bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence and risk factors of non‐alcoholic fatty liver disease among Korean adults
Authors: PARK SEUNG H , JEON WOO K , KIM SANG H , KIM HONG J , PARK DONG I , CHO YONG K , SUNG IN K , SOHN CHONG I , KEUM DONG K , KIM BYUNG I 
Published: February 2006

AbstractBackground and Aim:  Differences in the prevalence of non‐alcoholic fatty liver disease (NAFLD) between Eastern and Western populations are primarily attributable to differences in definitions and biased population selection. Thus, the aim of the present study was to accurately determine the actual prevalence of NAFLD by sonography and to characterize the risk factors for NAFLD.Methods:  The present cross‐sectional study was performed with data obtained from 6648 subjects, all of whom were older than 20 years of age (3530 men and 3118 women). The term ‘non‐drinker’ was applied to men who consumed less than 30 g alcohol/day and to women who consumed less than 20 g alcohol/day. Non‐alcoholic fatty liver disease was defined as a sonographically detected fatty liver in the absence of viral hepatitis in a non‐drinker.Results:  Of the 1613 subjects who were diagnosed with sonographic fatty liver, 1240 were non‐drinkers and had no viral hepatitis. Overall, the unadjusted and age‐adjusted prevalences of NAFLD were 18.7% (23% in men, 13.7% in women) and 16.1% (21.6% in men, 11.2% in women), respectively. Multivariate analysis revealed that several risk factors were profoundly associated with the prevalence of NAFLD, including obesity, insulin resistance, hyperlipidemia and hyperglycemia in both genders, as well as age, menopausal status and estrogen medication in women only.Conclusions:  These results demonstrate that the prevalence of NAFLD in Korean adults, according to sonographic surveys, is comparable to that seen in more developed countries. From the perspective of increasing obesity, the high prevalence rates noted in the study may herald an increased burden of chronic liver disease in the Korean population.
Short‐term effects of magnetic sacral dermatome stimulation for idiopathic slow transit constipation: Sham‐controlled, cross‐over pilot study
Authors: LEE KWANG JAE , KIM JIN HONG , CHO SUNG WON 
Published: February 2006

AbstractBackground and Aim:  An increase in recto‐sigmoid colon activity through electrical stimulation of the sacral dermatomes has previously been reported. It has not been evaluated whether or not sacral dermatome stimulation has beneficial effects on constipation symptoms and anorectal function in constipated patients. Our aim was to evaluate short‐term effects of magnetic stimulation of the sacral dermatomes on constipation symptoms and anorectal function in patients with idiopathic slow transit constipation.Method:  Fourteen patients with idiopathic slow transit constipation were enrolled. Constipation symptoms, stool form and anorectal function were assessed before treatment, and at 3 and 6 weeks of treatment. Six‐week treatment consisted of either a 3‐week period of sham treatment or a 3‐week period of magnetic stimulation of the S2‐S3 dermatomes, which was performed in a randomized cross‐over design.Results:  During the stimulation period, the frequency score of spontaneous bowel movements decreased in eight of the 14 patients (2.9 [2–3]vs 1.4 [0–2]), whose threshold volumes for urge to defecate and maximum tolerable volumes were significantly greater than those of the non‐responders, and significantly decreased at the end of treatment. The degree of straining on defecation also significantly decreased in the responders. Responders had shorter right colonic transit time and longer left colonic transit time compared to the non‐responders. Sham treatment did not affect constipation symptoms, stool form and rectal sensation.Conclusion:  Sacral dermatome stimulation may offer potential for therapeutic benefit for a subset of patients with idiopathic slow transit constipation, particularly constipated patients with rectal hyposensation or hindgut dysfunction.
Predictors of fibrosis in Asian patients with non‐alcoholic steatohepatitis
Authors: TSANG STEVEN WOON CHOY , NG WING FUNG , WU BRIAN PING YING , CHOW DAVID ALAN , LI ERIC TING HO , WONG TAK CHEUNG 
Published: February 2006

AbstractBackground and Aim: Non‐alcoholic steatohepatitis (NASH) is increasingly recognized as an important cause of chronic liver disease. However, data on Asians with NASH is lacking in the literature. The aim of the present study was to describe the clinical, biochemical and histological characteristics of NASH in Asians and to determine the predictors for septal fibrosis.Method: Sixty consecutive patients aged over 18 years with elevated serum alanine transferase, sonographic evidence of steatosis, and consent for liver biopsy were included. Patients with chronic hepatitis B or C, alcoholic, autoimmune, genetic, or drug‐induced liver disease were excluded. Clinical, biochemical and histological variables were tested for association with septal liver fibrosis (F2/3).Results: Median age of the cohort was 45.5 years (range 21–75 years) and 63% were male. Ninety percent of patients were obese (body mass index [BMI]≥ 25), 70% had hypertriglyceridemia, 68% had hypercholesterolemia, 58% had metabolic syndrome, 53% had hypertension, 47% had diabetes mellitus (DM), and 18% had obstructive sleep apnea. Sixty‐eight percent had gamma‐glutamyl transferase (GGT) ≥ 2 × upper limit of normal (ULN), 55% had alanine aminotransferase (ALT) ≥ 2 × ULN, and 23% had aspartate aminotransferase (AST) ≥ 2 × ULN. Of the 40 non‐diabetic patients undergoing oral glucose tolerance testing, 45% had normal tests, 30% had impaired glucose tolerance, 23% DM, and 2% impaired fasting glucose. Eighteen patients (30%) had septal fibrosis (F2/3), but none had cirrhosis. Necroinflammatory grade ≥ 2 (odds ratio [OR] 13), AST ≥ 2 × ULN (OR 5.3) and DM (OR 5) were significantly and independently correlated with septal fibrosis.Conclusion: Septal fibrosis is common in Asians with NASH. Necroinflammatory grade ≥ 2, AST ≥ 2 × ULN and DM are independent predictors for septal fibrosis.
Role of transferrin receptor 2 in hepatic accumulation of iron in patients with chronic hepatitis C
Authors: MIFUJI RUMI , KOBAYASHI YOSHINAO , MA NING , QIANG QIN LI , URAWA NAOHITO , HORIIKE SHINICHIRO , IWASA MOTOH , KAITO MASAHIKO , MALAVASI FABIO , ADACHI YUKIHIKO 
Published: February 2006

AbstractBackground and Aim:  Iron deposition in the liver is a common finding in patients with chronic hepatitis C (CH‐C). The mechanism of this hepatic accumulation of iron is not completely understood. This study assessed if the protein expression of transferrin receptor 2 (TfR2) is upregulated in the liver of patients with CH‐C and if TfR2 protein mediates iron accumulation during hepatitis C virus (HCV) infection.Method:  Liver specimens from patients with CH‐C that underwent interferon (IFN) therapy (n = 23) and from patients with CH‐B (n = 18) were evaluated. Hepatic expression of TfR2 protein was analyzed by immunohistochemistry. Total hepatic iron score (THIS) was evaluated by Prussian blue staining.Results:  TfR2 protein was expressed in the cell membrane and cytosol of hepatocytes. Cytosol TfR2 protein was found to co‐localize with Tf. THIS (P = 0.0198) and hepatic TfR2 (P = 0.0047) expression were significantly higher in CH‐C than in CH‐B. The change in THIS values (rho = 0.580, P = 0.0079) and the grade of histological activity (rho = 0.444, P = 0.0373) were significantly correlated with changes in TfR2 expression after IFN therapy.Conclusions:  The protein expression of TfR2 is significantly associated with iron deposition in the liver in patients with CH‐C. HCV infection may affect the hepatic expression of TfR2, leading to iron accumulation in the liver.
Fas‐associated phosphatase‐1 promotes Fas‐mediated apoptosis in human colon cancer cells: Novel function of FAP‐1
Authors: MIYAZAKI TAKAKO , ATARASHI YOSHINARI , YASUMURA SATOSHI , MINATOYA ISAO , OGAWA KOHEI , IWAMOTO MASAYA , MINEMURA MASAMI , SHIMIZU YUKIHIRO , SATO TAKA‐AKI , WATANABE AKIHARU , SUGIYAMA TOSHIRO 
Published: February 2006

AbstractBackground and Aim:  Fas‐associated phosphatase‐1 (FAP‐1) has been thought as an inhibitor in Fas‐mediated apoptosis. Here, we investigated the role of FAP‐1 in Fas‐mediated apoptosis of human colon cancer cells.Method:  The viability of four colon cancer cell lines treated with agonistic anti‐Fas antibody was determined using WST‐1 assay and cell death detection ELISA. pRc/CMV‐FAP‐1 was transfected to a FAP‐1‐negative, Fas‐resistant colon cancer cell line SW480 by lipofection and the clones expressing FAP‐1 protein were selected by limiting dilution. In the clones, expression of 550 genes was analyzed by cDNA microarrays. Protein expression of FAP‐1 and molecules related to apoptosis was examined by western blot.Results:  We obtained two FAP‐1 overexpressed clones which were much more susceptible to Fas‐mediated apoptosis than control cells. In the clones, caspase 8 and caspase 3 were fully activated by agonistic anti‐Fas antibody treatment. Bcl‐2 family proteins were not related to the high susceptibility of these clones, because caspase 9 was not activated. Transfection of FAP‐1 did not suppress the survival actions of insulin‐like growth factor (IGF‐1) which enhanced survival signal through Akt phosphorylation. Upregulation in 21 genes and downregulation in 29 genes was revealed by cDNA arrays. We confirmed protein expression of p21 and phosphorylated p21 were much more enhanced in the clones than in control cells.Conclusions:  Overexpression of FAP‐1 enhanced susceptibility to Fas‐mediated apoptosis in SW480 and upregulation of p21 may contribute to this phenomenon. Our results indicate a novel function of FAP‐1 in Fas‐mediated apoptosis of human colon cancer cells.
Slow‐wave photic stimulation relieves patient discomfort during esophagogastroduodenoscopy
Authors: NOMURA TSUTOMU , HIGUCHI KAZUHIDE , YU HIDENORI , SASAKI SHIN‐ICHI , KIMURA SHUJI , ITOH HIROYUKI , TANIGUCHI MICHIYO , ARAKAWA TETSUO , KAWAI KOKI 
Published: February 2006

AbstractBackground and Aim:  Although pretreatment with a sedative drug is effective in relieving pain during esophagogastroduodenoscopy (EGD), such drugs can cause significant side‐effects. The aim of this study was to examine the effect of slow‐wave photic stimulation on discomfort and/or pain felt during EGD.Methods:  Forty consecutive patients (25 men and 15 women) who underwent diagnostic EGD in our hospital were included in the study. Twenty patients received photic stimulation for 25 min, and underwent electroencephalographic recording, in addition to the usual premedications. Twenty control patients received the same treatment but without photic stimulation. All patients evaluated the discomfort/pain felt during endoscopy against a five‐grade scale in comparison with what they had experienced in their previous examination.Results:  Patients with an improved discomfort/pain score were 18/20 and 3/20 in the treated and control groups, respectively. Overall comparison of pain scores between both groups was significant (P < 0.0001). The proportion of slow‐wave activity recorded in patients’ electroencephalograms significantly increased in the treated group compared to control values (36.6 ± 6.8% vs 29.1 ± 3.4%, P < 0.001). There was a close correlation between the degree of discomfort/pain felt during endoscopy and the proportion of slow‐wave activity (P < 0.001).Conclusion:  Slow‐wave photic stimulation shows promise as a treatment for relieving the discomfort and/or pain felt by patients undergoing EGD.
Endoscopic characteristics and Helicobacter pylori infection in NSAID‐associated gastric ulcer
Authors: KAMADA TOMOARI , HATA JIRO , KUSUNOKI HIROAKI , SUGIU KUNIAKI , TANIMOTO TATSURO , MIHARA MITSUHIRO , HAMADA HIROSHIGE , KIDO SOICHIRO , DONGMEI QIAN , HARUMA KEN 
Published: February 2006

AbstractBackground and Aim:  Helicobacter pylori infection and non‐steroidal anti‐inflammatory drugs (NSAIDs) are deeply involved in the etiology of gastric ulcers. The aim of our study was to clarify the endoscopic characteristics and H. pylori infection status of NSAID‐associated gastric ulcers.Methods:  The study group comprised 50 patients (23 men, 27 women; mean age 66.5 years) with NSAID‐associated gastric ulcers and 100 sex‐ and age‐matched patients with gastric ulcer associated with other factors (control group). Ulcer morphology, size and number of lesions, onset site and incidence of hemorrhagic ulcers were investigated endoscopically in both groups. H. pylori infection was diagnosed by serology, histology and 13C‐urea breath test.Results:  Multiple lesions (68% vs 20%, P < 0.001), occurrence in the antrum (56% vs 6%, P < 0.001), and hemorrhagic ulcer (34% vs 4%, P < 0.001) were significantly more prevalent in patients with NSAID‐associated gastric ulcers than in patients with non‐NSAID‐associated gastric ulcer. The H. pylori infection rate was significantly lower in NSAID‐associated gastric ulcer patients than in non‐NSAID‐associated gastric ulcer patients (48% vs 96%, P < 0.001). In the NSAID‐associated gastric ulcer group, the prevalence of H. pylori infection was significantly lower in patients with ulcers in the antrum than in those with ulcers in the angulus or corpus (25% vs 77.3%, P < 0.001).Conclusions:  In contrast to non‐NSAID‐associated gastric ulcers, NSAID‐associated gastric ulcers frequently occur in the antrum with bleeding. The rate of H. pylori infection in NSAID‐associated gastric ulcers is significantly lower than that in non‐NSAID‐associated gastric ulcers.
Efficacy of interferon α‐2b and lamivudine combination treatment in comparison to interferon α‐2b alone in chronic delta hepatitis: A randomized trial
Authors: Canbakan Billur , Senturk Hakan , Tabak Fehmi , Akdogan Meral , Tahan Veysel , Mert Ali , Sut Necdet , Ozaras Resat , Midilli Kenan , Ozbay Gulsen 
Published: February 2006

AbstractBackground and Aim:  Delta hepatitis is characterized by rapidly progressive liver disease with adverse prognosis in most patients. Patients benefit from high doses and prolonged courses of interferon (IFN) therapy; however, lamivudine as a single agent has been disappointing. Data relating to the efficacy of IFN and lamivudine in combination is limited. The aim of this study was to test the efficacy of IFN‐α 2b and lamivudine combination treatment in comparison to IFN‐α 2b alone in patients with chronic delta hepatitis.Methods:  Twenty‐six patients with chronic delta hepatitis were randomized into two groups. Twelve patients received IFN‐α 2b alone (eight men, four women; mean ± SD age: 43.83 ± 8.57 years), and 14 patients received IFN‐α 2b plus lamivudine combination (seven men, seven women; mean ± SD age: 42.5 ± 11.02 years). The dose of IFN‐α 2b was 10 MU t.i.w. and of lamivudine was 100 mg/day. The groups were comparable in reference to serum alanine aminotransferase (ALT), aspartate aminotransferase, bilirubin, albumin levels, histological activity and stage. Four patients (33.3%) in the IFN group and two (14.3%) in the combination group had cirrhosis (P = 0.2). The duration of treatment was 48 weeks with an untreated follow‐up period of at least 96 weeks (mean ± SD, 3.1 ± 1.9 years). A liver biopsy was performed at the end of treatment.Results:  Eight patients from the IFN group and 11 from the combination group completed treatment. Serum ALT values became normal in 8/14 patients (57.1%) treated with IFN plus lamivudine and in 5/12 patients (41.7%) treated with IFN alone (P = 0.43). Serum hepatitis delta virus RNA was no longer detectable in nine of 14 (64.3%) patients treated with IFN plus lamivudine as compared to five of 12 (41.6%) patients treated with IFN alone (P = 0.024). In both groups female patients had significantly better virological response rate (P = 0.007). There was a significant improvement in histological activity in the combination group (mean decrease 5.27 ± 1.08 score, P = 0.001), but not in the IFN group (mean decrease 1.44 ± 1.59 score, P = 0.39). No significant improvement was observed in regards to fibrosis. Four of the 14 patients (28.6%) treated with combination therapy as compared to two of 12 patients treated with IFN (16.7%) were sustained virological responders (P = 0.47). The 5‐year survival rate was 65% in the IFN group and 85% in the combination group (P > 0.05).Conclusion:  Interferon and lamivudine in combination is an encouraging treatment method and may be superior to IFN alone in chronic delta hepatitis.
Surface structure of antral gastric mucosa represents the status of histologic gastritis: Fundamental evidence for the evaluation of antral gastritis by magnifying endoscopy
Authors: Kim Sunjin , Ito Masanori , Haruma Ken , Egi Yasuo , Ueda Hiroyuki , Tanaka Shinji , Chayama Kazuaki 
Published: February 2006

AbstractBackground:  Recent studies have demonstrated the diagnostic potential of magnifying endoscopy in cases of histologic gastritis. The aim of the present study was to clarify whether the mucosal surface structure reflects the degree of histologic gastritis below the surface.Methods:  Gastric biopsy specimens were obtained from 1018 Japanese patients and were stained with hematoxylin and eosin. In 863 sections examined, gastritis was graded by means of the updated Sydney system, and the surface structure was classified as one of four types: flat, irregular, papillary, or non‐structured. In addition, 103 patients underwent gastric examination by magnifying gastroscopy.Results:  The surface structure of most biopsy sections with normal mucosa and no Helicobacter pylori infection was classified as the flat type. Grades of histological gastritis were statistically lower in flat‐type sections than in other types. Histologic gastritis was found in 91% of sections with a non‐flat surface structure. Helicobacter pylori infection was confirmed in 96% of these cases. Most biopsy sections in patients with abnormal magnifying endoscopy features were of the non‐flat type and showed histologic gastritis.Conclusions:  The surface structure of the gastric mucosa reflects the status of histologic gastritis. Magnifying gastroscopy could be a useful non‐invasive method of diagnosing histologic gastritis.
Non‐steroidal anti‐inflammatory drugs have bacteriostatic and bactericidal activity against Helicobacter pylori
Authors: Shirin Haim , Moss Steven F , Kancherla Sandy , Kancherla Kevin , Holt Peter R , Weinstein I Bernard , Sordillo Emilia M 
Published: February 2006

AbstractBackground:  Helicobacter pylori infection and non‐steroidal anti‐inflammatory drugs (NSAIDs) are each associated with gastrointestinal mucosal damage, but the extent and direction of their interactions remain controversial. Therefore, the purpose of the present paper was to examine whether specific NSAIDs inhibit the growth of Helicobacter pylori in vitro.Methods:  Sodium salicylate, ibuprofen, indomethacin, the selective cyclooxygenase‐2 inhibitor NS‐398 and two derivatives of sulindac sulfoxide were tested against two laboratory strains of H. pylori, the mouse‐adapted Sydney strain, and against seven fresh clinical isolates of Helicobacter pylori. Possible effects on Campylobacter jejuni, Staphyloccoccus aureus, Escherichia coli, Salmonella typhimurium, and Shigella boydii were also examined.Results:  Certain NSAIDs possess antibacterial activity against Helicobacter pylori at therapeutically achievable doses; an effect that appears to be independent of cyclooxygenase enzymes inhibition. For Helicobacter pylori, >90% growth inhibition and bactericidal activity were observed consistently for sulindac sulfide at ≤70 µg/mL and sulindac sulfone at ≤175 µg/mL. The minimal inhibitory concentration against Helicobacter pylori was 125 µg/mL for ibuprofen, 100 µg/mL for indomethacin and 300 µg/mL for NS‐398 but much higher concentration of sodium salicylate (4000 µg/mL) and sulindac sulfoxide (≥1250 µg/mL) were required to inhibit the growth of Helicobacter pylori.Conclusions:  The decreased prevalence of Helicobacter pylori in specimens from some NSAID users and the chemopreventive effects of NSAIDs in gastric cancer may be related to inhibition of Helicobacter pylori growth.
Hepatitis B post‐partum e antigen clearance in hepatitis B carrier mothers: Correlation with viral characteristics
Authors: Lin Ho‐Hsiung , Wu Wen‐Yih , Kao Jia‐Horng , Chen Ding‐Shin 
Published: February 2006

AbstractBackground:  The purpose of the present paper was to correlate hepatitis B virus (HBV) genotype, e antigen titer, HBV‐DNA level and precore/basal core promoter mutations with post‐partum e antigen clearance in hepatitis B e antigen (HBeAg)‐positive carrier mothers.Methods:  A total of 40 consecutive HBeAg‐positive carrier mothers were studied from January 2002 to January 2003. The blood samples were taken at delivery, 3–4 months and at 1 year after delivery, and the follow‐up period was until 1 year after delivery. All sera were assayed for HBeAg, HBV‐DNA level, HBV genotype and precore/basal core promoter mutations. The correlation between HBV characteristics and post‐partum e antigen clearance was analyzed by Mann–Whitney, Pearson χ2 and multiple logistic regression tests.Results:  The mean age of the 40 HBeAg‐positive carrier mothers was 29.9 ± 5.3 years with a mean parity of 1.4 ± 0.7. Five of them (group I) had post‐partum e antigen clearance, which persisted thereafter, whereas the remaining 35 carrier mothers (group II) had persistent positivity of HBeAg during the follow‐up period. The prepartum comparisons of HBV characteristics between groups I and II were comparable in terms of demographics and distributions of HBV genotype and precore/basal core promoter mutations. In contrast, group I carrier mothers had lower HBeAg titer and HBV‐DNA level than group II carrier mothers (1:80 vs 1:4000, P = 0.02, and 3.75 × 105 vs 3 × 108 copies/mL, P = 0.028, respectively).Conclusions:  Post‐partum e antigen clearance in HBeAg‐positive carrier mothers is closely associated with prepartum low HBeAg titer or HBV‐DNA level.
Origin of neovascular structure in an early stage of hepatocellular carcinoma: Study of alpha‐smooth muscle actin immunohistochemistry in serial thin sections of surgically resected cancer
Authors: IKEDA KENJI , KOBAYASHI MASAHIRO , SAITOH SATOSHI , SOMEYA TAKASHI , HOSAKA TETSUYA , SEZAKI HITOMI , SUZUKI YOSHIYUKI , SUZUKI FUMITAKA , AKUTA NORIO , ARASE YASUJI , KUMADA HIROMITSU 
Published: February 2006

AbstractBackground:  To elucidate the origin of the neovascular structure found in well‐differentiated hepatocellular carcinoma (HCC), an immunohistochemical study was performed on sequential thin section specimens.Method:  Eleven surgically resected specimens of well‐differentiated HCC were analyzed for neovascular structure using monoclonal alpha‐smooth muscle actin (α‐SMA) antibody. Each paraffin specimen was serially sliced to a thickness of 3 µm for immunohistochemistry. When a ring‐shaped structure was found unrelated to portal triads on α‐SMA staining, it was regarded as abnormal neovascularity (non‐triadal vessel or unaccompanied vessel).Results:  All of the 11 liver cancers had thin‐walled, round‐ or oval‐shaped non‐triadal vessels in their well‐differentiated parts. Immunohistochemistry of serial thin sections of HCC showed that these non‐triadal vessels were connected to portal veins in portal triads in well‐differentiated cancer in a total of nine patients (81.8%). This type of neovascular structure found in a well‐differentiated cancer seemed to be a surviving portal vein among diminishing and disappearing arteries and bile ducts. All 11 tumors showed isovascular staining on ordinary digital subtraction angiography, and four of the tumors showed negative enhancement on intra‐arterial carbon dioxide‐enhanced ultrasonography or computerized tomographic (CT) hepatic arteriography, suggesting a relative arterial blood scarcity in the tumor nodules.Conclusion:  At an early stage of HCC, non‐triadal vessels originate from ordinary portal veins in intratumoral portal triads. This fact sufficiently explains the reason why a well‐differentiated liver cancer can sometimes show arterial blood paucity on CT arteriography or enhanced ultrasonography.