bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gastric juice ascorbic acid is related to Helicobacter pylori infection but not ethnicity
Authors: Fraser Alan G , Woollard Gerald A 
Published: March 2003

Abstract
Background
: Maori and Pacific Island ethnic groups in New Zealand have a high risk for gastric cancer. Low levels of gastric juice ascorbic acid (vitamin C) have been suggested to be a risk factor for gastric cancer. Previous studies have shown that gastric juice ascorbic acid may be independently associated with both ethnicity and Helicobacter pylori infection. This study aimed to examine the interrelationship between H. pylori and ethnicity in New Zealand.
Methods
: Gastric juice was collected into 70% perchloric acid preservative and stored at –80°C. Ascorbic acid was analysed by high‐performance liquid chromatography using ion‐pair chromatography and electrochemical detection. Inflammation and atrophy was graded from biopsies from multiple sites in the antrum and body. Gastric juice was collected from 89 patients during routine endoscopy.
Results
: There was a wide range of measured gastric juice ascorbic acid from 0.001 to 410 μg/mL. The median concentration of ascorbic acid for H. pylori‐negative patients was 1.78 μg/mL (n = 57) and 0.12 μg/mL (n = 32) for H. pylori‐positive patients (P = 0.001). Gastric juice ascorbic acid concentration was not associated with age, endoscopic diagnosis or intestinal metaplasia, but was significantly associated with the degree of acute inflammation (P = 0.01) and the presence of atrophy (P = 0.04). The median ascorbic acid concentration for European patients was 0.92 μg/mL (n = 44) and 0.09 μg/mL (n = 38) for Maori and Pacific Island ethnic groups combined (P = 0.1). Multiple step‐wise regression analysis showed that only H. pylori infection was a significant factor for predicting ascorbic acid concentrations (r2 = 0.12).
Conclusions
: This study has confirmed that gastric juice ascorbic acid concentration is lower in the presence of H. pylori infection.© 1999 Blackwell Science Asia Pty Ltd
Congenital hepatic fibrosis in Indian children
Authors: Poddar Ujjal , Thapa Babur R , Vashishta Rakesh K , Girish Chakkodbail S , Singh Kartar 
Published: March 2003

Abstract
Background
: Congenital hepatic fibrosis (CHF) is an uncommon cause of portal hypertension in children. So far, there is no report of this from the subcontinent. We have studied the clinical spectrum of CHF in North Indian children.
Methods
: Fifteen children were diagnosed with CHF on the basis of their liver histology over a period of 6.5 years. Their clinical details were recorded. Oesophagogastroduodenoscopy and abdominal ultrasonography were performed in all cases. All siblings were examined clinically; and ultrasonography, endoscopy and liver biopsy were performed if there was firm hepatomegaly. Children with variceal bleeding were managed by endoscopic sclerotherapy. The median age of these children was 8 years with a male to female ratio of 1.5:1.
Results
: Only one sibling (of 33) was diagnosed as having CHF. The predominant presentations were variceal bleeding in six, abdominal distension in seven and incidental detection of organomegaly in two. Hepatomegaly was present in all patients and splenomegaly in all but one. Liver function and renal function tests were normal in all children, except for a raised serum alkaline phosphatase in six. Two children had associated renal cysts, two had choledochal cysts, one each had Caroli’s disease and biliary atresia and two children had portal vein thrombosis. Variceal obliteration was achieved in five children after an average 4.8 sclerotherapy sessions and one required a mesocaval shunt. On follow up (median 41 months, range 1–80 months) all are doing well.
Conclusions
: Congenital hepatic fibrosis is mainly sporadic in India and associated renal lesions are uncommon. Endoscopic sclerotherapy is effective in controlling variceal bleed and the prognosis is universally good in the absence of renal diseases.© 1999 Blackwell Science Asia Pty Ltd
Hepatocyte growth factor/scatter factor enhances the thrombopoietin mRNA expression in rat hepatocytes and cirrhotic rat livers
Authors: Yamashita Kiyoshi , Matsuoka Hitoshi , Ochiai Toshimasa , Matsushita Ryuji , Kubuki Youko , Suzuki Muneou , Tsubouchi Hirohito 
Published: March 2003

AbstractBackground: Although thrombopoietin (TPO) is mainly produced in the liver, the regulatory mechanism ofTPOgene expression in hepatocytes remains unclear. The role of TPO in thrombocytopenia associated with liver cirrhosis has not been identified.Methods: We examined the effects of various growth factors and cytokines on TPO mRNA expression in adult rat hepatocytes in primary cultures using a semiquantitative reverse transcription‐polymerase chain reaction assay.Results: Among them, only hepatocyte growth factor/scatter factor (HGF/SF) enhanced TPO mRNA expression; other growth factors (epidermal growth factor and transforming growth factor‐β) and cytokines (erythropoietin, granulocyte‐colony stimulating factor, granulocyte‐macrophage‐colony stimulating factor, interleukin (IL)‐3, IL‐6 and interferon‐γ) did not. Next, we examined TPO mRNA expression in the livers of rats with CCl4‐induced cirrhosis, the effects of HGF/SF on hepatic TPO mRNA expression and peripheral platelet and bone marrow megakaryocyte counts in the cirrhotic rats. In the cirrhotic rats, both the peripheral platelet count and TPO mRNA expression in the livers were markedly decreased compared with those of the normal rats. The administration of HGF/SF to the cirrhotic rats stimulated TPO mRNA expression in the livers and resulted in significant increases of peripheral platelets and bone marrow megakaryocytes.Conclusions: These results suggest that HGF/SF is a possible regulatory factor for TPO gene expression and that HGF/SF increases platelet production through an enhancement of TPO mRNA expression in the livers of cirrhotic rats.
Apoptosis in the intestinal epithelium: Its relevance in normal and pathophysiological conditions
Authors: Ramachandran Anup , Madesh Muniswamy , Balasubramanian Kunissery A 
Published: March 2003

AbstractApoptosis is now recognized as an important process responsible for maintenance of the cellular balance between proliferation and death. Apoptosis is distinct from necrosis in that it is a programmed form of cell death and occurs without any accompanying inflammation. This form of cell death can be induced by a wide range of cellular signals, which leads to activation of cell death machinery within the cell and is characterized by distinct morphological changes. Apoptosis is especially relevant in the gastrointestinal tract, as the mammalian intestinal mucosa undergoes a process of continual cell turnover that is essential for maintenance of normal function. Cell proliferation is confined to the crypts, while differentiation occurs during a rapid, orderly migration up to the villus. The differentiated enterocytes, which make up the majority of the cells, then undergo a process of programmed cell death (apoptosis). Although apoptosis is essential for the maintenance of normal gut epithelial function, dysregulated apoptosis is seen in a number of pathological conditions in the gastrointestinal tract. The cellular mechanisms regulating this tightly regimented process have not been clearly defined and this topic represents an area of active investigation as delineation of this process will lead to a better understanding of normal gut mucosal growth.
Amino acid substitutions in codons 9–11 of hepatitis C virus core protein lead to the synthesis of a short core protein product
Authors: Yeh Chau‐Ting , Lo Shih‐Yen , Dai Dar‐In , Tang Jui‐Hsiang , Chu Chia‐Ming , Liaw Yun‐Fan 
Published: March 2003

Abstract
Background
: Previous in vitro experiments have indicated that if the ninth codon of the hepatitis C virus (HCV) core gene is mutated from arginine to lysine, a short 16‐kDa (P16) instead of a 21‐kDa (P21) core protein will be produced. In this study, we aimed to investigate whether similar mutations existed in patients with chronic HCV infection and whether such mutations led to the expression of P16.
Methods
: The core gene was isolated from patients’ sera by reverse transcription–polymerase chain reaction and sequenced.
Results
: Three of 10 patients with hepatocellular carcinoma were found to have mutant viruses with missense mutations at codons 9–11: arginine‐to‐glycine mutation at codon 9 (case 1); lysine‐to‐glutamine mutation at codon 10 (case 5); and lysine‐to‐asparagine/threonine‐to‐alanine double mutations at codons 10 and 11 (case 8). Site‐directed mutagenesis and in vitro translation experiments revealed that P16 was expressed by all three mutants. Using gel‐purified P21 and P16 proteins obtained from transformed Escherichia coli, the serum titres of anti‐P21 and anti‐P16 were assayed. Unequal titres of anti‐P16 and anti‐P21 were found in only cases 1, 5 and 8. A rabbit antibody directed against P16 but not P21 was thus generated for immunohistochemical analysis. P16 was detected in the nuclei of hepatocytes in the peri‐hepatoma tissue of a single case (case 1).
Conclusions
: These data indicate that missense mutations at codons 9–11 can occur during chronic HCV infection, which results in the expression of P16 core protein.
Pathophysiology of the intrahepatic biliary epithelium
Authors: Strazzabosco Mario , Spirlì Carlo , Okolicsanyi Lajos 
Published: March 2003

AbstractThe intrahepatic bile duct epithelium modulates the fluidity and alkalinity of the primary hepatocellular bile from which it reabsorbs fluids, amino acids, glucose and bile acids, while secreting water, electrolytes and immunoglobulin A. The transport function of the intrahepatic biliary epithelium is finely regulated by a number of gastrointestinal hormones, neuropeptides and neurotransmitters that promote either secretion or absorption. The intrahepatic biliary epithelium appears to be a primary target in a broad group of chronic cholestatic disorders that represent an important cause of morbidity and mortality. The spectrum of cholangiopathies ranges from conditions in which a normal epithelium is damaged by disordered autoimmunity, infectious agents, toxic compounds or ischaemia, to genetically determined disorders arising from an abnormal bile duct biology, such as cystic fibrosis or biliary atresia. Probably as a result of the known heterogeneity in cholangiocyte function, different portions of the biliary tree appear to be preferentially affected in specific cholangiopathies. From a pathophysiological point of view, cholangiopathies are characterized by the coexistence of cholangiocyte loss (by apoptotic or lytic cell death) with cholangiocyte proliferation and various degrees of portal inflammation, fibrosis and cholestasis. These basic disease mechanisms are discussed in detail. Better understanding of cholangiocyte pathophysiology, in particular the immune regulation of cholangiocyte function, will help in designing newer genetic or pharmacological approaches to treat cholangiopathies.© 2000 Blackwell Science Asia Pty Ltd
Dysphagia after prophylactic endoscopic injection sclerotherapy for oesophageal varices: Not fatal but a distressing complication
Authors: Nozoe Tadahiro , Matsumata Takashi , Sugimachi Keizo 
Published: March 2003

Abstract
Background
: Although dysphagia resulting from oesophageal strictures induced by endoscopic injection sclerotherapy (EIS) is not a fatal complication, it is often quite distressing for the patients. The aim of the current study was to clarify the relationship between dysphagia resulting from oesophageal stricture following prophylactic EIS and the volume of sclerosant consumed in the EIS series.
Methods
: Fifty‐two patients with oesophageal varices, who had been treated by prophylactic EIS, were selected as the subjects.
Results
: Seventeen (32.7%) patients developed dysphagia following prophylactic EIS, and five patients with a severe stricture required bougie dilatation to take meals. The volume of sclerosant used in the initial session of EIS for patients with subsequent dysphagia (24.9 ± 4.0 mL) was significantly larger than that for patients without dysphagia (18.4 ± 5.1 mL; P < 0.001). The mean volume of sclerosant consumed per session during the EIS series for patients with dysphagia (16.5 ± 3.0 mL) was also significantly larger than that for patients without dysphagia (13.1 ± 3.8 mL; P < 0.01).
Conclusions
: The injection of a superfluous amount of sclerosant in prophylactic EIS brings about distressing dysphagia with oesophageal stricture in the patients with oesophageal varices who had no such complaint or symptoms before the therapy.© 2000 Blackwell Science Asia Pty Ltd
Helicobacter pylori infection and gastric carcinoma in animal models
Authors: Fujioka Toshio , Honda Shoji , Tokieda Masashi 
Published: March 2003

AbstractMany epidemiological studies have shown a strong association between chronic Helicobacter pylori infection and the subsequent development of gastric carcinoma in humans. To confirm this link more clearly, it is necessary to use this bacterium in experimental studies to develop gastric carcinoma in suitable experimental animals. Persistent H. pylori infection has recently been achieved in the Mongolian gerbil model, with results demonstrating that the sequential histopathological changes in the gastric mucosa closely mimic the gastric mucosal changes caused by H. pylori infection in humans. These studies have demonstrated that H. pylori infection enhances gastric carcinogenesis in combination with known carcinogens, such as N‐methyl‐N‐nitroso‐urea and N‐methyl‐N‐nitro‐N′‐nitrosoguanidine and have also demonstrated that H. pylori infection alone can result in the development of gastric carcinoma. These important results provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of H. pylori infection and assist the planning of eradication therapy to prevent gastric carcinoma.
Wilson’s disease with superimposed autoimmune features: Report of two cases and review
Authors: Milkiewicz Piotr , Saksena Sushma , Hubscher Stefan G. , Elias Elwyn 
Published: March 2003

AbstractWe describe two females, 15 and 23 years old, respectively, who presented with classical features of Wilson’s disease (WD) and several features of autoimmune hepatitis (AIH). The first patient was initially diagnosed as AIH and treated with prednisolone which caused clinical improvement, with an increase of serum albumin from 22 to 30 g/L, and a decrease of aspartate aminotransferase from 103 to 47 U/L. Subsequent diagnosis of WD and introduction of penicillamine gave excellent improvement and complete normalization of liver function tests. The second patient, at first also diagnosed as having AIH, was treated with steroids and azathioprine with initial improvement, but subsequent deterioration. The diagnosis of WD was made 2 years after initial diagnosis of AIH, as the patient reached end‐stage liver disease and required a transplant. Therefore, d‐penicillamine treatment was not attempted. We conclude that, in patients with AIH, a thorough screening for WD is necessary, particularly when the response to steroid therapy is poor. Conversely, in patients suffering from WD with superimposed features of AIH, a combination of steroids and penicillamine may be of benefit.
Renovascular resistance assessed by color Doppler ultrasonography in patients with chronic liver diseases
Authors: Koda Masahiko , Murawaki Yoshikazu , Kawasaki Hironaka 
Published: March 2003

AbstractBackground and AimsRenal arterial vasoconstriction is known to be related to renal hemodynamic derangement in patients with liver cirrhosis. Using color Doppler ultrasonography in patients with chronic liver diseases, abnormal resistance in the renal artery was examined non‐invasively both cross‐sectionally and longitudinally to clarify the relationship between renal vascular resistance and liver function to neurohumoral factors.MethodsThe study comprised 118 patients with cirrhosis, 23 patients with chronic hepatitis, and 35 healthy controls. Pulsatility and resistive indices that were derived from renal artery velocity analysis were used as parameters of renal arterial resistance.ResultsBoth the pulsatility and resistive indices were significantly higher in cirrhotic patients (1.29 ± 0.37, P < 0.001 and 0.69 ± 0.07, P < 0.001, respectively) compared to controls (1.00 ± 0.12 and 0.62 ± 0.05, respectively) and compared to patients with chronic hepatitis (0.97 ± 0.13 and 0.60 ± 0.05, respectively). Both indices showed significant correlation with increased Child–Pugh grade. Each correlated significantly with plasma renin activity and plasma aldosterone and norepinephrine levels. Multivariate analysis of the relationship between neurohumoral factors and renal arterial resistance disclosed that plasma renin activity was a significant independent predictor. The longitudinal change in pulsatility index, resistive index and neurohumoral factors were examined in the cirrhotic patients who were followed‐up for longer than 6 months. Pulsatility and resistive indices increased according to the deterioration of liver function and the changes in both indices were closely related to the change in plasma renin activity.ConclusionsPulsatility index and resistive index as measured by color Doppler ultrasonography were closely related to the severity of cirrhosis and to the levels of neurohumoral factors, especially plasma renin activity, in this cross‐sectional and longitudinal study. Therefore, they are useful indices for assessing renal hemodynamics in patients with cirrhosis.
Molecular therapy with recombinant antisense c‐myc adenovirus for human gastric carcinoma cells in vitro and in vivo1,2
Authors: Chen Jie‐Ping , Lin Chen , Xu Cai‐Pu , Zhang Xue‐Yan , Fu Ming , Deng You‐Ping , Wei Yue , Wu Ming 
Published: March 2003

Abstract Background and Aims: This study used a recombinant antisense c‐myc adenovirus (Ad‐ASc‐myc) to evaluate how alterations of c‐myc expression in the SGC7901 human gastric carcinoma cells could influence the proliferation, apoptosis and the growth of human gastric tumors in nude mice.Methods: The human gastric carcinoma cell line, SGC7901, treated with Ad‐ASc‐myc or adenovirus recombinants carrying LacZ gene (Ad‐LacZ) were analyzed by using X‐gal stain, MTT, DNA ladder, TUNEL assay, flow cytometric analysis, polymerase chain reaction and western blot in vitro. The tumorigenicity and experimental therapy in nude mice models were assessed in vivo.Results: The Ad‐ASc‐myc could strongly inhibit cell growth and induce apoptosis in SGC7901 cells. The proliferation of the Ad‐ASc‐myc‐infected SGC7901 cells was reduced by 44.1%. The mechanism of killing gastric carcinoma cells by Ad‐ASc‐myc was found to be apoptosis, which was detected by the use of a DNA ladder, TUNEL and flow cytometric analysis. Infection of Ad‐ASc‐myc in nude mice showed that all three mice failed to form tumors from the 7 to 30 day period, compared with injection of Ad‐LacZ and parent SGC7901 cells. Experimental therapy on the nude mice bearing subcutaneous tumors of SGC7901 cells showed that intratumor instillation of Ad‐ASc‐myc inhibited the growth of the tumors. Recombinant antisense c‐myc adenovirus‐treated tumors were inhibited by 68.9%, compared with tumors injected with Ad‐LacZ and control (LacZ and phosphate‐buffered saline).Conclusion: The expression of Ad‐ASc‐myc can inhibit growth and induce apoptosis of gastric cancer cells in vitro and in vivo and thus is a potential clinical utility in gene therapy for the treatment of gastric carcinoma.
Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2‐type receptors
Authors: Loureiro‐Silva MaurÍcio R , Molina HercÍlia M , Borges Durval R 
Published: March 2003

AbstractBackground: We have shown that the portal hypertensive response to bradykinin in normal rats is mediated by B2 receptors.Methods: By using isolated and exsanguinated rat liver perfusion, we studied the portal hypertensive response to bradykinin or des‐Arg9‐bradykinin (B1 agonist) in inflamed or cirrhotic rat livers. Livers were perfused with bovine serum albumin Krebs–Henseleit buffer (pH 7.4; 37°C) at a constant flow rate, in the absence or presence of des‐Arg9[Leu8]‐bradykinin or HOE 140 (B1 and B2 receptor antagonists, respectively). Bradykinin (140 nmol) or des‐Arg9‐bradykinin was injected as a bolus via the afferent route to the liver.Results: Basal perfusion pressure in liver‐cirrhotic rats was higher than in normal rats. In normal, inflamed, or liver‐cirrhotic rats, the presence of the B1 antagonist did not change the portal hypertensive response to bradykinin, while the B2 antagonist abolished this response. A 140‐nmol dose of des‐Arg9‐bradykinin did not change the perfusion pressure; 700 nmol of this B1 agonist produced an insignificant perfusion pressure increase. The perfusion pressure increase induced by bradykinin in cirrhotic livers was lower than in normal livers.Conclusions: The portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 receptors, but not B1 receptors, and there is a contracting hyporeactivity to bradykinin in cirrhotic rat livers.
Strategy for retreatment of therapeutic failure of eradication of Helicobacter pylori infection
Authors: Nagahara Akihito , Miwa Hiroto , Ohkura Ryuichi , Yamada Toshio , Sato Kenji , Hojo Mariko , Sato Nobuhiro 
Published: March 2003

AbstractBackground and Aim:A proton pump inhibitor (PPI)‐based triple therapy consisting of a PPI, amoxicillin (A) and clarithromycin (C) or metronidazole (M) provides an eradication rate ranging from 80 to 90%. However, there have been few controlled studies with regard to the most effective regimen to re‐treat patients after failure of the first‐line therapy. Accordingly, we retrospectively reviewed our experiences and compared regimens with different combinations of antimicrobials to determine the optimal retreatment regimen.Methods:Out of 133 patients who had received second‐line therapy after failure of first‐line PPI/AC therapy, we selected, for review, patients who took the prescribed drugs for first‐line therapy equal to, or more than 80%. As a result, data on 114 patients (83 males and 31 females; mean age 49.1 ± 13.0 years; peptic ulcer n = 89; non‐ulcer dyspepsia, n = 25) were eligible for evaluation. They had either repeated the PPI/AC regimen (n = 34; 5–14 days), or had been administered the PPI/AM regimen (n = 80; 10 days). The cure rates of the two regimens were compared.Results:The eradication rates for second‐line therapy with the PPI/AC regimen versus the PPI/AM regimen were 52.9% (95% CI, 35–70) versus 81.3% (95% CI, 71–89) by intention‐to‐treat analysis (P < 0.01), and 62.1% (95% CI, 42–79) versus 91.4% (95% CI, 81–97) by per‐protocol analysis (P < 0.01).Conclusion:The eradication rate for the PPI/AM retreatment regimen was significantly higher than for the repeated PPI/AC regimen, suggesting that a 10‐day PPI/AM regimen can be recommended as a retreatment regimen for patients who had first‐line eradication therapy by PPI/AC regimens.