bluuebunny/crossref_metadata_2025_split huggingface dataset:
Efficacy of consensus interferon in the treatment of chronic hepatitis C
Authors: Kao Jia‐Horng , Chen Pei‐Jer , Lai Ming‐Yang , Chen Ding‐Shinn 
Published: March 2003

AbstractBackground and AimsConsensus interferon (CIFN) is a newly developed type I interferon. The aim of this study was to investigate the safety and efficacy of CIFN in the treatment of patients with chronic hepatitis C and to determine the predictors for sustained response.MethodsPatients were randomized to receive 3 μg or 9 μg CIFN three times a week for 24 weeks, followed by 24 weeks of observation. Efficacy was assessed by normalization of serum transaminase levels and disappearance of serum hepatitis C virus (HCV)‐RNA at the end of treatment and at 24 weeks after stopping treatment. Histologic response was defined as a decrease of at least two points in the Knodell necroinflammatory score at week 48 and was compared with baseline.ResultsThere were no serious adverse effects related to CIFN therapy. Overall, 44% of patients receiving 3 μg and 48% of patients receiving 9 μg had normalization of serum transaminase levels and disappearance of HCV viremia at the end of treatment. At 24 weeks after stopping treatment, 16% of patients in receiving 9 μg and 12% of patients receiving 3 μg had sustained responses. The histologic responses in patients receiving 9 μg and those receiving 3 μg were 60% and 36%, respectively. The necroinflammatory score was significantly reduced from baseline to week 48 in both groups. In addition, bodyweight < 60 kg and pretreatment serum HCV‐RNA level < 0.5 MEq/mL can serve as predictors for sustained response to CIFN treatment.ConclusionsThese findings suggest that 9 μg CIFN is safe and effective in the treatment of patients with chronic hepatitis C.
‘Pseudo‐aldosteronism’ induced by intravenous glycyrrhizin treatment of chronic hepatitis C patients
Authors: Rossum Tekla GJ Van , De Jong Frank H , Hop Wim CJ , Boomsma Frans , Schalm Solko W 
Published: March 2003

AbstractBackground and Aims: Treatment with intravenous glycyrrhizin reduces the progression of liver disease caused by chronic hepatitis C (HCV) infection. Glycyrrhetinic acid, a metabolite of glycyrrhizin, inhibits the renal conversion of cortisol to cortisone by inhibiting the enzyme 11β‐hydroxysteroiddehydrogenase in the kidney. The resulting excess of cortisol subsequently stimulates the mineralocorticoid receptor, leading to pseudo‐aldosteronism with hypertension, hypokalemia and eventually renin and aldosterone suppression. The aim of this study was to evaluate the occurrence of pseudo‐aldosteronism after treatment of chronic hepatitis C (HCV) patients with increasing doses of intravenous glycyrrhizin.Methods: Forty‐four HCV patients with chronic hepatitis or compensated cirrhosis were treated with intravenous glycyrrhizin 6 × 200 mg/week, 3 × 240 mg/week or 3 × 0 mg/week (placebo) for 4 weeks. In all patients, bodyweight, blood pressure and plasma concentrations of sodium, potassium, cortisol, DHEA‐S (dehydroepiandrosterone sulfate), renin and aldosterone were measured before, and at 0 and 4 weeks after treatment.Results: Within the placebo group, no significant changes were observed. Within the 1200 mg group systolic blood pressure was significantly higher at the end of treatment, while aldosterone was significantly lower; at the end of the follow‐up period these values had returned to baseline. The changes from baseline in systolic and diastolic blood pressure at the end of treatment were significantly higher in the 1200 mg group compared to the placebo group. The changes in aldosterone and potassium concentrations at the end of treatment increased with increasing dosage, although not significantly.Conclusion: Hepatitis C virus patients with chronic hepatitis or compensated cirrhosis show minor reversible symptoms of pseudo‐aldosteronism after treatment with 1200 mg glycyrrhizin weekly for 4 weeks.
Prevalence of hepatitis B or C virus infections in patients with non‐Hodgkin's lymphoma
Authors: Kuniyoshi Masami , Nakamuta Makoto , Sakai Hironori , Enjoji Munechika , Kinukawa Naoko , Kotoh Kazuhiro , Fukutomi Marie , Yokota Masaki , Nishi Hidehiro , Iwamoto Hiroaki , Uike Naokuni , Nishimura Junji , Inaba Shuichi , Maeda Yoshiaki , Nawata Hajime , Muta Koichiro 
Published: March 2003

AbstractBackground: Hepatitis C virus (HCV) and hepatitis B virus (HBV) are not only hepatotropic, but also lymphotropic viruses. Recently, some reports suggested that these viruses may participate in the development of malignant lymphoproliferative disorders.Methods: We investigated the prevalence of HCV or HBV infection in 348 patients with non‐Hodgkin's lymphoma (NHL). We also compared these prevalences with those in blood donors as a control group representing the general population in our area (n = 1 513 358). Next, we evaluated the clinical and pathologic characteristics of HCV‐ or HBV‐infected NHL cases. Non‐Hodgkin's lymphoma was classified according to the Working Formulation classification.Results: Thirty‐seven cases (14.9%) were found to be infected with HCV or HBV; of these, 20 (8.1%) were infected with HCV, and 17 (6.9%) with HBV. In male NHL patients, the rate of HCV infection was significantly higher than in an age‐ and sex‐matched population in the same area (P < 0.001, Mantel– Haenszel test). The rate of HBV infection also tended to be higher in the population (P = 0.0551). In contrast, in female NHL patients, the rate of HCV or HBV infection was not higher than in the general population. In HCV‐infected cases, 15 cases (75%) had B‐cell NHL and 16 cases (80%) were classified as being in the intermediate grade; B‐cell NHL comprised 83% of all NHL cases. In HBV‐infected NHL cases, 11 (65%) were of B‐cell type and 10 (58%) were classified as being in the intermediate grade.Conclusions: The high prevalence of HCV or HBV infections in our study population provides epidemiologic evidence suggesting that HCV and HBV infections may be involved in the development of a subgroup of NHL in males. Our investigation also revealed that both HCV‐ and HBV‐infected NHL patients showed certain similarities in clinical and pathologic manifestations.
Treatment of hepatocellular carcinoma by percutaneous laser hyperthermia
Authors: Christophi Christopher , Muralidharan Vijayaragavan 
Published: March 2003

AbstractBackground and Aim: The majority of patients with hepatocellular carcinoma (HCC) are unsuitable for partial liver resection or transplantation because of unfavorable tumor characteristics or underlying severe liver disease. Techniques of in situ tumor ablation may be an alternative to resection and have the advantage of reduced morbidity and mortality. Percutaneous laser‐induced hyperthermia produces predictable areas of tumor necrosis with minimal complications. This study assesses the effectiveness of percutaneous interstitial laser hyperthermia in eight patients with hepatocellular carcinoma occurring on a background of chronic liver disease.Methods: Patients with confirmed HCC with less than five tumor nodules of less than 7 cm maximum diameter were selected for treatment. Tumor response was monitored by dynamic CT, α‐fetoprotein levels and liver function tests. Patients were discharged within 24 h.Results: There were six males and two females, with liver disease of Child–Pugh grade C in five, and grade B in the others. Two patients had tumor recurrence following previous segmental resection. Four had solitary lesions, and individual lesion size ranged between 3 and 7 cm. Avascularity and significant necrosis of the tumor was achieved on all lesions less than 4 cm, but was unsuccessful in tumors greater than 5 cm despite repeated treatments. Survival of patients ranged from 3 to 18 months.Conclusions: Percutaneous laser hyperthermia produces significant tumor necrosis and has the advantage of low morbidity, and cost effectiveness. Further refinement is needed to achieve elimination of viable tumor cells at the tumor host interface by further knowledge of appropriate dosimetry levels, manipulation of blood flow and synergistic effects with other therapeutic modalities.
Effects and mechanisms of somatostatin analogs on apoptosis of pancreatic acinar cells in acute pancreatitis in mice
Authors: Yuan Yaozong , Gong Zihua , Lou Kaixian , Tu Shuiping , Di Zukang , Xu Jiayu 
Published: March 2003

AbstractAim:To investigate the effects of somatostatin analogs (SSa) on apoptosis of pancreatic acinar cells and apoptosis‐regulated gene bax, and p53 in treating acute pancreatitis in mice.Methods:In cerulein‐induced pancreatitis, with or without treatment of somatostatin, analogs (Octreotide) in CD‐1 (BALB/c × DΒΑ/1) mice, apoptosis of pancreatic acinar cells was detected by using the TdT‐mediated dUTP nick‐end labeling (TUNEL) method, and the expression of apoptosis‐regulated gene bax and p53 was determined by using the streptavidin‐peroxidase immunohistochemical technique and the RT‐PCR method, respectively.Results:On HE staining, acinar cells in the pancreas showed pyknotic nuclei and the formation of apoptotic bodies, which are the typical morphological features of apoptosis. Regarding TUNEL use, the apoptotic index of pancreatic acinar cells in the non‐treated group at 5 and 14 h after induction of acute pancreatitis was significantly lower than those of the SSa‐treated group, respectively (P < 0.01). On immunohistochemistry and RT‐PCR, there was an expression of neither bax nor p53 in normal pancreatic tissues. The expression of bax in the SSa‐treated group at 5 and 14 h after treatment of SSa was markedly higher than those of the non‐treated group, respectively (P < 0.01), but there was no significant difference in the expression of p53 between the SSa‐treated group and the non‐treated group.Conclusions:The induction of apoptosis in pancreatic acinar cells injury to reduce inflammatory reaction might be one of the mechanisms of SSa in treating acute pancreatitis in mice, and the mechanisms of apoptosis probably correlated with the expression of apoptosis‐regulated gene bax, but have no relationship with the expression of p53.
Post‐partum acute exacerbation of chronic hepatitis in a hepatitis C‐carrier mother
Authors: Chen Jin‐De , Chung Jing‐Liang , Kao Jia‐Horng , Chen Ding‐Shinn 
Published: March 2003

AbstractHepatitis C virus infection is a global health problem; however, the interaction between pregnancy and chronic hepatitis C remains controversial. A Taiwanese woman with chronic hepatitis C had an uncomplicated pregnancy and gave birth to a female baby through spontaneous vaginal delivery. The serum levels of alanine aminotransferase and hepatitis C virus (HCV) RNA were measured before pregnancy, in the first and third trimesters, 1 and 3 months after delivery, respectively. During her pregnancy, the serum aminotransferase levels became normalized, while the serum HCV‐RNA levels declined significantly and consecutively with the lowest viral load in the third trimester. One month after delivery, she had an abrupt elevation of serum HCV‐RNA level, paralleling a hepatitis flare with serum aminotransferase level more than 20‐fold the upper normal limit. The serum HCV‐RNA levels declined thereafter, and serum aminotransferase levels became normalized 3 months postdelivery. She was infected with HCV genotype 1a throughout the entire follow‐up period, and other causes of hepatitis flare were excluded. In conclusion, post‐partum acute exacerbation of chronic hepatitis may occur in HCV‐carrier mothers, and an abrupt elevation of serum HCV‐RNA level may be associated with the acute exacerbation.
Enhancement of tumor radioresponse by combined chemotherapy in murine hepatocarcinoma1
Authors: Seong Jinsil , Kim Sung Hee , Suh Chang OK 
Published: March 2003

AbstractBackground and Aims: Recent studies have shown that local radiotherapy can be an effective component of the treatment for hepatocellular carcinoma. To further improve therapeutic efficacy, use of drugs that can beneficially interact with radiation has been suggested. The purpose of this study was to identify drugs that can enhance radioresponse of murine hepatocarcinoma.Methods: C3H/HeJ mice bearing 8 mm tumors of murine hepatocarcinoma, HCa‐I, were treated with 25 Gy radiation and one of the following drugs: 5‐Fu, 150 mg/kg; adriamycin, 8 mg/kg; cisplatin, 6 mg/kg; paclitaxel, 40 mg/kg; and gemcitabine, 50 mg/kg. Tumor response to the treatment was determined by the use of a tumor growth delay assay and by an enhancement factor. The apoptotic level was assessed in tissue sections. The expression of regulating molecules was analyzed by using western blotting for p53, Bcl‐2, Bax, Bcl‐XL, Bcl‐XS, and p21WAF1/CIP1.Results: Among the drugs tested, only gemcitabine enhanced the antitumor effect of radiation, with an enhancement factor of 1.6. The induction of apoptosis by a combination of gemcitabine and radiation was shown as only an additive level. In the analysis of radiation‐induced expression of regulating molecules, the most significant change by combining gemcitabine with radiation was the activation of p21WAF1/CIP1.Conclusion: Gemcitabine is the first to show an enhancement of radioresponse of murine hepatocarcinoma when combined with radiation. The key element of enhancement is thought to be p21WAF1/CIP1.
Alterations of telomerase activity and terminal restriction fragment in gastric cancer and its premalignant lesions
Authors: Yang Shi‐Ming , Fang Dian‐Chun , Luo Yuan‐Hui , Lu Rong , Battle Paul D , Liu Wei‐Wen 
Published: March 2003

AbstractAims: In order to explore the role of alterations of telomerase activity and terminal restriction fragment (TRF) length in the development and progression of gastric cancer.Methods: Telomerase activity was detected in 176 specimens of gastric mucosa obtained through an operation or endoscopical biopsy by using the telomeric repeat amplification protocol (TRAP) assay. Meanwhile, the mean length of TRF was measured with the use of a Southern blot in part of those samples.Results: Telomerase activity was detected in 14 of 57 (24.6%) chronic atrophy gastritis patients, six of 18 (33.3%) intestinal metaplasia patients, three of eight (37.5%) dysplasia patients and 60 of 65 (92.3%) gastric cancer patients, respectively. Normal gastric mucosa revealed no telomerase activity. No association was found between telomerase activity and any clinicopathological parameters. The mean TRF length was decreased gradually with age in normal mucosa and in gastric cancer tissue. Regression analysis demonstrated that the reduction rate in these tissues was 41 ± 12 base pairs/year. Among 35 gastric cancers, TRF length was shown to be shorter in 20 cases (57.1%), similar in 12 cases (34.3%) and elongated in three cases (7.6%), compared to the corresponding adjacent tissues. The mean TRF length tended to decrease as the mucosa underwent chronic atrophy gastritis, intestinal metaplasia, dysplasia and into gastric cancer. The mean TRF length in gastric cancer was not statistically correlated with clinicopathological parameters and telomerase activity.Conclusions: Our results suggest that telomerase is expressed during the early stage of gastric carcinogenesis, and that the clinical significance of TRF length appears to be limited in gastric cancer.
Expression of B7 costimulatory molecules by cells infiltrating the colon in experimental colitis induced by oral dextran sulfate sodium in the mouse
Authors: Grose Randall H , Howarth Gordon S , Xian Cory J , Hohmann Arthur W 
Published: March 2003

AbstractBackground and Aim:T‐cell activation, mediated by the interaction with major histocompatibility complex (MHC)‐peptide complexes and B7 costimulatory molecules on antigen‐presenting cells, is an essential event in the pathogenesis of inflammatory bowel disease (IBD). We investigated the expression of B7 costimulatory molecules on cells in the colon in an experimental mouse model of IBD to determine whether the B7/ligand interaction could provide a target for therapeutic intervention in IBD.Methods:Experimental colitis was induced in mice by oral consumption of water substituted with 5% dextran sulfate sodium (DSS). Mice (n = 4) were killed 1, 2, 3, 4 and 7 days after commencing DSS consumption, and colonic tissue was collected and examined immunohistochemically for T cells, B cells, macrophages and cells expressing B7‐1 or B7‐2.Results:Compared to control mice drinking water, macrophage numbers in the colonic epithelium were elevated sevenfold by day 1 and T cells were elevated threefold by day 3 following commencement of DSS consumption. Numbers of infiltrating B7‐positive (B7+) cells were not significantly elevated until day 7 when B7‐1+, B7‐2+ cells and macrophages were increased 20‐fold compared to normal mice.Conclusion:These results demonstrate that an initial and rapid infiltration of the colonic epithelium by B7‐negative macrophages is followed by an infiltration of T cells and subsequent upregulation of the B7 costimulatory molecules potentiating the inflammatory reaction in this disease model. These results suggest an intervention strategy based on the blockade of the B7‐costimulatory axis could find application in the treatment of inflammatory bowel disease.
Synchronous triple cancers at middle and lower esophagus and stomach with different histological features and genetic alterations
Authors: CHANG YU‐TING , TSAI CHUN‐I , YANG TZENG‐HUEY , SHIH CHIA‐WEN , WU MING‐SHIANG , LIN JAW‐TOWN 
Published: March 2003

AbstractSynchronous multiple primary malignancies are relatively unusual. We describe a case of synchronous triple cancers located at the middle and lower esophagus and the stomach in a 59‐year‐old Taiwanese man who presented with progressive dysphagia, epigastralgia, and bodyweight loss in 1 month. Endoscopic and histological features, microsatellite instability status of genomic DNA, and immunohistochemical staining of p53, MUC2, Fhit, c‐erbB‐2 and E‐cadherin of all three cancers were demonstrated. We noted that these three cancers arose from different clones and that p53 mutation, instead of microsatellite instability, may play a major role in the development of multiple primary malignancies in this patient.
Fas (Apo‐1/CD95) and Fas ligand interaction between gastric cancer cells and immune cells
Authors: LEE TAE‐BUM , MIN YOUNG‐DON , LIM SUNG‐CHUL , KIM KYUNG‐JONG , JEON HO‐JONG , CHOI SEOK‐MIN , CHOI CHEOL‐HEE 
Published: March 2003

AbstractBackground and aims: It has been proposed that the expression of Fas ligand (Fas L) in tumors may play an important role in immune escape. This study was undertaken to test a ‘counterattack’ theory as a mechanism of immune escape in gastric carcinoma.Methods: Expression of Fas and Fas L was examined in the human gastric cancer cell lines

using reverse transcription–polymerase chain reaction. Cytotoxicity was determined

by the MTT [3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide] assay.

Apoptosis of target Jurkat cells was examined after coculture with the effector gastric

cancer cells in vitro. Immunohistochemical staining was performed for the

detection of Fas and FasL in tumor‐infiltrating lymphocytes (TIL) and gastric cancer

cells in vivo. Apoptosis was detected by terminal deoxynucleotidyl transferase

(TdT)‐mediated dUTP nick‐end labeling (TUNEL) method in vitro and in vivo.Results: Fas and FasL mRNA were found to be differentially expressed in gastric cancer cell lines. The coculture experiment showed that apoptosis of Jurkat was induced by a FasL‐overexpressing effector gastric cell SNU‐484. In a Fas‐expressing gastric cell SNU‐638, Fas expression was upregulated by the treatment of gamma‐interferon in a time‐ and concentration‐dependent manner. SNU‐638 treated with gamma‐interferon was more sensitive to anti‐Fas antibody‐mediated cytotoxicity than was the control cell line, suggesting an increase of functional Fas in gastric cancer cells. The expression of FasL in gastric cancer cells and of Fas in apoptotic TIL was also detected in

vivo.Conclusion: The data indicate that the FasL expression of gastric cancer cells supports a ‘counterattack

theory’ in gastric cancer cells and that the upregulation of Fas by IFN‐γ

in SNU‐638 may accelerate the apoptosis pathway through the Fas and FasL interaction

between gastric cancer cells and immune cells. This result is supported by the expression

of FasL in gastric cancer cells and apoptotic TIL in vivo. It is implicated that the different biological behaviors of gastric cancer cells could be at least in part explained by Fas and FasL interaction with immune cells.
Automated enzymatic mitochondrial antibody assay for the diagnosis of primary biliary cirrhosis: Applications of a routine diagnostic tool for the detection of antimitochondrial antibodies
Authors: HAZAMA HIROAKI , OMAGARI KATSUHISA , MASUDA JUN‐ICHI , OHBA KAZUO , KINOSHITA HIDEKI , MATSUO ISAO , ISOMOTO HAJIME , MIZUTA YOHEI , MURASE KUNIHIKO , MURATA IKUO , KOHNO SHIGERU 
Published: March 2003

AbstractBackground and Aims: An automated enzymatic mitochondrial antibody assay (EMA) kit for the diagnosis of primary biliary cirrhosis (PBC) has become commercially available recently. The aim of this study was to assess the clinical utility of the enzyme inhibition assay using this EMA kit for the diagnosis of PBC.Methods: We tested the immunoreactivity of sera from 54 histologically confirmed Japanese PBC patients to the 2‐oxo‐acid dehydrogenase complex (2‐OADC) enzymes by enzyme inhibition assay using commercially available TRACE (EMA) assay kit, and compared the results with those of indirect immunofluorescence, commercial enzyme‐linked immunosorbent assay (ELISA) using MESACUP Mitochondria M2 kit, and immunoblotting on bovine heart mitochondria.Results: Of the 54 sera, 43 (80%) were positive for antimitochondrial antibodies
(AMA) by immunofluorescence, 39 (72%) for enzymatic inhibitory antibody to
pyruvate dehydrogenase complex (PDC) by EMA, 33 (61%) for immunoglobulin
G (IgG) class anti‐PDC antibody by ELISA, and 53 (98%) for IgG, IgM, or IgA
class antibodies against at least one of the 2‐OADC enzymes by immunoblotting. Of
these, 43 (80%) were positive for IgG, IgM, or IgA class antibodies against
the E2 subunit of PDC (PDC‐E2) by immunoblotting. Thirty‐six of the 54 sera (67%)
showed identical results in all of the four assays, and 40 (74%) were all
negative or positive by EMA, ELISA, and immunoblotting in PDC‐relevant reactivity.
There was a significant correlation between the number of detected immunoglobulin
classes of anti‐PDC‐E2 by immunoblotting and anti‐PDC by EMA (P < 0.0001),
and a significant inverse correlation between IgG class anti‐PDC by ELISA and units
of PDC activity by EMA (r = −0.87, P < 0.0001).Conclusions: Although EMA had lower sensitivity compared with immunofluorescence and immunoblotting, this assay should be included among the routine diagnostic tools for the detection of AMA specific to PBC in clinical laboratories because of its high specificity, objective read‐out, and rapid turnaround time.© 2002 Blackwell Science Asia Pty Ltd