bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biogeochemical contrasts between mid‐Cretaceous carbonate platforms and Cenozoic reefs
Authors: Iryu Yasufumi , Yamada Tsutomu 
Published: March 2003

AbstractCarbonate sediments of mid‐Cretaceous platforms on Allison and Resolution Guyots, Mid‐Pacific Mountains (ODP Leg 143, Sites 865, 866, 867 and 868) and those of upper Oligocene to Pliocene reefs of the Kita‐daito‐jima Borehole were studied. The mid‐Cretaceous platforms abound with abiotic (?) precipitates (ooids) and microbial carbonate grains/sediments (oncoids and ‘algal’ laminites), whereas the Cenozoic reefs consist mainly of coral and non‐geniculate coralline algae, major frame‐builders, benthic foraminifers and codiacean alga (Halimeda). There exists a remarkable difference in a mode of calcification between the mid‐Cretaceous platforms and Cenozoic reefs. The major reef‐builders of Cenozoic reefs precipitated carbonates within closed to semiclosed spaces within their bodies. In contrast, the mid‐Cretaceous platforms contain abundant grains/sediments formed by chemical (?) precipitations and biotic extracellular calcification. This contrasting feature reflects different modes of biogeochemical cycles between the mid‐Cretaceous and Cenozoic. Increased CO2 (degassed by active volcanism) and resultant high temperature and intensive weathering may have brought high concentration of Ca2+ and HCO3− into the mid‐Cretaceous sea, which enhanced abiotic and extracellular calcification. Inverse processes are true for the Cenozoic.
Hepatic fibrosis: From bench to bedside
Authors: SCHUPPAN DETLEF , POROV YURY 
Published: March 2003

Abstract Antifibrotic therapies are preferentially targeted to the activated mesenchymal cells in the liver that synthesize an excess of matrix proteins and resemble the myofibroblasts of healing wounds. These cells derive from normally quiescent hepatic stellate cells and (myo‐) fibroblasts. Their activation is triggered and maintained by several fibrogenic modulators and cytokines, but also by mechanical stress. Whereas many agents inhibit stellate cell/myofibroblast proliferation and collagen synthesis in vitro, only few of them are tolerable or effective in suitable animal models in vivo. An antifibrotic effect was demonstrated for silymarin, a defined mixture of flavonoids, sho‐saiko‐to which contains the related compound baicalein, for halofuginone, another plant‐derived agent, for the phosphodiesterase inhibitor pentoxifylline and for LU135252, an oral inhibitor of the endothelin‐A‐receptor. The retrospective finding that interferon‐α therapy for hepatitis C may halt or even reverse fibrosis, has to be confirmed in prospective randomized trials. Strategies to inhibit the profibrogenic cytokines transforming growth factor (TGF)‐β or connective tissue growth factor (e.g. by soluble decoy receptors) are evolving, but have not been convincing yet. Drug targeting to the fibrogenic liver cells is now possible by use of cyclic peptides that bind to receptors which are specifically up‐regulated on activated stellate cells, for example those for platelet‐derived growth factors or collagen type VI. In addition, blockade of such activation receptors can induce stress‐relaxation which reverts the fibrogenic cells to a fibrolytic, collagen degrading phenotype. Combined with the evolving validation of serological markers of fibrogenesis and fibrolysis an effective and individualized treatment of liver fibrosis can be anticipated.© 2002 Blackwell Publishing Asia Pty Ltd
Apolipoprotein A‐I in bile inhibits cholesterol crystallization and modifies transcellular lipid transfer through cultured human gall‐bladder epithelial cells
Authors: Secknus Roger , Darby Gwendolyn , Chernosky Ann , Juvonen Tatu , Moore Edward , Holzbach R Thomas 
Published: March 2003

Background: Apolipoprotein A‐I (Apo A‐I), conventionally purified by several steps including organic solvent‐delipidation from plasma, inhibits cholesterol crystallization in bile. To observe a significant effect in vitro, however, supraphysiological concentrations above 100 μg/mL are required. For this reason, this protein has not been considered to play a physiological role in vivo. In the present study, we examined the cholesterol crystal growth‐inhibiting effect of biliary Apo A‐I at its physiological concentration, the modification of transcellular transfer of biliary lipids through cultured human gall‐bladder epithelial cells (GBEC) by Apo A‐I at its physiological concentration and the binding and secretion of Apo A‐I by GBEC.Methods and Results: We purified biliary Apo A‐I to near homogeneity using immobilized artificial membrane chromatography. At 5 μg/mL, biliary Apo A‐I reduced cholesterol crystal mass by 50%, whereas plasma‐derived, solvent‐delipidated Apo A‐I had no effect. Using an antibody‐capture enzyme‐linked immunosorbent assay, we found reduced Apo A‐I concentrations in bile samples from gallstone patients when compared with bile samples from gallstone‐free controls (medians, 2.35 and 9.4 μg/mL, respectively). In a GBEC line, Apo A‐I (5 μg/mL) enhanced transfer of phospholipid and cholesterol from the mucosal to the serosal side of cell monolayers by approximately 50%. These cells appear to bind Apo A‐I reversibly in a dose‐ and time‐dependent manner, compatible with receptor‐type binding. Cultured human gall‐bladder epithelial cells also showed basal secretion of Apo A‐I, which was greatly increased by exposure to model bile solutions.Conclusions: Apolipoprotein A‐I in bile, thus, has both a direct effect on cholesterol crystal formation and enhances lipid removal from gall‐bladder bile by GBEC. This effect may be specific and receptor mediated. These observations support two separate roles for human biliary Apo A‐I and suggest that this protein may be important in preventing the formation of cholesterol crystals (the initial step in gallstone formation) in supersaturated bile.
Acquisition of resistance to apoptosis and necrosis by Bcl‐xL over‐expression in rat hepatoma McA‐RH8994 cells
Authors: Fukuda Kazunori , Yamamoto Masahiro 
Published: March 2003

Background: Bcl‐xL is the predominant anti‐apoptotic Bcl‐2 family member in the liver. Suppression of cell death promotes carcinogenesis and contributes to resistance to radiation and chemotherapeutic agents. Methods: Direct effects of Bcl‐xL protein on apoptosis and necrosis were investigated in rat hepatoma cells. Rat hepatoma cell line McA‐RH8994 cells were transfected with expression plasmids containing a whole coding sequence of rat bcl‐xL cDNA of sense orientation. Stable transfectant cell lines expressing bcl‐xL cDNA (designated as RH8994/Bcl‐xL‐S), or control plasmid DNA (designated as RH8994/pT) were established. Results: Cellular amounts of Bcl‐xL in RH8994/Bcl‐xL‐S cells were demonstrated to be more than 20‐fold that of RH8994/pT and parental cells. Three independent clones of RH8994/Bcl‐xL‐S were isolated and their susceptibility to various cell death stimuli was compared with that of the control cells. Transforming growth factor‐β1 and tumour necrosis factor‐α induced apoptosis dose dependently in these cells, but the 50% cytotoxicity concentrations of these factors in RH8994/Bcl‐xL‐S cells were more than 10‐fold higher than those in RH8994/pT and parental cells. Similarly, RH8994/Bcl‐xL‐S cells were shown to be significantly less susceptible to necrotic cell death induced by a calcium ionophore, A23187; a mutagen, N‐methyl‐N′‐nitro‐N‐nitrosoguanidine; and UV‐irradiation when compared with the control cells. Conclusions: Over‐expression of Bcl‐xL was shown to provide protection against apoptotic and necrotic cell death in rat hepatoma cells.
C ASE R	EPORT: Lamivudine therapy for submassive hepatic necrosis due to reactivation of hepatitis B following chemotherapy
Authors: Maguire Cliona M , Crawford Darrell Hg , Hourigan Luke F , Clouston Andrew D , Walpole Euan T , Powell Elizabeth E 
Published: March 2003

AbstractThis report describes the case of a 53‐year‐old woman who developed severe hepatitis following chemotherapy for breast carcinoma. The patient was hepatitis B surface antigen positive, e antigen negative and e antibody positive and had high levels of hepatitis B virus‐DNA. Liver biopsy revealed submassive hepatic necrosis, consistent with reactivation of hepatitis B. Treatment with lamivudine resulted in rapid loss of hepatitis B virus‐DNA, resolution of hepatitis and clinical recovery.
CASE REPORT: Adenocarcinoma arising in a Crohn’s stricture of the jejunum
Authors: Barwood Nigel , Platell Cameron 
Published: March 2003

AbstractPatients with Crohn’s disease affecting the small intestine appear to have an increased risk of developing adenocarcinoma. However, it remains an uncommon complication of an uncommon disease. The diagnosis is difficult to make both pre‐ and intra‐operatively, and is most commonly made postoperatively on histopathology. Hence, at laparotomy, consideration should be given to performing a frozen section on all small bowel strictures due to Crohn’s disease to define the presence of dysplasia or cancer. This will assist the surgeon in deciding whether to perform a stricturoplasty or a resection.© 1999 Blackwell Science Asia Pty Ltd
Percutaneous endoscopic gastrostomy: A review of indications, complications and outcome
Authors: Nicholson Fiona B , Korman Melvyn G , Richardson Maureen A 
Published: March 2003

AbstractPercutaneous endoscopic gastrostomy (PEG) was first described in 1980 as an effective method of feeding via the stomach in situations where oral intake is not possible. Its simplicity has led to its potential use in areas of dubious clinical benefit. Our unit has faced a major increase in referrals for PEG insertion over the last 2 years. For this reason we decided to audit our PEG insertion procedures with regard to indications, complications, outcome and follow up. We studied 168 patients who had an initial PEG insertion during the period 1 February 1996–31 January 1998. The medical records of these patients were reviewed with regard to the procedure, antibiotic use and complications. All patients (or carers or next of kin) were contacted by telephone to provide details regarding late complications and follow up. There were 87 females and 81 males (aged 16–98 years, median age 70 years). At 2 years, 67% were alive. The most frequent indication for PEG insertion was a neurological condition, the commonest being stroke. Most patients received either ticarcillin/clavulanic acid or cephazolin antibiotic prophylaxis before and after the procedure. In six patients (3.6%) infection at the PEG site required intravenous antibiotics. Four of these six patients did not have antibiotic prophylaxis. Only two deaths could be directly related to the procedure. Three died within 7 days of the procedure due to unrelated medical complications. Sixteen patients died within 1 month, the majority of these patients did not leave hospital. One‐fifth of the patients (35/168) had their PEG removed due to the reestablishment of oral feeding, with median time of use, 4.3 months. It is a safe, effective feeding method in the elderly, but experience with case selection, the procedure and careful follow up remain essential. The use of prophylactic antibiotics resulted in few significant infections of the PEG site. Up to one‐fifth of patients will require their PEG only for a short term.
Autoimmune cholangitis with features of autoimmune hepatitis: Successful treatment with immunosuppressive agents and ursodeoxycholic acid
Authors: Li Chung‐Pin , Tong Myron J , Hwang Shinn‐Jang , Luo Jiing‐Chyuan , Co Ruth L , Tsay Shyh‐Haw , Chang Full‐Young , Lee Shou‐Dong 
Published: March 2003

AbstractWe report a 42‐year‐old Chinese female with elevated serum levels of liver aminotransferases, alkaline phosphatase, γ‐glutamyl transpeptidase, cholesterol and immunoglobulin M. Serum antimitochondrial antibody was negative, but antinuclear antibody was strongly positive. Liver histology showed features of both autoimmune cholangitis and autoimmune hepatitis. Combination therapy with immunosuppressive (prednisone and azathioprine) and choleuretic agents (ursodeoxycholic acid) was given. Serum aminotransferases and biliary enzymes showed much improvement after treatment. A follow‐up liver biopsy showed improvement of both hepatic necroinflammation and bile duct damage. Biliary enzymes rose after withdrawal of the immunosuppressive agents and declined again with reinstitution of prednisone. This case demonstrates that a combination of immunosuppressive agents and ursodeoxycholic acid may effectively treat patients with features of both autoimmune cholangitis and autoimmune hepatitis.
K‐ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction
Authors: Lord Reginald Vn , O’Grady Roslynn , Sheehan Catherine , Field Andrew F , Ward Robyn L 
Published: March 2003

Abstract
Background
: Activation of the ras oncogene is commonly found in gastrointestinal tract cancers, but the role of ras in the development and progression of Barrett’s oesophagus and associated cancers is uncertain.
Methods
: The frequency of K‐ras codon 12 point mutations was assessed in 52 paraffin‐embedded tissues from 44 patients with oesophageal pathology. The specimens were classified pathologically as follows: adenocarcinoma of the oesophagus or oesophagogastric junction (n = 23), Barrett’s high‐grade dysplasia (n = 5), low‐grade dysplasia (n = 14), intestinal metaplasia (n = 4), normal oesophagus (n = 5) or normal stomach (n = 1). DNA was extracted from three consecutive sections of each paraffin block and mutations at bases 1 and 2 of K‐ras codon 12 were identified using a novel restriction endonuclease‐mediated selective polymerase chain reaction method.
Results
: Mutations were found in 7 of 23 (30.4%) adenocarcinomas and in 2 of 5 (40%) high‐grade dysplasia specimens. No mutations were found in specimens of low‐grade dysplasia, intestinal metaplasia without dysplasia, or normal oesophagus and stomach. There were no significant associations between the presence of mutations and clinicopathologic features in the patients with cancer. One patient who progressed from low‐grade to high‐grade dysplasia was found to have developed mutant K‐ras in the course of this transformation.
Conclusion
: These results suggest that K‐ras codon 12 mutations may occur frequently in patients with Barrett’s oesophagus with high‐grade dysplasia or adenocarcinoma of the oesophagus or oesophagogastric junction. K‐ras mutation may be a late event in the Barrett’s metaplasia–dysplasia– adenocarcinoma sequence.
Recurrence of biliary symptoms after endoscopic sphincterotomy for choledocholithiasis in patients with gall bladder stones
Authors: Yi Sun Young 
Published: March 2003

Abstract
Background
: There are a few reports regarding the long‐term results of endoscopic sphincterotomy (EST). However, little data is available on the recurrence of biliary symptoms after EST for choledocholithiasis, in patients with gall bladder stones.
Methods
: All patients had gall bladder and common bile duct stones (n = 60; age 32–84 years, median age 55 years), and had received an EST. One group of these patients had a laparoscopic or open cholecystecomy (n = 39; group A), while the other group did not (n = 21; group B). The follow‐up period ranged from 5 to 54 months (average 22 months).
Results
: Complications included the recurrence of common bile duct stones, recurrent acute cholecystitis, postoperative bile leakage and papillary stenosis. Nine patients (15%) had a recurrence of biliary symptoms. Two significant prognostic factors for the recurrence of biliary symptoms were identified by multivariate analysis; namely an intact gall bladder and a dilated common bile duct. The recurrence rate of biliary symptoms in group B was 20.4%, while in group A it was 10.3% (P < 0.01). Patients with a larger than average common bile duct diameter (mean diameter 14 mm) were more prone to the recurrence of symptoms than those with a smaller common bile duct diameter (mean diameter 10 mm, P < 0.016). The hospital stay period was 8.9 ± 3.1 days in group A and 2.8 ± 1.9 days in group B (P < 0.01).
Conclusions
: Biliary symptom recurrence occurred in a considerable proportion of patients after EST for the treatment of choledocholithiasis, in patients with gall bladder stones. The prognostic factors associated with the recurrence of biliary symptoms were an intact gall bladder and a dilated common bile duct diameter. Regardless of their short stay in hospital, non‐cholecystectomy patients had a higher rate of recurrent biliary symptoms than cholecystectomy patients.
Serum amino‐terminal propeptide of type III procollagen and 7S domain of type IV collagen correlate with hepatic iron concentration in patients with chronic hepatitis C following α‐interferon therapy
Authors: Shimizu Ichiro , Omoya Toshihiro , Takaoka Tukasa , Wada Satoshi , Wada Hisanori , Taoka Masayo , Hayashi Hideki , Hayashi Shigehito , Honda Hirohito , Sano Nobuya , Ito Susumu 
Published: March 2003

AbstractBackground: It has been reported that chronic infection with hepatitis C virus is associated with excess iron deposits in the liver of subjects who are neither alcoholics nor recipients of blood transfusions. However, little is known about the relationship between hepatic iron concentration (HIC) and the serum levels of hepatic fibrogenesis markers, which were caused by interferon therapy for chronic hepatitis C. Therefore, changes in the serum amino‐terminal propeptide of type III procollagen (P‐III‐P) and the 7S domain of type IV collagen (7S‐IV) in 16 patients treated with α‐interferon (IFN‐α) were studied, and their HIC and histological assessment evaluated. Hepatic iron concentrations were measured by using liver biopsy specimens obtained before and 6 months after the cessation of treatment.Methods and Results: Eight subjects (50%) who had normal alanine transaminase levels at 6 months after therapy showed significantly lowered HIC, and attenuated hepatic iron staining with decreased serum levels of P‐III‐P and 7S‐IV compared to the remaining subjects. The HIC was significantly correlated with the serum levels of P‐III‐P and 7S‐IV in all subjects.Conclusions: These findings suggest that IFN‐α treatment may decrease stimuli for fibrogenesis, at least in part, by reducing the hepatic iron deposition in patients with chronic hepatitis C.
Isocitrate dehydrogenase as a marker of centrilobular hepatic necrosis in the experimental model of rats1
Authors: Chung Young‐Hwa , Kim Jeong A , Song Byung‐Cheol , Song Il Han , Koh Moon Soo , Lee Han Chu , Yu Eunsil , Lee Yung Sang , Suh Dong Jin 
Published: March 2003

AbstractBackground and Aims: Serum alanine aminotransferase (ALT) and aspartate aminotransferase may not detect centrilobular hepatic necrosis (CLN) of a mild degree because these enzymes are known to be located predominantly in the periportal area. The aim of this study was to evaluate the usefulness of plasma isocitrate dehydrogenase (ICDH), which is located predominantly in the centrilobular zone, as a marker of CLN.Methods: In 56 adult male rats, centrilobular (n = 21) and periportal hepatic necrosis (PPN; n = 21) were induced experimentally by the intraperitoneal injection of bromobenzene and allylalcohol, respectively. Seven rats were used as solvent controls in both groups. Isocitrate dehydrogenase and ALT activities were measured in the plasma of rats with mild to moderate hepatic necrosis (17 CLN and 19 PPN). Isocitrate dehydrogenase and ALT were compared according to the sampling time (12, 24 and 48 h) and the location of hepatic necrosis. Ratios of ICDH/ALT were also calculated and compared between CLN and PPN groups at any time points.Results: Plasma ICDH activities were higher in rats with CLN than in those with PPN. In contrast, plasma ALT levels were higher in rats with PPN than in those with CLN at 12 h and were similar in both groups after 12 h. The ICDH/ALT ratios were much higher in rats with CLN compared to those with PPN (P < 0.001). The ratios were above 1.0 in 13 of 17 rats (77%) with CLN in contrast to none of the 19 rats with PPN.Conclusions: Our data suggested that the plasma ICDH/ALT ratio might be useful to differentiate between mild to moderate degrees of CLN from PPN, at least in the experimental model of rats.
Efficacy of treatment with chimeric monoclonal antibody (Infliximab) to tumor necrosis factor‐α for Crohn's disease in Japan: Evaluation by rapid turnover proteins, and radiologic and endoscopic findings
Authors: Asakura Hitoshi , Yao Tsuneyoshi , Matsui Toshiyuki , Koganei Kazutaka , Fukushima Tsuneo , Takazoe Masakazu , Hobara Reiko , Nakano Hiroshi , Okamura Shouzou , Matsueda Kei , Kashida Hiroshi , Makiyama Kazuya , Hiwatashi Nobuo , Kashiwagi Kazuhiro , Hibi Toshifumi 
Published: March 2003

AbstractBackground: Several studies have reported that the chimeric monoclonal antibody to tumor necrosis factor (TNF)‐α (Infliximab) is extremely valuable in the treatment of Crohn's disease. The aim of this study was to clarify the efficacy of this treatment in Japanese patients with Crohn's disease.Methods: A 12‐week multicenter, open trial of Infliximab was carried out and involved 25 patients with moderate to severe Crohn's disease who were resistant to conventional treatment. Patients received a single 2‐h intravenous infusion of Infliximab at a dose of 1, 3, 5 or 10 mg/kg bodyweight. Clinical evaluation of this treatment response was defined as a reduction in the index of the inflammatory bowel disease (IOIBD) and of the Crohn's disease activity index scores (CDAI), and in serum levels of C‐reactive protein (CRP) at 2, 4, 8 and 12 weeks, and as an increase in serum levels of rapid turnover proteins as well as improvement of radiologic and endoscopic findings at 4 weeks.Results: The IOIBD score was reduced after 4 weeks in 66.7% of the group receiving 1 mg/kg Infliximab, 71.4% in the group receiving 3 mg/kg, 80.0% in the group receiving 5 mg/kg, and 85.7% in the group receiving 10 mg/kg. Improvement was better maintained over 12 weeks in the 5 and 10 mg/kg groups compared with the 1 and 3 mg/kg groups. Similar results were obtained for the CDAI scores. Serum levels of rapid turnover proteins significantly increased to within the normal ranges after infusion in all groups. Seven of the 11 (63.6%) patients evaluated showed improvement of radiologic and endoscopic findings.Conclusions: A single infusion of Infliximab was effective for the treatment of Japanese patients with Crohn's disease. Serum rapid turnover proteins reflected the clinical response to antibody for TNF‐α well.