Investigation of Components in Roasted Green Tea That Inhibit Streptococcus mutans Biofilm Formation.

Streptococcus mutans form oral biofilms (BFs) and cause dental caries. Roasted green tea (RGT) is prepared by roasting the tea plant, and RGT-specific polyphenols are produced during the roasting process. Catechins, polyphenols in green tea, have BF inhibitory activity against S. mutans; therefore, RGT-specific polyphenols are also expected to have this activity. However, there are few reports on the structural and functional properties of RGT. This study aimed to investigate the inhibitory activity of RGT against S. mutans BF formation and to investigate the active compounds. RGT extract fractionation and BF inhibitory assay were performed. Strong activity was confirmed in the RGT fractions that had medium-high hydrophobicity, were rich in phenolic hydroxyl groups, and lacked catechins. A peak comprising compounds with molecular weights of 918 (mw918) and 1050 (mw1050) was purified from the fraction. Since BF inhibitory activity was confirmed for this peak, these compounds were considered to be part of the active ingredients. The mw918 polyphenol was detected only in RGT and it was thought to be produced during the roasting process. The results of this research will serve as a basis for the future application of RGT as a safe and effective anti-caries agent.

Decreased risk of hepatocellular carcinoma in patients with chronic hepatitis C whose serum alanine aminotransferase levels became less than twice the upper limit of normal following interferon therapy.

AIM: The incidence of hepatocellular carcinoma (HCC) in C-viral chronic hepatitis (CH) and liver cirrhosis (LC) patients after interferon (IFN) therapy was evaluated according to alanine aminotransferase (ALT) levels. PATIENTS: Two hundred sixty-nine patients with C-viral CH and LC were treated with natural IFN-alpha. The efficacy of IFN therapy was evaluated based on virologic response and ALT levels using the following groups: virologic-sustained responders (VSR); biochemical-sustained responders (BSR); partial responders (PR), which consisted of BSR patients whose serum ALT levels later relapsed; non-responders (NR)1, which included patients with serum ALT levels that were usually less than 80 IU/l; and NR2, NR with ALT levels persistently more than 80 IU/l. RESULTS: Of the 269 patients, 22 (8.2%) developed HCC after IFN therapy. The incidence of HCC (%/patient/year) was 0.78%, 0%, 0%, 0.17%, 4.68% in VSR, BR, PR, NR1, NR2, respectively. Multivariate analysis revealed that an increase in ALT levels to more than 80 IU/l is an important risk factor for the occurrence of HCC. CONCLUSIONS: We concluded that the patients with ALT levels less than twice the upper limit of normal after IFN therapy have a reduced risk of progression to HCC from C-viral chronic liver disease.

Patients with severe liver cirrhosis followed up by L-[1-(13)C] phenylalanine breath test.

Compared to healthy subjects, patients with severe liver cirrhosis (LC) are reported to show lower values in the L-[1-(13)C] phenylalanine breath test (PBT). We performed this test several times during the clinical course in two patients with severe liver cirrhosis (LC). Patient 1 was a 67-year-old woman with non-B, non-C LC and hepatocellular carcinoma (HCC) in the lateral hepatic segment. Because the patient wanted to receive nonsurgical treatment for HCC, intraarterial administration of zinostatin stimalamer was performed. The patient was hospitalized four times before her death from liver failure on December 20, 2000. During her clinical course, PBT was performed four times. Values for both the rate of hepatic phenylalanine oxidation (%(13)C dose h(-1)) and %(13)C cumulative excretion gradually decreased during her clinical course. Patient 2 was a 57-year-old man with hepatitis C virus (HCV)-positive LC. He was hospitalized seven times between December 1998 and his death on May 24, 2001. During his clinical course, PBT was performed four times. Values for both %(13)C dose h(-1) and %(13)C cumulative excretion decreased during his clinical course. We confirmed that PBT was useful for following the course of LC.

Long-term outcome, with monitoring of platelet counts, in patients with chronic hepatitis C and liver cirrhosis after interferon therapy.

OBJECTIVE: Because the determination of the stage of fibrosis depends on rather subjective judgment, more objective parameters are needed. In this study, we followed the long-term outcome, with monitoring of platelet counts, in patients with chronic hepatitis C or liver cirrhosis (LC) who had undergone interferon (IFN) therapy. METHODS: 596 patients who were diagnosed at our institute from 1987 to 1998 with chronic hepatitis C and LC were treated with IFNs. A further 58 patients were not treated (NT). The annual rate of changes in platelet counts were calculated and compared for IFN-treated and NT patients. RESULTS: The relationship between the efficacy of IFN therapy and the incidence of hepatocellular carcinoma (HCC) showed that the patients who were virologic sustained responders (VSR) had a significantly lower incidence of HCC than the nonresponders (NR) and NT patients. The change in platelet counts was +4,350/microl/year in the VSR, +1,010/microl/year in the biochemical sustained responders (BSR), -4,540/microl/year in the NR and -6,180/microl/year in the NT patients, indicating a significant platelet increase in the VSR, a decrease of the same magnitude in the NR and NT patients, and no change in the BSR. The cumulative probability of developing HCC and liver failure was significantly higher in groups with decreased platelet counts than in groups with increased platelet counts among patients who had undergone IFN therapy. Multivariate analyses revealed that a decrease in platelet counts was the cardinal risk factor for development of HCC and liver failure in chronic hepatitis C or LC patients. CONCLUSION: Investigation of platelet counts was useful for determining the long-term outcome of patients who had undergone IFN therapy and for predicting the development of HCC.

The clinical significance of GBV-C/HGV exposure in C-viral chronic liver disease and blood donors.

Aims: The relationship between the hepatitis G virus (HGV) RNA-positive state or the HGV anti-E2 antibody-positive state, and various clinical parameters among patients with C-viral chronic liver disease and blood donors, was examined. Patients and methods: The subjects consisted of 166 patients with hepatitis C virus (HCV) RNA-positive liver disease, and 157 blood donors. Serum samples were tested for the presence of HGV RNA by the polymerase chain reaction method. The HGV E2 antibody level was measured with an enzyme-linked immunosorbent assay kit. Results: HGV RNA was detected in 1.3% of the blood donors, and HGV E2 antibodies were detected in the sera of 2.5% of the blood donors. The detection rate of HGV RNA and HGV E2 antibodies among the patients with C-viral liver disease was 4.8 and 28.3%, respectively. The detection rates of HGV RNA and HGV E2 antibody among those in each F stage were 0 and 25.0% among those in the F1 stage, 2.6 and 34.2% among those in F2, 11.1 and 27.8% among those in F3, 12.5 and 29.2% among those in F4, and 11.1 and 27.8% among those with hepatocellular carcinoma (HCC). The detection rate of HGV RNA increased with the progression of the F stage and HCC, however, the detection rate of HGV E2 antibody among the four F stages and HCC did not significantly differ. In addition, the clinical parameters and background of those who did or did not have HGV E2 antibodies or HGV RNA, did not significantly differ. Conclusion: HGV exposure may promote the progression of liver fibrosis (F stage) in C-viral liver diseases.