bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of gut motility in type II diabetes by the radiopaque marker method
Authors: Iida Motoyuki , Ikeda Masahiko , Kishimoto Michihiko , Tsujino Takafumi , Kaneto Hideaki , Matsuhisa Munehide , Kajimoto Yoshitaka , Watarai Takao , Yamasaki Yoshimitsu , Hori Masatsugu 
Published: March 2003

Abstract
Background
: The clinical usefulness of the radiopaque marker method for detecting diabetic gastrointestinal motility disturbances, was evaluated by examining 21 type II diabetes subjects who did not have any neuropathic symptoms.
Methods
: After administration of a Sitzmark capsule®, markers were located using plain abdominal radiographs, and the transit time of the markers through seven areas of digestive tract was calculated by Arhan’s methods. The plasma concentration of acetaminophen at 45 min after oral administration was measured to evaluate gastric emptying time. The coefficient of variation of R‐R intervals on the electrocardiograms (CVR‐R) was measured to evaluate parasympathetic autonomic function.
Results
: In the diabetics, the average (± SD) transit time through upper digestive tracts was slightly but not significantly elongated compared with control subjects (14.4 ± 8.3 vs 9.9 ± 6.1 h). Significant elongation was observed in transit time through the lower digestive tracts or the whole gut (44.6 ± 20.9 and 57.9 ± 22.3 h, respectively) compared with control subjects (23.3 ± 8.5 and 33.2 ± 11.0 h). The transit time of the markers from stomach to small intestine was highly correlated (r = 0.693) with plasma concentration of acetaminophen. The transit time through either the whole colon (r = 0.564) or the whole gut (r = 0.630) was highly correlated with CVR‐R.
Conclusions
: These findings suggest that the radiopaque marker method is a useful tool for detecting the sections of the digestive tract responsible for gut motility disturbances. In type II diabetics with no neuropathic symptoms, the lower digestive tracts may deteriorate prior to the impairment of upper digestive tracts.
Effect of nucleoside analogue therapy on duck hepatitis B viral replication in hepatocytes and bile duct epithelial cells in vivo
Authors: Nicoll Amanda , Locarnini Stephen , Chou Sheung To , Smallwood Richard , Angus Peter 
Published: March 2003

Abstract
Background
: Recent studies have implicated bile duct epithelial cells (BDEC) as a reservoir of hepatitis B virus (HBV) infection that may be particularly important in the development of post‐liver transplant recurrence of hepatitis B. The aim of this study was to compare the effects of antiviral therapy on duck HBV (DHBV) expression in hepatocytes and BDEC and to determine if this was affected by biliary hyperplasia.
Methods
: Ducklings congenitally infected with DHBV received penciclovir (10 mg/kg per day) treatment from 9 days of age. In order to mimic the biliary hyperplasia that often accompanies severe post‐liver transplant HBV recurrence, half the animals underwent bile duct ligation. Duck HBV‐DNA in serum was measured at day 1, and serum and liver DHBV‐DNA were determined when the animals were killed on day 17. Intrahepatic expression of viral preS1 antigen and DHBV‐DNA was measured by immunohistochemistry and in situ hybridization, respectively.
Results
: Viraemia became undetectable in the penciclovir‐treated animals at day 17, following 8 days of therapy. Examination of liver tissue revealed that all hepatocytes and the majority of BDEC contained DHBV preS1 antigen and DHBV‐DNA. Penciclovir greatly reduced the intrahepatic viral burden, but there was no antiviral effect on viral markers within BDEC. Despite the increased number of BDEC after bile duct ligation, the same proportion of BDEC was seen to be infected, and this was unaffected by antiviral therapy.
Conclusions
: In the duck model with and without biliary hyperplasia, penciclovir controls DHBV replication and reduces viral burden in hepatocytes, but not in BDEC. The BDEC appear to be an important reservoir of virus that is relatively unaffected by antiviral treatment, and may play an important role in disease persistence and relapse following cessation of therapy.© 2000 Blackwell Science Asia Pty Ltd
Case selection for interferon treatment of hepatitis C
Authors: Zeniya Mikio , Toda Gotaro 
Published: March 2003

AbstractTo establish a case selection algorithm for the treatment of hepatitis C, predictive factors were studied and reported articles were reviewed and analysed. Because of the relatively poor efficacy of interferon (IFN) monotherapy, which is ineffective in 60–70% of patients, case selection at present is determined by the likelihood of attaining a sustained response (SR; defined by normalizing serum ALT and eliminating serum HCV RNA after treatment) to therapy. According to the present study, viral load and genotype, and IL‐10 and IL‐1ra serum levels, are the most predictive of achieving SR after IFN monotherapy given in a comparatively high dose regimen for 6 months. In addition, reported studies with logistic analyses were carefully reviewed and analysed for the most effective predictive factors of case selection. The results again indicated that viral load and HCV‐genotype (serotype) were closely related to SR. Age, gender, and histological changes at treatment were also considered for case selection. These results, however, relate solely to IFN‐monotherapy. Future development of more effective strategies for treating hepatitis C could alter the exclusion criteria for IFN treatment and will negate the need for the case selection algorithm discussed here.
Hepatitis C: Retreatment and treatment of patients with renal failure
Authors: Chow Wan‐Cheng 
Published: March 2003

AbstractThis paper addresses two difficult issues in the treatment of hepatitis C: patients who fail to achieve a sustained response after the first course of treatment, and those who simultaneously suffer from chronic renal failure. With the recent improvements in firstline treatment, retreatment is mainly applicable to those who have previously received 6‐month of interferon monotherapy at 3 MU thrice weekly. For those who had an end‐of‐treatment response but relapsed, there is a choice between interferon monotherapy at increased dose and/or duration of treatment, or a 6‐month course of combination therapy. Retreatment of non‐responders is generally unsuccessful, but some patients may respond to interferon‐alpha 3 MU and ribavirin 1.0–1.2 g/day. For patients with chronic renal failure and hepatitis C, combination treatment is not possible because ribavirin is contraindicated. Interferon given at a dose of 1.5 MU thrice weekly was reported to be fairly well tolerated by patients who were on dialysis and resulted in end‐of‐treatment and sustained biochemical and virological response in some cases. Interferon given in the usual doses may be associated with severe adverse effects in patients with renal failure, and can precipitate allograft rejection in patients who have undergone renal transplantation.
Natural history of chronic hepatitis C
Authors: Yatsuhashi Hiroshi , Yano Michitami 
Published: March 2003

AbstractThe natural history of chronic hepatitis C is one of a slow progression from early stage chronic hepatitis without fibrosis to cirrhosis or hepatocellular carcinoma (HCC). The disease progresses to advanced stage chronic hepatitis C over 10–30 years. Data from Japan indicate that mortality associated with chronic hepatitis C results mainly from the development of HCC. We studied 186 patients referred between 1968 and 1994. The mean follow‐up interval was 8.6 (2–23) years. HCC developed in 34 patients (18%). The cumulative probability of HCC development was 4% at 5 years, 18% at 10 years and 45% at 15 years. Univariable analysis indicated that age at entry, fibrosis stage, inflammation activity and the status of IFN treatment (treated vs untreated) were predictive risk factors for developing HCC in patients with chronic hepatitis C. Multivariable analysis of these risk factors indicated that age at entry (> 50 vs < 50; Risk Ratio = 3.2, P < 0.005) and fibrosis stage (F3 vs F0; Risk Ratio = 5.6, P < 0.005) are independent risk factors for HCC. From these results it was concluded that (1) 20% of patients referred to liver clinics with chronic hepatitis C in Japan can be expected to develop HCC over a 10 year period; (2) the risk of HCC increases with progression of liver fibrosis (F3, F4) and age (greater than 50 years old) at the time of diagnosis and (3) the degree of liver fibrosis is a critical predictive factor for the occurrence of HCC.
Water extract of Helicobacter pylori stimulates interleukin‐8 secretion by a human gastric epithelial cell line (JR‐St) through protein tyrosine phosphorylation
Authors: Yakabi Koji , Ro Shoki , Okazaki Ryo , Shiojima Junko , Tsuda Katsuhiko , Mimura Harumi , Tomono Hiroki , Nakamura Takashi 
Published: March 2003

Abstract
Background
: Infection by Helicobacter pylori induces cytokine production in gastric mucosal cells. Production of interleukin‐8 (IL‐8) is known to be markedly increased and is believed to play an important role in gastric mucosal inflammation. The aim of this study was to elucidate the effects of soluble factors of H. pylori on IL‐8 production in a gastric epithelial cell line, JR‐St.
Methods
: JR‐St cells were cocultured with a H. pylori water extract, live H. pylori or culture medium supernatant for 24 h, then the IL‐8 secreted into the culture medium was assayed. The effects of three different inhibitors; (i) an inhibitor of protein kinase C (PKC); (ii) an inhibitor of PKC and protein kinase A (PKA); and (iii) an inhibitor of protein tyrosine kinase (PTK) were also compared. Specific induction of IL‐8 mRNA was also examined.
Results
: Water extract of H. pylori increased IL‐8 secretion 7.72‐fold, more than the control. The increase was concentration dependent. Live bacteria, supernatant and water extract significantly stimulated IL‐8 secretion. Addition of live bacteria increased IL‐8 secretion most strongly, while the effect of water extract was small (22% that of live bacteria). Secretion was not inhibited by the PKC inhibitor staurosporine or the inhibitors of PKA and PKC H7. However, secretion was significantly reduced by the PTK inhibitor herbimycin in a dose‐dependent manner. Furthermore, 24 h exposure to water extract increased IL‐8 mRNA expression, suggesting water extract increased production of IL‐8.
Conclusions
: Some soluble factors of H. pylori can stimulate IL‐8 production by JR‐St cells. Stimulation was not dependent on PKA or PKC but was, at least partially, dependent on protein tyrosine phosphorylation. This suggests that soluble factors of H. pylori can play an important role in mediating the inflammatory response of H. pylori gastritis.© 2000 Blackwell Science Asia Pty Ltd
Sho‐saiko‐to: Japanese herbal medicine for protection against hepatic fibrosis and carcinoma
Authors: Shimizu Ichiro 
Published: March 2003

AbstractHerbal medicines, which have been used in China for thousands of years, are now being manufactured in Japan, in standardized form in terms of quality and quantities of ingredients. The Chinese herbal medicine Sho‐saiko‐to is a mixture of seven herbal preparations, which is widely administered in Japan to patients with chronic hepatitis and cirrhosis. In a prospective study, this herbal medicine was found to play a chemopreventive role in the development of hepatocellular carcinoma in cirrhotic patients. However, little is known about the mechanism by which Sho‐saiko‐to protects against hepatic fibrosis and carcinoma. Several laboratories, including ours, have clearly demonstrated the preventive and therapeutic effects of Sho‐saiko‐to on experimental hepatic fibrosis, as well as its inhibitory effect on the activation of hepatic stellate cells, which are the major types of collagen‐producing cells. We provided evidence that Sho‐saiko‐to functions as a potent anti‐fibrosuppressant via the inhibition of oxidative stress in hepatocytes and hepatic stellate cells and that its active components are baicalin and baicalein. In addition, Sho‐saiko‐to has anti‐carcinogenic properties in that it inhibits chemical hepatocarcinogenesis in animals, acts as a biological response modifier and suppresses the proliferation of hepatoma cells by inducing apoptosis and arrests the cell cycle. Among the active components of Sho‐saiko‐to, baicalin, baicalein and saikosaponin‐a have the ability to inhibit cell proliferation. It should be noted that baicalin and baicalein are flavonoids with chemical structures very similar to silybinin, which shows anti‐fibrogenic activities. This may provide valuable information on the search for novel anti‐fibrogenic agents.
Plaunotol suppresses interleukin‐8 secretion induced by Helicobacter pylori: Therapeutic effect of plaunotol on H. pylori infection
Authors: Takagi Atsushi , Koga Yasuhiro , Aiba Yuji , Kabir Abu Ma , Watanabe Sumio , Ohta‐Tada Uki , Osaki Takako , Kamiya Shigeru , Miwa Takeshi 
Published: March 2003

Abstract
Background
: It has been suggested that gastric mucosal injury induced by Helicobacter pylori infection is mediated by interleukin‐8 (IL‐8).
Methods
: We studied the effect of plaunotol, a drug extracted from the Plau‐noi tree of Thailand, and reported it to be effective in the treatment of ulcers, of IL‐8 secretion induced by H. pylori and of the inhibitory adhesion activity of the bacterium to gastric epithelial cells. Moreover, the therapeutic effect of plaunotol on H. pylori infection was assessed by using the gnotobiotic murine model.
Results
: Plaunotol inhibited the growth of H. pylori (1.5 × 10
4 c.f.u./mL) at high doses (24–48 μg/mL), but not at low doses (3–6 μg/mL). Interleukin‐8 secretion induced by H. pylori was inhibited by coculture with plaunotol in a dose‐dependent manner. The adhesion of H. pylori to MKN45 cells was also suppressed by coculture with plaunotol in a dose‐dependent manner. An in vivo study showed that plaunotol improved histological gastritis and decreased the H. pylori antibody titre.
Conclusions:
These findings suggest that plaunotol has a therapeutic effect on gastritis induced by H. pylori.
Influence of RNA titre and amino acid changes in the NS5A region of GB virus C/hepatitis G virus on the effectiveness of interferon therapy
Authors: Fujisawa Tomoki , Horiike Norio , Michitaka Kojiro , Onji Morikazu 
Published: March 2003

Abstract
Background
: A relationship between the pretreatment RNA titre of GB virus C/hepatitis G virus (GBV‐C/HGV) and the effectiveness of interferon (IFN) therapy has been reported previously. However, the influence of changes in the amino acid sequence of the NS5A region of GBV‐C/HGV on the effectiveness of IFN therapy has not been examined, although this influence has been explored in patients with chronic hepatitis caused by hepatitis C virus. We examined the relationship between changes in the amino‐acid sequence of the NS5A region and the effectiveness of IFN therapy.
Methods
: The subjects were 10 patients with chronic hepatitis C coinfected with GBV‐C/HGV and treated with IFN. The pretreatment level of GBV‐C/HGV‐RNA (copies/mL) in their sera was measured by real‐time detection polymerase chain reaction (PCR) assay. At 6 months after cessation of therapy, four of 10 patients had become negative for GBV‐C/HGV‐RNA (CR, complete response) and six patients were still positive for GBV‐C/HGV‐RNA (NR, non‐response). We determined the nucleotide sequence of the NS5A region (amino acid residues 1865–2279; NS5A1865–2279) of pretreatment GBV‐C/HGV‐RNA by direct sequencing.
Results
: The pretreatment GBV‐C/HGV‐RNA level of CR patients (7.8 × 104–6.2 × 105, mean 3.30 × 105) was significantly lower than that of NR patients (6.3 × 107–7.2 × 108, mean 3.55 × 108; P < 0.01). The number of amino acid substitutions in NS5A1865–2279 was five to seven (mean 5.8 ± 1.0) in CR patients, and four to eight (mean 6.8 ± 1.6) in NR patients, a difference that is not significant. Moreover, there were no amino acid substitutions or sites of substitution in NS5A1865–2279 that were specific to either group.
Conclusions
: The effectiveness of IFN therapy for GBV‐C/HGV is strongly related to the pretreatment GBV‐C/HGV‐RNA level, but is not related to changes in NS5A1865–2279.
Telomerase activity in peripheral blood for diagnosis of hepatoma
Authors: Tatsuma Toshiro , Goto Shigeru , Kitano Seigo , Lin Yu‐Chun , Lee Chuan‐Mo , Chen Chao‐Long 
Published: March 2003

Abstract
Background
: Telomerase activity may be used as a molecular marker for the detection of circulating hepatoma cells in blood of patients with hepatoma.
Methods
: Telomerase activity in peripheral blood from hepatocellular carcinoma (HCC) patients was assessed by using a highly sensitive and non‐radioisotope telomerase polymerase chain reaction (PCR) ELISA. Initially, tissue telomerase activity was measured in the hepatoma and non‐tumour portions by using PCR ELISA within the same specimen, to compare its sensitivity with the conventional telomeric repeat amplification protocol (TRAP) method. Second, telomerase activity was measured in the peripheral blood obtained from patients with HCC, patients with chronic liver disease and in healthy controls.
Results
: Of the 17 HCC patients, telomerase activity was found to be positive in 14 (82%) by using TRAP and 15 (88%) by using PCR ELISA, indicating that PCR ELISA is a reliable tool for the measurement of telomerase activity. By using the Telomerase PCR ELISA assay, telomerase activities in the peripheral blood of 20 HCC patients was 1.65 ± 0.78 units. This was significantly greater than the results obtained for 20 chronic liver disease patients (0.43 ± 0.36 units) and 20 healthy controls (0.39 ± 0.14 units; P < 0.0001). When the arbitrary cut‐off level was set at 0.7 units (maximum value of healthy controls + 0.1), the positive frequency of telomerase activity was 25% for chronic liver disease and 80% for HCC patients (sensitivity 80%, specificity 75%). Among the HCC patients, high telomerase activity in the peripheral blood was shown at stage III HCC with vascular invasion (2.10 ± 0.62 units, n = 9). This was significantly higher than patients at stage II of HCC (1.28 ± 0.72 units, n = 11, without vascular invasion; P = 0.012).
Conclusion
: These results suggest that peripheral blood telomerase activity, which may reflect haematogenous micrometastasis, is potentially a practical diagnostic/predictive marker of HCC.
L‐Arginine protects and exacerbates ethanol‐induced rat gastric mucosal injury
Authors: Kalia Nalia , Bardhan Karna Dev , Reed Malcolm Wr , Jacob Samuel , Brown Nicola Jane 
Published: March 2003

Abstract
Background and Aims
: We have previously demonstrated that 60% ethanol (EtOH) increases macromolecular leakage and induces focal lesion formation in areas of permanent flow stasis within gastric mucosal vessels. Nitric oxide (NO) may prevent lesion formation by inhibiting leakage. This study used fluorescent in vivo microscopy to investigate (i) whether
L‐arginine (NO precursor) prevented EtOH induced injury and (ii) the mechanisms of protection.
Methods
: Experiments were carried out on anaesthetized rats (hypnorm/diazepam) receiving either intra‐arterial fluorescein isothiocyanate–bovine serum albumin (0.2 mL/100 g), a marker for quantitating leakage, or Acridine red (0.1 mL/100 g) which labels leukocytes. Animals then received 100, 300 or 500 mg/kg
L‐arginine (i.a.) followed by 60% EtOH or distilled water, topically applied to the gastric mucosa (n = 6 for each group). Vessel diameter, macromolecular leakage of labelled albumin from post capillary venules (PCV) and capillaries and leukocyte activity were quantitated using image analysis.
Results
:
L‐Arginine (100 mg/kg) did not increase vessel diameter or prevent EtOH‐induced lesion formation and leakage. Both 300 mg/kg and 500 mg/kg alone induced significant and sustained increases in PCV diameter after 15 (P < 0.01) and 5 min (P < 0.001), respectively. Lesion formation was only prevented by 300 mg/kg
L‐arginine, whereas 500 mg/kg exacerbated haemorrhagic lesion formation over the entire exposed mucosa. Neither 300 mg/kg nor 500 mg/kg
L‐arginine prevented leakage following EtOH. No leukocyte activity was observed following EtOH with or without
L‐arginine pretreatment.
Conclusion
:
L‐Arginine (300 mg/kg) prevented lesion formation. The mechanism of protection probably involved the increased blood flow in the dilated PCV and not the inhibition of leakage. The combined effects of EtOH and the possible high NO levels exacerbate gastric mucosal damage despite the increases observed in vessel diameter.
Acute and chronic effects of isosorbide‐5‐mononitrate administration on effective renal plasma flow and the renin‐aldosterone system in cirrhotic patients
Authors: Chen Shy‐Den , Hsieh Jih‐Fang , Tsai Shih‐Chuan , Lin Wan‐Yu 
Published: March 2003

Abstract
Background and Aims
: Isosorbide‐5‐mononitrate (ISMO) has been shown to be effective in reducing the risk of variceal bleeding in patients with cirrhosis. However, recent studies have suggested that this drug compromises renal function. The present study was conducted to assess the acute and chronic effects of ISMO on effective renal plasma flow (ERPF) and the renin‐aldosterone profile in cirrhotic patients.
Methods
: Fifteen cirrhotic patients were included in the present study. The mean arterial pressure (MAP), heart rate (HR), serum renin concentration (SR), ERPF and plasma aldosterone concentration (PA) were checked before ISMO treatment (baseline study), after a single oral dose of 20 mg ISMO (acute effect study) and after 3 weeks of ISMO treatment (chronic effect study).
Results
: Our data showed that the oral administration of a single dose (20 mg) of ISMO to cirrhotic patients was associated with significant decreases in ERPF (from 405.18 to 369.06 mL/min) and MAP (from 93.26 to 86.40 mmHg), and increases in HR (from 65.53 to 70.06 beats/min), SR (from 24.15 to 54.41 pg/mL), and PA (from 105.1 to 148.7 pg/mL). However, no significant changes were observed in HR, MAP, PA, SR, or ERPF after 3 weeks of ISMO treatment when compared with the baseline study.
Conclusions
: The administration of ISMO causes a decrease in ERPF in cirrhotic patients and its use in patients with renal impairment should be considered cautiously.