bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of gallstone disease in Iran
Authors: Massarrat Sadegh 
Published: March 2003

AbstractBackground: Prevalence of gallstone disease is different depending on the geographic region involved. Few studies, in Asia but not from Iran, about the frequency of gallstone disease have been published. The aim of this study is to examine the prevalence of gallstone disease in Iran.Methods: Four hundred and seventy‐seven nomads from southern Iran, 513 industrial laborers older than 34 years, and 421 laborers from a pharmaceutical company above 30 years of age, and 471 elderly persons from three nursing homes near Tehran underwent abdominal sonography.Results: There were 1373 men and 509 women. Eighty‐nine subjects had gallstone disease and 10.1% of them were cholecystectomized. While the prevalence in the men and women in the age group 31–40 years was very low (0.3% in men and 1.8% in women), it increases sharply in men older than 60 years and women older than 50 years to more than 10‐fold (12.5 and 24.6% in male and female with an age 71–80 years, respectively).Conclusion: In Iran, gallstone disease is very uncommon in middle‐aged people, but increases sharply in older people. However, this does not reach the high prevalence seen in Western countries. The intake of a high fiber‐containing diet, a low number of overweight people, smoking habit and hyperlipidemia are probably the cause for this low prevalence.
Modulation of acid secretion in common bile duct ligation‐related gastropathy in Wistar rats
Authors: Kaur Simran , Kaur Upjeet , Agnihotri Navneet , Tandon Chandan D , Majumdar Siddhartha 
Published: March 2003

AbstractBackground: Portal hypertensive gastropathy is associated with fundic gland atrophy, resulting in a decrease in chief and parietal cells, and diminished acid secretion.Methods: Acid secretion by isolated parietal cells was measured (acridine orange retention), along with the levels of various second messengers (intracellular Ca2+, cyclic adenosine monophosphate and protein kinase C) in the common bile duct, ligated portal hypertensive rats and compared with sham‐operated controls.Results: There was a significant decrease in the response of isolated parietal cells to the secretagogues histamine and carbachol. This resulted in the blunted acid secretion in the common bile duct ligated group. In addition, all the second messengers studied were significantly decreased as compared with the sham‐operated controls.Conclusion: These results suggest that the blunted acid secretory response in the portal hypertensive rat is caused by an alteration in the intracellular signal transduction mechanism.
Therapeutic effects on intestinal Behçet’s disease of an intravenous drug delivery system using dexamethasone incorporated in lipid emulsion
Authors: Nakase Hiroshi , Okazaki Kazuichi , Kawanami Chiharu , Uchida Kazushige , Ohana Masaya , Uose Suguru , Nishi Toshiki , Itoh Toshiyuki , Okano Akihiro , Nishio Akiyoshi , Takakuwa Hiroshi , Chiba Tsutomu 
Published: March 2003

AbstractRecurrent intestinal ulcer is a frequent problem in the management of Behçet’s disease. However, no standard therapy for intestinal Beheçt’s disease has been established. We report two patients with intestinal Behçet disease and recurrent ileal ulcers who were treated successfuly with a lipid emulsion of dexamethasone. In one patient, the cecal ulcer did not relapse after the intravenous administration initiation of a lipid emulsion of dexamethasone once a week, despite the discontinuation of prednisolone. In the other patient, the cecal ulcer showed a healing tendency, and oral administration of prednisolone was reduced from 40 to 15 mg/day after intravenous administration of a lipid emulsion of dexamethasone. Both patients experienced no complications associated with the administration of the emulsion. These results suggest that an intravenous drug delivery system using a lipid emulsion of dexamethasone is useful for treatment of intestinal Behçet’s disease.
Cisapride improves gallbladder emptying and bile lipid composition in patients with gallstones
Authors: Dhiman Radha K , Reddi Rajashekhar , Sharma Arpita , Singh Rajinder , Kohli Krishan K , Gupta Sanjay , Suri Sudha , Chawla Yogesh 
Published: March 2003

AbstractBackground and Aim: Biliary cholesterol supersaturation, gallbladder stasis and delayed intestinal transit are the key events in cholesterol gallstone formation. We studied the effect of cisapride, a prokinetic drug, on gallbladder emptying and bile composition in patients with gallstone disease undergoing cholecystectomy.Methods: Gallbladder emptying, cholesterol saturation index (CSI) and nucleation time were studied in 21 patients with gallstone disease. Eleven patients (cisapride group, age 41.9 ± 2.9 years) received tablet cisapride 10 mg t.i.d. for 2 weeks, while 10 patients (placebo group, age 42.1 ± 1.9 years) received placebo for the same duration. Gallbladder emptying was repeated in all patients after a 2‐week treatment with cisapride or placebo. Gallbladder bile was obtained at the time of surgery for the measurement of CSI and nucleation time.Results: Residual volume of the gallbladder decreased (mean ± SE, 18.6 ± 2.5 mL vs 10.0 ± 1.1 mL, P = 0.007), and the ejection fraction increased (43.5 ± 5.3%vs 60.0 ± 3.2%, P = 0.007) in patients in the cisapride group, while no change was observed in placebo group patients. Nucleation time was higher in the cisapride group than in the placebo group (14.9 ± 1.3 days vs 8.0 ± 0.9 days, P = 0.003). Patients in the cisapride group had a significantly lower cholesterol concentration (molar percentage, 5.1 ± 0.3%vs 6.8 ± 0.8%, P = 0.049) and CSI (1.0 ± 0.1 vs 1.36 ± 0.11, P = 0.034) than patients in the placebo group.Conclusion: Cisapride improves gallbladder emptying and bile lithogenicity in patients with gallstone disease.
Comparison of real‐time quantitative polymerase chain reaction with three other assays for quantitation of hepatitis C virus
Authors: Enomoto Masaru , Nishiguchi Shuhei , Shiomi Susumu , Tanaka Motoharu , Fukuda Katsuhiko , Ueda Tadashi , Tamori Akihiro , Habu Daiki , Takeda Tadashi , Yano Yoshihisa , Otani Shuzo 
Published: March 2003

AbstractBackground and Aims: Evaluation of serum levels of hepatitis C virus (HCV) is important for predicting the response to interferon treatment and monitoring its therapeutic efficacy. The aim of this study was to evaluate real‐time quantitative polymerase chain reaction (PCR) as a method for the measurement of HCV‐RNA.Methods: The subjects were 50 patients with chronic hepatitis C: 36 with genotype 1b, eight with genotype 2a, and six with genotype 2b. Samples were tested for HCV‐RNA by using real‐time quantitative PCR with the ABI Prism 7700 sequence detection system, a branched DNA signal amplification assay, and an Amplicor monitor test; and for HCV core protein by using a fluorescent enzyme immunoassay.Results: The detection range of the real‐time quantitative PCR was between 101–108 copies/mL of HCV‐RNA. Hepatitis C virus RNA was detectable in all 50 samples by the use of real‐time quantitative PCR, but was undetectable in 14 samples by the use of a branched DNA assay and in two samples by using the Amplicor monitor test; HCV core protein was undetectable in three samples. A significant correlation was found between the results of real‐time quantitative PCR and those of the three other assays: branched DNA assay (r = 0.837, P < 0.0001), Amplicor monitor test (r = 0.853, P < 0.0001), and HCV core protein concentrations (r = 0.549, P < 0.0001).Conclusions: Our results showed that the real‐time quantitative PCR was a highly sensitive assay for the measurement of HCV‐RNA.
An audit of metal stent palliation for malignant biliary obstruction
Authors: Mcdougall Neil I , Edmunds Simon EJ 
Published: March 2003

AbstractBackground and Aims: Endoscopic stent insertion is the optimum method of palliation for malignant biliary obstruction. Metal stents have several advantages over the polyethylene alternatives, but are significantly more expensive. It has been reported that patients need to survive beyond 6 months to make metal stents more cost‐effective. The aim of this study was to audit the performance of expanding metal biliary stents in our endoscopy unit, and to identify factors that might help with patient selection.Methods: The records of all patients who were selected for endoscopic metal stent insertion at the Royal Perth Hospital for malignant biliary obstruction between September 1994 and November 1998 were reviewed.Results: Thirty‐two patients (16 males, mean age 71 years (range 34–88 years) were identified and followed up for a mean 201 days (range 3–810 days). Fifteen (47%) had cholangiocarcinoma, 13 (41%) had pancreatic cancer, and four had metastatic disease as the cause of obstruction. Mortality rates after metal stent insertion were 16, 41 and 55% at 30, 90 and 180 days, respectively. In total, 24 (75%) patients died during the follow‐up period. Eleven (34%) stents became obstructed during follow up with a median time to occlusion of 125 days (range 44–729 days). Patients with cholangiocarcinoma had significantly longer survival than pancreatic cancer cases (median 286 vs 58 days, P = 0.04). No other factors were found to correlate with the survival or stent complications.Conclusions: Less than half of this mixed cohort survived beyond 6 months. Metal stent palliation of malignant biliary obstruction should probably be targeted at those with cholangiocarcinoma, as these patients tend to survive longer.
FR167653, a potent suppressant of interleukin‐1 and tumor necrosis factor‐α production, ameliorates colonic lesions in experimentally induced acute colitis1
Authors: Blandino Ivan I Pacheco , Otaka Michiro , Jin Mario , Komatsu Koga , Odashima Masaru , Konishi Noriaki , Sato Toshihiro , Kato Sayuri , Watanabe Sumio 
Published: March 2003

AbstractBackground: Interleukin‐1 (IL‐1) and tumor necrosis factor‐α (TNF‐α) are believed to play a significant role in the pathogenesis of inflammatory bowel disease (IBD). Interleukin‐1 and TNF‐α possess overlapping and synergetic activities inducing the production in cascade of other cytokines, adhesion molecules, arachidonic acid metabolites, as well as activating immune and non‐immune cells. FR167653 (C24H18FN5O2.H2SO4.H2O) is a newly synthesized organic compound with a potent inhibitory effect on IL‐1β and TNF‐α production. We hypothesized that the suppression of IL‐1 and TNF‐α induced by FR167653 could effectively attenuate experimentally induced colonic damage.Methods: Colonic lesions were induced in male Sprague–Dawley rats (250–300 g) by intrarectal instillation of 4% acetic acid. The effect of FR167653 administration at 1.0, 1.5, 2.5 mg/kg per 6 h subcutaneously on acetic acid‐induced colonic damage was assessed. The lesion area, microscopic findings, colonic and serum levels of TNF‐α and IL‐1β were also evaluated.Results: Treatment with FR167653 at 1.5 and 2.5 mg/kg per 6 h was able to ameliorate the gross macroscopic appearance of colonic lesions significantly, as well as ameliorate the lesion area induced by acetic acid. Colonic mucosal TNF‐α and IL‐1β levels of rats treated with FR167653 showed significant decrease in a dose‐dependent fashion compared with the control group. In the same manner, serum TNF‐α of rats treated with FR167653 was significantly lower than that of respective controls.Conclusions: Subcutaneous administration of FR167653 was able to ameliorate the acute changes induced by acetic acid instillation in a dose‐dependent manner. This is the first report to evaluate the dual inhibition of the production of IL‐1 and TNF‐α, offered by FR167653, in acute experimental colitis. Further studies are necessary to evaluate FR167653's efficacy and safety on long‐term conditions.
A Japanese herbal medicine, Sho‐saiko‐to, prevents gut ischemia/reperfusion‐induced hepatic microvascular dysfunction in rats
Authors: Horie Yoshinori , Kajihara Mikio , Yamagishi Yoshiyuki , Kimura Hiroyuki , Tamai Hironao , Kato Shinzo , Ishii Hiromasa 
Published: March 2003

AbstractBackground and Aim:We have reported that gut ischemia/reperfusion (I/R) causes hepatic microvascular dysfunction. Nitric oxide (NO) has been found to be a modulator of the adhesive interactions between leukocytes, platelets, and endothelial cells. Sho‐saiko‐to (TJ‐9), a Japanese herbal medicine, is reported to have protective effects against liver injury and to regulate NO production. The objective of this study was to determine whether TJ‐9 affects hepatic microvascular dysfunction elicited by gut I/R, and to investigate the role of NO.Methods:Male Wistar rats were exposed to 30 min of gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment and the number of non‐perfused sinusoids (NPS). Plasma tumor necrosis factor (TNF)‐α and alanine aminotransferase (ALT) activities were measured. In another set of experiments, TJ‐9 (1 g/kg per day intragastrically) was administered to rats for 7 days. In some experiments, dexamethasone (ST) (2 mg/kg per day intravenously) was administered.Results:In control rats, gut I/R elicited increases in the number of stationary leukocytes, NPS, and plasma TNF‐α and ALT activities, and these changes were mitigated by the pretreatment with TJ‐9. Pretreatment with an NO synthase inhibitor diminished the protective effects of TJ‐9 on the increase in leukostasis in the pericentral region, NPS, and plasma TNF‐α levels, but not its effect on the increase in leukostasis in the midzonal region, total number of stationary leukocytes, or plasma ALT activities. Pretreatment with TJ‐9 increased plasma nitrite/nitrate levels. The responses caused by gut I/R were attenuated by the pretreatment with ST. Pretreatment with an NO synthase inhibitor did not affect the effect of ST.Conclusions:These results suggest that TJ‐9 attenuates the gut I/R‐induced hepatic microvascular dysfunction and inflammatory responses such as TNF‐α production in the early phase via enhancement of NO production, and sequential hepatocellular damage via its anti‐inflammatory effect like corticosteroid effect.
Endothelin‐3 induces both human and opossum gallbladder contraction mediated mainly by endothelin‐B receptor subtype in vitro
Authors: AL‐JIFFRY BILAL O , TOOULI JAMES , SACCONE GINO TP 
Published: March 2003

AbstractBackground: Endothelins are produced by gallbladder epithelial cells, suggesting a role in the regulation of gallbladder function.Aims: To characterize the effect of endothelin‐3 (ET‐3) on human and Australian possum gallbladder contractility and identify the receptor(s) involved.Methods: Human and possum gallbladder muscle strips were exposed to cumulative concentrations
of ET‐3 (10 pmol/L–100 nmol/L). Strips were pretreated with either tetrodotoxin
(TTX) (1 μmol/L), the selective ET receptor antagonists BQ‐123 (ETA),
BQ‐788 (ETB), alone or together, or the mixed ET antagonist tezosentan
(all 1 μmol/L). Maximal changes in tone were measured and expressed as percentage
of carbachol (100 μmol/L)‐induced tone. ANOVA was used for statistical analysis.Results: Endothelin‐3 induced a concentration‐dependent increase in tone in both human and
pos‐sum strips (P < 0.05) and at 100 nmol/L represented 44.2 ± 4.5%
and 40.3 ± 4.6% of carbachol‐induced tone, respectively. The effect
on human strips was TTX insensitive, whereas the possum concentration–response
curve was shifted to the right. Individually, BQ‐123 and BQ‐788 shifted the human
concentration‐response curve to the right, but a greater inhibition by BQ‐788 was
achieved in the possum (P < 0.05). However, BQ‐123 plus BQ‐788 further
reduced the ET‐3 effect (P < 0.001) to a level comparable to that observed in the presence of tezosentan in both human and possum strips.Conclusion: Endothelin‐3 produces potent gallbladder contraction in vitro, acting mainly
via ETB receptors and also interacting with ETA receptors. The receptors are located on the smooth muscle, but in possum gallbladder, neural receptors may also be involved. These findings suggest that ET‐3 may regulate motility of possum and human gallbladder.© 2002 Blackwell Science Asia Pty Ltd
Management of peptic ulcer disease not related to Helicobacter
Authors: Yeomans Neville D 
Published: March 2003

Abstract  Most peptic ulcers not due to Helicobacter pylori are caused by non‐steroidal anti‐inflammatory drugs (NSAID), among which an important subset are due to vascular protective (‘low‐dose’) aspirin therapy. Non‐steroidal anti‐inflammatory drugs ulcers heal quite quickly when treated with a proton pump inhibitor (PPI), even though the NSAID is continued. If the NSAID can be stopped, the ulcers heal readily with either a PPI or a histamine H2‐receptor antagonist (H2‐RA). If anti‐inflammatory treatment is still needed after ulcers are healed, prophylactic co‐therapy with a PPI or misoprostol will reduce the risk of ulcer recurrence by about 60–80%. The alternative of switching to a highly selective cyclooxygenase‐2 inhibitor has been shown to reduce the risk of a complicated ulcer by about 50–60%, unless low‐dose aspirin treatment needs to be given as well for vascular disease. Idiopathic ulcers are becoming more frequent as H. pylori prevalence falls. Some may be sequelae of previous NSAID ulceration even though the NSAID has been ceased and the original ulcer had healed. These are best treated with an H2‐RA or a PPI, followed by long‐term maintenance with either of these (often in half the healing dosage) to prevent recurrence. Ulcers due to Zollinger–Ellison syndrome and other hypergastrinemia syndromes are rare, and largely beyond the scope of this review.© 2002 Blackwell Publishing Asia Pty Ltd
Advances in the management of irritable bowel syndrome
Authors: Kellow John E 
Published: March 2003

Abstract  Recent advances in different aspects of irritable bowel syndrome have led to a need to reassess the overall management of this common, complex disorder. Important areas include: first, the heterogeneity of symptom patterns and the role of specific diagnostic symptom criteria for use in both clinical practice and in clinical research; second, the growing interest in the potential interaction between ‘peripheral’ and ‘central’ pathophysiological mechanisms; and third, the development of novel and effective drugs designed to target specific receptor systems in the enteric nervous system. This review covers each of these aspects and emphasizes an approach to management of patients based on pathophysiological considerations.© 2002 Blackwell Publishing Asia Pty Ltd
Suppression of Helicobacter pylori‐induced interleukin‐8 production in gastric cancer cell lines by an anti‐ulcer drug, geranylgeranylacetone
Authors: Yoshimura Naoki , Suzuki Yasuo , Saito Yasushi 
Published: March 2003

Abstract
Background:
Geranylgeranylacetone (GGA) is an antigastritis and anti‐ulcer agent, with as yet an unknown mechanism of action. In this study, we investigated the effect of GGA on Helicobacter pylori‐induced interleukin (IL)‐8 production and IL‐8 mRNA expression in KATOIII cells, an established gastric cell line.
Methods:
Interleukin‐8 production in H. pylori‐infected KATOIII cells was measured by using enzyme‐linked immunoassay. The cytotoxicity of H. pylori on KATOIII cells was measured by a 51Cr release assay. The effect of GGA on H. pylori‐induced IL‐8 mRNA expression was measured by using northern blotting.
Results:
Interleukin‐8 production increased with time and H. pylori dose; the most significant increase was seen within 6–24 h of coculture with H. pylori. A dose of 0.1 mmol GGA suppressed IL‐8 production (P = 0.0077) and inhibited H. pylori‐induced IL‐8 mRNA expression (P = 0.0019). Furthermore, H. pylori‐induced gastric mucosal cell injury associated with IL‐8 and neutrophil activation was enhanced by NH3, and this enhancement was suppressed by GGA (P = 0.0043).
Conclusions:
Helicobacter pylori‐
infected gastric mucosal cells produce IL‐8, which can promote neutrophil activation, thus contributing to mucosal tissue injury associated with
H. pylori
infection. Agents like GGA, which can suppress IL‐8 production may have a protective role in the treatment of mucosal tissue damage seen in
H. pylori infection.© 2002 Blackwell Publishing Asia Pty Ltd
Non‐alcoholic fatty liver disease: An overview
Authors: Mulhall Brian P , Ong Janus P , Younossi Zobair M 
Published: March 2003

AbstractNon‐alcoholic fatty liver disease (NAFL) includes a spectrum of clinicopathological conditions with increasing prevalence in the developed world. Although steatosis alone seems to have a benign course, those patients with the diagnosis of non‐alcoholic steatohepatitis (NASH) can have a progressive course. Additionally, there is now evolving, indirect evidence that some of the patients with cryptogenic cirrhosis may be the result of ‘burned‐out’ NASH. Although NAFL and NASH are associated with insulin‐resistance syndrome, some patients with NAFL may have no obvious risk factors. Despite preliminary data from a number of pilot studies, no established therapies can be offered to patients with NASH. Over the next few years, a number of exciting research projects dealing with the epidemiology as well as the pathogenesis of NAFL are expected to be completed. It is anticipated that, through a better understanding of NAFL, more effective treatment protocols can be developed targeting only those patients with NASH that are at the highest risk for progression to cirrhosis and liver failure.© 2002 Blackwell Publishing Asia Pty Ltd
Effects of insulin‐like growth factors‐IR and ‐IIR antisense gene transfection on the biological behaviors of SMMC‐7721 human hepatoma cells
Authors: YANG JIAN‐MIN , CHEN WEN‐SHENG , LIU ZHI‐PENG , LUO YUAN‐HUI , LIU WEI‐WEN 
Published: March 2003

AbstractBackground and Aims: Insulin‐like growth factors (IGFs) are closely related to hepatocellular carcinoma growth. The study aim was to investigate the effects of IGF‐IR and IGF‐IIR antisense gene transfection on the biological behaviors of SMMC‐7721 human hepatoma cells.Methods: 7721‐IGF‐IR‐AS cells (human hepatoma SMMC‐7721 cells transfected with IGF‐IR antisense gene in our previous study) were transfected with a plasmid vector expressing IGF‐IIR cDNA in the antisense orientation by DOTAP liposome.7721‐IGF‐R‐AS cells were obtained by selection with G418 and hygromycin. Morphological changes of the cells were observed with optic and electron microscopes. In vitro growth of the 7721‐IGF‐R‐AS cells was observed with a soft agar test, MTT test and with naked mice inoculation test in vivo.Results: The following changes were found in the SMMC‐7721 cells after being transfected with the IGF‐IR and IGF‐IIR antisense genes: (i) the degree of malignancy of the tumor cells as revealed by cell morphology was ameliorated; (ii) the growth capability of the tumor cells in soft agar and their tumorigenicity in naked mice were significantly depressed. However, in the control groups, the SMMC‐7721 cells transfected both with IGF‐IR and IGF‐IIR sense cDNA and SMMC‐7721 cells transfected without any external genes, had no such changes. However, the cell growth curves had no significant differences among these three groups.Conclusion: IGF‐IR and IGF‐IIR antisense genes could significantly restrain the malignant behavior of human hepatoma cells and might be useful in investigating a potential route for hepatocellular carcinoma gene therapy.