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Biomedical subjects

T Monna

Publications and source records attributed to T Monna.

At least 37 records · Page 2Linked to original sources
PubMed1995

Prospective study of chemoprevention of hepatocellular carcinoma with Sho-saiko-to (TJ-9).

BACKGROUND: Most hepatocellular carcinomas (HCC) arise in patients with cirrhosis, in whom its incidence is high. The prevention of HCC in patients with cirrhosis is important. METHODS: A prospective, randomized, nonblind controlled study was performed to evaluate the preventive effect of Sho-saiko-to (TJ-9) on HCC development. TJ-9 is a Chinese herbal medicine that contains crude extracts of seven herbs; it has antitumor effects in experimental animals. Two hundred sixty patients with cirrhosis were randomly assigned to two groups, matched for age, sex, presence of hepatitis B surface antigen, and the severity of liver damage. The patients in the trial group were given TJ-9 at a daily oral dose of 7.5 g in addition to the conventional drugs given to the control patients. The patients were prospectively monitored for 60 months and the cumulative incidence of HCC and the survival rate in the two groups were calculated. RESULTS: The cumulative incidence curve for 5 years of the trial group was lower than that of the control group (P = 0.071). For the patients without HBs antigen, the difference was significant (P = 0.024). The survival curve for 5 years of the trial group was higher than that of the control group (P = 0.053). For the patients without HBs antigen, the difference was significant (P = 0.043). CONCLUSIONS: TJ-9 helped to prevent the development of HCC in patients with cirrhosis, particularly in patients without HBs antigen.

Adult↗
PubMed1995

Telomere shortening in chronic liver diseases.

We measured the telomere length in patients with chronic hepatitis or liver cirrhosis and found a significant telomere shortening in the liver with chronic liver disease compared to that in the normal liver. The telomere length tended to decrease with the progression of chronic liver disease.

Adult↗
PubMed1994

Effect of combined alanine and glutamine administration on the inhibition of liver regeneration caused by long-term administration of alcohol.

We studied the effect of administration of a mixture of alanine and glutamine on the inhibition of liver regeneration caused by alcohol in rats undergoing partial hepatectomy 6 weeks after the start of alcohol administration. DNA synthesis was inhibited 24 hr after partial hepatectomy in rats given alcohol, but treatment with alanine and glutamine partially prevented this inhibition. To identify the mechanism of this effect, polyamine metabolism was studied. Administration of alcohol or alanine plus glutamine had no effect on the activity of ornithine decarboxylase, a rate-limiting enzyme of polyamine metabolism. In the liver, of the three polyamines, only the spermine concentration changed significantly. It decreased during long-term administration of alcohol, and this decrease was prevented by treatment with alanine and glutamine. The level of N(1)-acetylspermidine, the acetylated product of spermidine, was increased by alcohol, and its elevation was significantly less when alanine and glutamine were given. Hepatic spermidine/spermine N(1)-acetyltransferase, the key enzyme of polyamine acetylation, was induced by long-term administration of alcohol, and this induction was suppressed by alanine plus glutamine. The results suggest that treatment with alanine and glutamine can help to prevent the inhibition of liver regeneration caused by alcohol by maintaining the spermine level and suppressing the acetylation of spermidine.

Alanine↗
PubMed1993

Long-term therapeutic efficacy of interferon for patients with chronic hepatitis C.

Interferon is being used for therapy of chronic hepatitis C, but its long-term results have not been reported. We studied 65 patients with this disease who were monitored for at least 2 years after completion of the therapy. Almost all patients who had responded to therapy at 6 months after the end of therapy had normal levels of alanine aminotransferase (ALT) when evaluated later. The level of ALT became normal for the first time in some patients more than 6 months after therapy ended. The level of ALT in many of the patients without HCV RNA had become normal 6 months after the end of the therapy. One of three schedules was employed: three times weekly long-term; daily for two weeks and none for two weeks in a cycle; and daily for several weeks; 57%, 29%, and 17% of the patients on these schedules came to have normal ALT levels. Patients without HCV RNA at six months after completion of therapy tended to have higher responses in terms an increased level of 2',5'-oligoadenylate synthetase of mononuclear cells in vitro before therapy began. However, therapy three times per week was effective even for some patients judged not responsive to IFN by this test. The results showed that IFN therapy was effective for chronic hepatitis C when judged by long-term results.

Adult↗
PubMed1993

Gender-related differences in the inhibitory effect on liver regeneration in alcohol-treated rats: study of polyamine metabolism.

We studied gender-related differences in the effect of a single dose of ethanol (EtOH) on liver regeneration following partial hepatectomy in male and female rats by determining polyamines and their related enzymes. When rats were orally treated with EtOH at 3 g/kg 1 hr before partial hepatectomy, liver ornithine decarboxylase (ODC) activity at 4 hr post-hepatectomy was found to be lower in EtOH-treated female than male rats (51% vs. 42%, P < 0.01). Although no EtOH effect was observed on spermidine acetyltransferase (SAT) activity, female rats showed significantly higher values than male rats. Among intra-hepatic polyamines, putrescine was strongly affected by EtOH and significantly reduced in both male and female rats, but the effect was more marked in female than in male rats (88% vs. 51%, P < 0.01). With respect to spermidine and spermine, male rats were unaffected by EtOH, whereas EtOH-treated female rats had lower levels. The gender-related differences became more distinct in terms of total polyamine; the decrease in total polyamine due to EtOH was observed in female rats only. These results suggested that there was a gender-related difference in the effect of EtOH on liver regeneration after partial hepatectomy, with the variations in polyamines probably affecting the subsequent process of liver regeneration.

Acetyltransferases↗
PubMed1993

Effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment.

We studied the effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment after partial hepatectomy (PH) in rats. When rats were dosed i.p. with ethanol at 2 g/kg at the time of PH, DNA synthesis 48 hr after PH was significantly inhibited, but it was completely reversed by the combined use of alanine and glutamine. Although hepatic ornithine decarboxylase (ODC) activity in the alcohol-treated group 4 hr after PH was significantly inhibited, there was a tendency towards recovery of the ODC inhibition in the alanine and glutamine-treated group. The putrescine (PUT) level in liver which was decreased by ethanol was also increased by the administration of alanine and glutamine. However, the levels of spermidine (SPD) and spermine (SPM) in liver were unaffected either by ethanol or by alanine and glutamine. These results suggest that alanine and glutamine show a protective effect on the inhibition of liver regeneration caused by acute ethanol treatment by improving polyamine metabolism, particularly by increasing hepatic PUT levels.

Alanine↗
PubMed1993

Vertical transmission of hepatitis C virus (HCV) detected by HCV-RNA analysis.

The rate of transmission of hepatitis C virus (HCV) from patients with chronic hepatitis C to their children was studied. Of the 64 children with a parent with chronic hepatitis C, two (3%) had abnormal alanine aminotransferase (ALT) activities, six (9%) had anti-HCV detected by c100 ELISA, seven (11%) had anti-HCV detected by ELISA-II, and 21 (33%) had HCV-RNA by polymerase chain reaction (PCR). Anti-HCV detected by ELISA-II disappeared within six months in all six infants. Of the five children whose mothers were given a blood transfusion after the child's first birthday, none had anti-HCV or HCV-RNA. In the five families whose elder or eldest offspring had HCV-RNA, all of the younger offspring had HCV-RNA. The vertical transmission rate of HCV was low if judged by the presence of anti-HCV or abnormal ALT values, but the rate was high (33%) if judged by the presence of HCV-RNA.

Adolescent↗
PubMed1992

Increased 5-lipoxygenase activity in massive hepatic cell necrosis in the rat correlates with neutrophil infiltration.

Rats were treated with heat-killed Propionibacterium acnes and subsequent injection of a small amount of lipopolysaccharide after 7 days. After 24 hr most of the rats died of massive liver cell necrosis. Nonparenchymal liver cells were isolated from this liver injury model and incubated with arachidonic acid. Reverse-phase high-pressure liquid chromatography detected the 5-lipoxygenase metabolites (leukotriene B4 and 5-hydroxy-arachidonic acid), whereas these compounds were produced in negligible amounts when the rats were treated with P. acnes only. Immunohistochemical studies with 5-lipoxygenase antiserum revealed that the injured livers contained a large number of positively stained round cells with segmented nuclei, which were rarely found in the livers treated with P. acnes only. These positively stained cells were histologically identified as neutrophils. The results suggested that the increased 5-lipoxygenase activity in the injured rat liver is attributable to the infiltrating neutrophils rather than to nonparenchymal hepatic cells.

Animals↗
PubMed1992

Possible induction of fatty acid cyclo-oxygenase in lipopolysaccharide-stimulated rat Kupffer cells.

In response to stimulation with lipopolysaccharide, isolated rat Kupffer cells released increased amounts of prostaglandin E2, prostaglandin D2, 6-keto-prostaglandin F1 alpha, and thromboxane B2. There was a lag of 2-6 hours before a significant release of these metabolites into the medium was detected. Nonstimulated Kupffer cells converted exogenous arachidonic acid to prostaglandins and thromboxane B2, and a major product was prostaglandin D2. Twenty-four hours after stimulation with lipopolysaccharide, Kupffer cells produced approximately 7 times more prostaglandin E2 and 2 times more prostaglandin D2, 6-keto-prostaglandin F1 alpha; and thromboxane B2 than nonstimulated cells. Western immunoblotting of microsomal proteins prepared from the stimulated rat Kupffer cells showed a 70-kilodalton component that was immunoreactive with a polyclonal anticyclo-oxygenase antibody. The intensity of the band increased with the time of the lipopolysaccharide stimulation. These results suggest that the accelerated arachidonate metabolism in lipopolysaccharide-stimulated rat Kupffer cells might be attributed to an induction of the cyclo-oxygenase enzyme.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Enhancement of prostaglandin E2 production by liver macrophages (Kupffer cells) after stimulation with biological response modifiers.

PGE2 production by liver macrophages (Kupffer cells) activated by biological response modifiers was examined. Kupffer cells obtained from a normal rat liver possessed cyclooxygenase activity and produced TXB2, PGD2, and PGE2 from (1-14C)arachidonic acid. The major product was PGD2. When Kupffer cells were incubated in the presence of lipo-polysaccharide (LPS), OK-432, or heat-killed Propionibacterium acnes for 24 h, the amount of arachidonate cyclooxygenase products increased and the major product changed from PGD2 to PGE2. When liver macrophages including Kupffer cells were prepared from rats after an injection of LPS, OK-432, or heat-killed P. acnes, it was noticed that the number of cells obtained and PGE2 production increased compared with those of normal rat. These results suggested that PGE2 production by rat liver was induced when they were treated with biological response modifiers.

Animals↗