitis B who respond to interferon and lose hepatitis B e antigen (HBeAg) from serum. The other mutations may also be responsible for the loss of HBeAg and response. METHODS: Forty six consecutive patients with HBeAg-positive chronic hepatitis B received recombinant-alpha 2 a interferon (total dose: 702 MU). The mutation for stop codon 28 in the precore region was determined by restriction fragment length polymorphism, and mutations in the core promoter were searched for in five HBV DNA clones propagated from each patient. RESULTS: HBeAg was cleared at 6 months after interferon in 11 (61%) of 18 patients with the precore mutation and in 12 (43%) of 28 without it. Of these 28 patients, 19 with mutations in the core promoter in all five HBV DNA clones lost HBeAg more frequently than the remaining nine who had at least one clone among the five that lacked such mutations (58 vs 11%, p < 0.05). CONCLUSIONS: HBeAg-positive patients infected with HBV variants having mutations for an HBeAg-negative phenotype would respond better to interferon by clearing HBeAg from serum. Such mutations may not necessarily be in the precore region but also in the core promoter, which would interfere with the synthesis and secretion of HBeAg either at the translation or transcription level.

Adult↗
PubMed1995

HCV RNA monitoring for tailored regimens of interferon therapy in hepatitis C.

Sustained non-viraemia is prerequisite for a virological cure of hepatitis C virus (HCV) disease. We monitored serum HCV RNA in our patients during interferon therapy and for 6 months of follow-up. The rate of sustained responders (RNA-negative at the end of follow-up) differed significantly by whether or not RNA became sero-negative within 24 weeks of the initiation of therapy (71% vs 7%); and also by whether or not the RNA-seronegativity lasted for 12 weeks during therapy (88% vs 11%). Thus, by monitoring viraemia in individual patients, we can tailor the duration of therapy and minimize waste of interferon.

Follow-Up Studies↗
PubMed1995

Interferon-alpha 2a for chronic hepatitis B with e antigen or antibody:comparable antiviral effects on wild-type virus and precore mutant.

Recombinant interferon-alpha 2a (IFN-alpha 2a) in a total dose of 702 MU was given to 31 patients: nine with wild-type hepatitis B virus (HBV) and hepatitis B e antigen (HBeAg) (A); four with HBeAg and a mixed infection with wild-type HB and precore mutants (B); 11 with antibody to HBeAg (HBeAb) and a mixed infection (C); and seven with HBeAb and precore mutants alone (D). HBV DNA was not cleared in any patient in groups A and B. By contrast, in patients with HBeAb, HBV DNA was ultimately lost in four patients in group C, as well as in 10 patients in group D. Thus, patients with HBeAb and infected with precore mutants alone (D) lost serum HBV DNA more often than those with HBeAg and wild-type HBV (A). Patients with low pretreatment levels of HBV DNA cleared virus more frequently, and the response of precore mutant to IFN was comparable with that of wild-type HBV in patients who had a mixed infection. Based on these results, precore mutants do respond to IFN, and therefore, IFN is indicated in patients with HBeAb, especially those with low serum HBV DNA levels.

Adult↗
PubMed1995

Clearance of serum hepatitis C virus RNA after interferon therapy in relation to virus genotype.

The effect of recombinant interferon-alfa on serum HCV RNA levels in Japanese patients with chronic hepatitis C was investigated. At 24 weeks of treatment, 41 (32.5%) of 126 patients lost HCV RNA from serum, and aminotransferases were normalized in 31 (75.6%) of these 41 cases. HCV genotypes were categorized into four types (Type I, II, III, IV); the frequencies among the patients were: Type I: 0%, Type II: 70.6%, Type III: 20.6%, and Type IV: 6.3%. At the end of the 24-week treatment, HCV RNA levels were remarkably decreased in Type III patients and became undetectable in 18 (69.2%) of 26. In contrast, only 18 (20.2%) of 89 patients with Type II and two of eight with Type IV lost HCV RNA from sera. The relation between HCV genotype (Type III) and response to IFN therapy was also confirmed using a logistic regression model. HCV genotype seems to be an important factor in determining the response to IFN in patients with chronic hepatitis C.

Alanine Transaminase↗
PubMed1995

Effect of senegin-II on blood glucose in normal and NIDDM mice.

The hypoglycemic effect of senegin-II, the main component of Polygala senega (Polygalaceae), was examined in normal and KK-Ay mice, one of the model animals of non-insulin-dependent diabetes mellitus (NIDDM). Senegin-II (2.5 mg/kg) reduced the level of blood glucose in normal mice from 220 +/- 8 to 131 +/- 5 mg/dl 4 hours after intraperitoneal administration (P < 0.001), and also significantly lowered the blood glucose of KK-Ay mice from 434 +/- 9 to 142 +/- 6 mg/dl under similar conditions (P < 0.001).

Animals↗
PubMed1995

Hypoglycemic effect of the rhizomes of ophiopogonis tuber in normal and diabetic mice.

The hypoglycemic effect of the rhizomes of Ophiopogonis Tuber (Liliaceae) was investigated in normal and streptozotocin-induced diabetic mice. The n-butanol extract of rhizomes of Ophiopogonis Tuber (BM) (100 mg/kg) reduced the blood glucose of normal mice from 201 +/- 13 to 151 +/- 7 mg/100 ml 4h after intraperitoneal administration (p < 0.054), and also significantly lowered the blood glucose of streptozotocin-induced diabetic mice from 590 +/- 28 to 470 +/- 37 mg/100 ml under similar conditions (p < 0.05). BM also tended to suppress epinephrine-induced hyperglycemia in mice. We concluded that the hypoglycemic effect of BM does not alter the insulin concentration.

Animals↗
PubMed1995

Anti-liver/kidney microsome-1-positive chronic hepatitis C with type I cryoglobulinemia responding to interferon.

A 53-year-old man was admitted to our hospital for close examination of his liver. Serum hepatitis C virus (HCV) RNA and anti-liver/kidney microsome (LKM) 1 were positive. Benign monoclonal gammopathy and type I cryoglobulinemia (both of IgG lambda class) which are rarely seen in association with chronic hepatitis C, were found to be present. Interferon therapy was given, resulting in the disappearance of both HCV-RNA and type I cryoglobulin in the blood. We propose a hypothesis that the primary cause of anti-LKM-1-positive chronic hepatitis C is HCV infection which triggers secondary autoimmune phenomena presenting anti-LKM-1 and cryoglobulinemia.

Autoantibodies↗