bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of association between cassava consumption and tropical pancreatitis syndrome
Authors: NARENDRANATHAN M. , CHERIYAN ASOK 
Published: March 2008

AbstractPrevious studies suggesting an association between use of tubers of cassava and tropical pancreatitis have been weak and conflicting. To test a possible association the cassava consumption of 40 consecutive cases of tropical pancreatitis syndrome were compared with age‐matched and sex‐matched healthy hospital visitors. The sociodemographic characteristics of the two groups were comparable. There was no association between cassava consumption and tropical pancreatitis syndrome (odds ratio = 0.56; 95% confidence interval = 0.21–1.45). Controlling for the possible confounding effects of low socio‐economic status and vegetarian diet did not alter the odds ratio. Testing for interaction also failed to show any effect modification of the association of cassava by economic status, chilli consumption or vegetarian diet. A significantly higher number of cases gave a positive family history of diabetes compared to the controls (odds ratio = 4.11; 95% confidence interval = 1.04–16.30; P= 0.04). In this case‐control study which had sufficient power to detect an odds ratio ? 3.5, there was no association between cassava consumption and tropical pancreatitis syndrome.
Clinicopathological study of minimum‐sized hepatocellular carcinoma: An approach to the definition of early hepatocellular carcinoma
Authors: KIM SOO RYANG , KANG KYONG BOO , SOH CHANG GYO , KIM JUNG HYO , HAYASHI YOSHITAKE , HANIOKA KEISUKE , ITOH HIROSHI 
Published: March 2008

AbstractClinicopathologic examination of 33 nodules from 23 cases of minimum‐sized hepatocellular carcinoma (HCC), less than 15 mm in diameter, was carried out by imaging and clinical follow up. On ultrasound (US), 16 hypoechoic nodules (48%) and 15 hyperechoic nodules (45%) on angiography 7 tumour stains (21%) and on computerized tomography (CT) 3 low density nodules (9%) were detected. Of 27 nodules on lipiodol CT (LpCT), 7 lipiodol‐deposited nodules (26%) were detected. Of 16 nodules on CO2US angiography (US‐angiography), 7 hypervascular (44%), 5 hypovascular (31%) and 4 isovascular nodules (25%) were detected. Of 13 nodules on CT during arterial portography (CTAP), 7 perfusion defect nodules (54%) were detected. The nodules were graded according to the Edmondson & Steiner Classification. Three nodules were resected; grossly, two were not distinct and one was poorly demarcated. Histologically, they were highly differentiated with irregularly‐thin trabecular‐patterned HCC where portal triads were detected. Cancer cells invaded the non‐cancerous liver cells by replacement, and the border between the cancerous and non‐cancerous regions was unclear; the latter region manifested chronic hepatitis or liver cirrhosis without hyperplasia. Minimum‐sized HCC is characteristically hypovascular in arterial and portal supply of blood, of multicentric origin and of a well‐differentiated pattern. Because the three resected nodules did not damage the liver acinus structure, they were considered to be an early stage of HCC.
Prediction of interferon‐alpha‐induced thyroid dysfunction in patients with chronic hepatitis C
Authors: MURAKAMI TSUKASA , MASUMOTO TOSHIKAZU , MICHITAKA KOJIRO , HORIIKE NORIO , HINO HISAKO , OKADA SHINICHI , KITAI KOICHIRO , ONJI MORIKAZU 
Published: March 2008

AbstractTo predict interferon‐alpha (IFN‐α)‐induced thyroid dysfunction, anti‐thyroglobulin (anti‐TgAb) and anti‐thyroid peroxidase antibodies (anti‐TPOAb) were determined by radio‐immunoassay (RIA) before IFN‐α treatment in 30 patients with chronic hepatitis C in whom the conventional haemagglutination test had failed to detect anti‐thyroid auto‐antibodies. Seven patients developed thyroid dysfunction during IFN‐α treatment (transient thyrotoxicosis in four patients, transient hypothyroidism in two, and Graves’ disease in one). Anti‐TgAb and/or anti‐TPOAb were detectable before IFN‐α treatment in six of these seven patients, while these antibodies were detected before treatment in only four of 23 patients who did not develop any thyroid dysfunction. The prevalence of these antibodies was significantly higher (P= 0.002) in the former group of patients than in the latter. In four patients with detectable anti‐TgAb before treatment but no subsequent thyroid dysfunction, the antibody disappeared during IFN‐α treatment. Haemagglutination tests for anti‐thyroid microsomal antibodies have previously been reported to be a useful predictive marker of IFN‐α‐induced thyroid dysfunction. In conclusion, sensitive detection of anti‐thyroid auto‐antibodies using RIA may also be useful for the prediction of IFN‐α‐induced thyroid dysfunction in patients with a negative haemagglutination test.
Restoration of gap junctions in the regenerative process of ethanol‐induced gastric mucosal injury
Authors: ENDO KEIICHIRO , WATANABE SUMIO , NAGAHARA AKIHITO , HIROSE MIYOKO , SATO NOBUHIRO 
Published: March 2008

AbstractGap junctions mediate intercellular communication and play an important role in cell proliferation and differentiation. The present study examined the expression of the gap junction protein connexin 32 in rat gastric mucosa during the regenerative process of ethanol‐induced gastric mucosal injury. Absolute ethanol (0.5 mL/100 g bodyweight) was administered to rats via gastric intubation. Following the treatment, rats were killed periodically, and gastric tissues were processed for indirect immunofluorescence microscopy using an anti‐connexin 32 antibody. Haematoxylin and eosin (H&E), periodic acid Schiff (PAS) and Bromodeoxyuridine (BrdU) staining were also performed in serial sections. Gastric injuries were limited in the mucosal layer. The injury was most severe 1 h after treatment, and was completely resolved by the 4th day after treatment. The number of immunoreactive spots for gap junctions was markedly decreased 1 h after the ethanol treatment. Reappearance of these immunostaining gap junctions occurred with repair of the injury. The reappearance of connexin 32 after injury was delayed in comparison with both the histologic resolution of the injury and the normalization of PAS‐stained mucus. In contrast, the time course of reappearance of gap junctions closely paralleled the appearance of BrdU‐labelled cells. These results indicate that morphologic repair is different to the recovery of cell maturity and cell proliferation in the regenerative gastric mucosa.
Primary liver cancer is of multifactorial origin: Importance of hepatitis B virus infection and dietary aflatoxin
Authors: SARACCO GIORGIO 
Published: March 2008

AbstractPrimary liver cancer has a variable incidence worldwide, occurring most frequently in South‐East Asia and China, which indicates that environmental factors are important in its aetiology. Although hepatitis B virus and chemical agents are the major risk factors for primary liver cancer, current evidence strongly suggests that it is of multifactorial origin. Aflatoxins are thought to be important because they are common food contaminants and are potent liver carcinogens in a wide variety of animal species. Evidence for the possible interactions between aflatoxin and hepatitis B infection, and their effects on the prevalence of primary liver cancer, is obtained from animal data and epidemiological studies. The risk of developing primary liver cancer following exposure to hepatitis B infection and aflatoxin is shown to be increased and the possible molecular mechanisms involved are discussed.
Aflatoxin and p53 abnormality in duck hepatocellular carcinoma
Authors: IMAZEKI FUMIO , YOKOSUKA OSAMU , OHTO MASAO , OMATA MASAO 
Published: March 2008

AbstractRecent studies have revealed that a point mutation at codon 249 in the p53 gene predominates in hepatocellular carcinoma (HCC) cases from Southern Africa and China, where infection with hepatitis B virus (HBV) and contamination of aflatoxin B1 in food are risk factors for HCC. This unique mutation from G to T at the third base in codon 249 observed in human HCC cases is suggested to be linked to aflatoxin exposure. Six ducks with HCC, five of which were fed a diet containing aflatoxin B1 for 1–2 years, were analysed for the presence of point mutations at this codon of the p53 gene by polymerase chain reaction and direct nucleotide sequencing. None of the six ducks with HCC showed the change at this codon regardless of duck hepatitis B virus infection. This suggests that aflatoxin B1 itself might not be involved in the unique mutation at codon 249 in hepatocar‐cinogenesis, or that other factors coincident with aflatoxin may be responsible for this unique mutation.
Clinical and radiological pictures of hepatocellular carcinoma with intracranial metastasis
Authors: YEN FU‐SHUN , WU JAW‐CHUNG , LAI CHUNG‐RU , SHENG WEN‐YANG , KUO BENJAMIN ING‐TIAU , CHEN TRONG‐ZONG , TSAY SHYH‐HAW , LEE SHOU‐DONG 
Published: March 2008

AbstractHepatocellular carcinoma (HCC) with extrahepatic spreading is not uncommon. In order to delineate the clinical and radiological pictures of HCC with intracranial metastasis, 33 documented cases were analysed. Eighteen had brain parenchymal metastasis without skull involvement; the other 15 cases disclosed skull metastasis with brain invasion. The underlying HCC are mainly of expanding (13/33, 39.4%) and multifocal (13/33, 39.4%) types. Eighteen cases (18/33, 54.5%) had mental changes not related to hypoglycaemia or hepatic encephalopathy. Eighteen cases (18/20, 90%) disclosed hyperdense mass lesions by non‐contrast computed tomography (CT) scans and 17 cases showed homogeneous enhancement (17/22, 77.3%) by post‐contrast CT images. In the non‐skull involved group, five cases (5/12, 41.7%) disclosed ring‐shape enhancement and 14 cases (14/16, 87.5%) had perifocal oedema, which were not seen in the skull involved group. Eight cases (8/33, 24.2%) presented as intracerebral haemorrhage. Twelve (12/33, 36.4%) died of brain herniation. Most (14/18, 77.8%) non‐skull involved cases had simultaneous lung metastasis without bony metastasis, while the skull involved group often (10/15, 66.7%) disclosed extracranial bony metastasis without lung metastasis. The difference in extracranial metastasis was statistically significant (P<0.05). The multivariate survival analysis disclosed that lower lactate dehydrogenase level (≤316 U/L, P= 0.029) and treatments (surgery or radiation, P= 0.001) were positively associated with longer survival.In conclusion, HCC with intracranial metastasis is symptomatic and life‐threatening. Half the cases may come from pulmonary metastasis and the other half may be from bony metastasis. Brain irradiation or surgery can prolong their survival.
Effect of hepatitis C antibody screening in blood donors on post‐transfusion hepatitis in Taiwan
Authors: WANG JIN‐TOWN , WANG TEH‐HONG , LIN JAW‐TOWN , LEE CHA‐ZE , SHEU JIN‐CHUAN , CHEN DING‐SHINN 
Published: March 2008

AbstractA national screening programme for antibody to hepatitis C virus (HCV) in blood donors in Taiwan began in July 1992 using a second‐generation immunoassay. To study the impact of this screening on post‐transfusion hepatitis in Taiwan, a prospective study on post‐transfusion hepatitis, that was started in 1987, was continued. As of June 1994, 245 patients who received a blood transfusion after July 1992 had completed a follow‐up period for more than 6 months post‐transfusion. Of them, seven (2.8%) recipients developed acute post‐transfusion hepatitis. The hepatitis in six cases could not be attributed to infection by hepatitis A, B, C, D, E viruses or cytomegalovirus (CMV) or Epstein‐Barr virus (EBV). The remaining patient seroconverted to both IgG and IgM anti‐CMV. All seven patients recovered in 6 months without development of chronicity, and the mean peak alanine aminotransferase level was lower compared with that of the cases before anti‐HCV screening (i.e. pre‐July 1992). These results indicate that the current anti‐HCV screening has effectively interrupted HCV transmission through blood transfusion in Taiwan.
Effect of changes in vascular tone on the haemodynamic characteristics of the portal vascular bed of the isolated perfused rat liver
Authors: GROSSMAN HOWARD J , GROSSMAN VIRGINIA L , BHATHAL PRITHI S 
Published: March 2008

AbstractThe effect of altered vascular tone on the haemodynamic characteristics of the intrahepatic portal vascular bed was studied in the isolated perfused rat liver preparation. The relationship between portal venous inflow (Q) and portal perfusion pressure (P) was determined in the presence of a maximally effective concentration of a vasoconstrictor agent (noradrenaline, NAmax, 3 × 10−5mol/L), an intermediate concentration (NAmed, 1 × 10−6mol/L) or a vasodilator agent (papaverine, PAP, 6 × 10−4mol/L). At flow rates greater than 20 mL/min, the pressure‐flow relationship could be regarded as linear (P < 0.001), with mean values for the extrapolated intercept with the pressure axis (Po) of 6.8 ± 0.9 mmHg for NAmax, 4.5 ± 0.5 mmHg for NAmed, and 1.65 ± 0.05 mmHg for PAP‐treated preparations. Over the full flow range (0–70 mL/min), in both NA‐ and PAP‐treated preparations, portal vascular conductance (G = Q/P) was related directly to perfusion pressure. Thus, G = C.P, where C is a constant (mean values for NAmax, NAmed, and PAP‐treated preparations were 0.0090 ± 0.0020, 0.023 ± 0.005, and 0.26 ± 0.02 mL/min per g per mmHg2, respectively). It is concluded that both C and Po may be useful indices of tone in the isolated perfused rat liver, and that analysis of hepatic portal haemodynamics in this manner may have considerable practical value in studies of the action of vasoactive agents.
Hepatitis C and liver transplantation
Authors: CHAZOUILLERES OLIVER , WRIGHT TERESA L 
Published: March 2008

AbstractHepatitis C virus (HCV) is important to the liver transplant recipient for several reasons. First, chronic HCV infection is a frequent cause of end‐stage liver disease in North America and Europe, where the majority of liver transplants are performed. Second, recurrence of HCV after liver transplantation is almost universal so that many liver transplant recipients with and without overt hepatitis are viraemic. Third, HCV infection in the organ donor and/or in the blood transfused in the peri‐transplant period make acquisition of HCV possible. Finally, liver transplantation for chronic HCV infection represents a major financial burden to the health‐care system in the USA and worldwide.Histological hepatitis not due to HBV or cytomegalovirus (CMV) is present in 14–35% of allografts from patients undergoing liver transplantation, and the majority of this is due to HCV infection. HCV infection recurs post‐transplant in almost all patients with pre‐transplant infection. Proof that HCV does recur has been provided by the sequencing of the hypervariable domain of the E2/NS1 region. The magnitude of HCV infection is underestimated by using serological assays in this immunosuppressed population. Using the b‐DNA assay, HCV‐RNA levels have been shown to increase in patients with recurrent infection.The long‐term consequences remain to be defined but post‐transplantation HCV infection is generally much less devastating than post‐transplantation HBV infection, and many patients have clinically silent disease. It is likely that a carrier state exists in immunosuppressed transplant recipients since high HCV‐RNA levels occur in the absence of liver damage. In one study, 1, 2 and 3 year patient survival rates were shown to be comparable in patients with chronic active HCV infection and with cryptogenic cirrhosis (94, 89 and 87%, and 84, 84 and 73%, respectively). A more recent study from the University of Pittsburgh which compared the outcome of a larger number of HCV‐infected patients (n= 237) with a large number of control patients with non‐viral disease (n= 801), showed that indeed HCV infection does impact negatively on both patient and graft survival (1, 2 and 3 year patient survival in the study and control groups of 78, 68 and 66% and 84, 82 and 78%, respectively, P= 0.001). Undoubtedly with time, the full impact of recurrent HCV infection will become apparent, although short‐term survival is sufficiently good to warrant continued transplantation of this group of patients.While the disease course in many patients is benign, aggressive post‐transplant HCV infection leading to liver failure is well documented. Factors which determine why some patients are more susceptible to liver damage than others are currently under study. It is likely that many interrelated variables are involved, including the level of pre‐transplant viraemia, genotype of the virus, amount of post‐transplantation immunosuppression, and ability of the host immune system to recognize HCV and mount an immune response.
New observations on cytoskeleton and fenestrae in isolated rat liver sinusoidal endothelial cells
Authors: BRAET FILIP , ZANGER RONALD DE , CRABBÉ EVELYNE , WISSE EDDIE 
Published: March 2008

AbstractFenestrae control the exchange of fluids, dissolved compounds and small particles between the blood and the space of Disse, and are primarily limited at one side by parenchymal cells. We recently described a simple and rapid method for the isolation, purification and cultivation of rat liver sinusoidal endothelial cells. With regard to the purity and morphology of liver endothelial cells, a detailed microscopic study was performed. Purity and viability after selective adherence was 74 and 95%, respectively. Liver endothelial cell purity was further enhanced to about 95% during adherence and spreading on collagen after 8 h of culture. Liver endothelial cells isolated by this method provide a viable cell population, enabling the study of structure and function of these cells in vitro. We investigated the cytoskeleton associated with fenestrae and sieve plates of liver endothelial cells. Cultured cells were slightly fixed and treated with cytoskeleton extraction buffer containing 0.1 % Triton. Whole mounts of extracted liver endothelial cells were prepared for scanning and transmission electron microscopy. Extracted liver endothelial cells show an integral, intricate cytoskeleton. Sieve plates and fenestrae are clearly delineated by cytoskeleton elements. Fenestrae are surrounded by a filamentous, fenestrae‐associated cytoskeleton ring with an average filament thickness of 16 nm. Additionally, sieve plates are surrounded and delineated by microtubuli, which form a network together with additional branching cytoskeletal elements. Microtubuli are sometimes found delineating linear arrangements of fenestrae. In conclusion, liver endothelial cells possess a cytoskeleton, that defines and supports sieve plates and fenestrae. Fenestrae‐associated cytoskeleton rings are involved in determining the size of fenestrae. The fenestrae‐associated cytoskeleton therefore probably controls the important hepatic function of endothelial filtration.
Role of Ito cells in the degradation of matrix in liver
Authors: ARTHUR MICHAEL JP 
Published: March 2008

AbstractLiver fibrosis is a dynamic process caused by changes in not only the synthesis of matrix proteins but also their degradation. Current evidence indicates that Ito cells, when activated to a myofibroblastic phenotype, play a very active role in regulating matrix degradation in liver. This is mediated via their ability to synthesize and release several members of the matrix metalloproteinase family, a class of enzymes which are responsible for degradation of matrix proteins in the extracellular space. Activated Ito cells have been demonstrated to release prostromelysin, progelatinase A and the pro‐enzyme form of interstitial collagenase. In addition, these cells can express appropriate systems for cleaving pro‐metalloproteinases to active forms (e.g. the plasminogen activator system, urokinase) as well as specific tissue inhibitors of the activated metalloproteinases (TIMP). In the early phases of liver injury, enzymes with the ability to degrade components of normal liver matrix are expressed (stromelysin and gelatinase A). In contrast, in the fibrotic phase of liver injury, during which fibrillar collagens accumulate, there is little (if any) expression of interstitial collagenase but marked expression of TIMP. These findings suggest that metalloproteinases and their inhibitors play a significant role in liver injury and fibrosis.
Non‐invasive means to study the functional status of sinusoidal liver endothelial cells
Authors: SMEDSRØD BÅRD 
Published: March 2008

AbstractCirculating connective tissue macromolecules are efficiently eliminated by receptor‐mediated endocytosis in liver endothelial cells (LEC). In patients with a seriously diseased liver, for example in liver cirrhosis or when a transplanted liver is about to be rejected, dysfunctional LEC or altered blood perfusion through the liver results in significantly increased serum levels of connective tissue macromolecules and other substances that are normally taken up by LEC. With the aid of high affinity antibodies or other kinds of binding proteins it has been possible to measure a number of connective tissue macromolecules in the blood, and some of these substances have been used to diagnose serious liver disease. However, the metabolic patterns of these molecules are such that it is difficult to extrapolate directly on the basis of increased serum levels to conclude that the main underlying cause of increased serum levels is dysfunctional LEC. Elevated serum levels of many connective tissue proteins may reflect either increased synthesis, increased release from cell or tissue depots, and/or decreased removal by LEC. Therefore, to use measurement of serum connective tissue molecule levels as indicators of LEC function, it is imperative to know the catabolic routes of these substances in health and disease. Due to the fact that we presently know more about the total metabolic pattern of hyaluronan (HYA) than of other connective tissue macromolecules that are cleared solely by LEC, serum HYA should be preferentially used to monitor the function of LEC, in particular in liver transplantation and cirrhosis.
Construction of retroviral vectors to induce strong hepatoma cell‐specific expression of cytokine genes
Authors: CAO GUANGWEN , KURIYAMA SHIGEKI , DU PING , SAKAMOTO TAKEMI , YANG WENGUO , MASUI KAZUHIRO , QI ZHONGTIAN 
Published: March 2008

ABSTRACTContinuing advances in molecular biology have provided tools for a promising approach to the treatment of cancer. Among the various strategies of gene therapy for cancer, many are aimed at killing tumour cells indirectly by the induction or reinforcement of a host immune response by gene transduction of various cytokines, major histocompatibility complex or immune accessory molecules. In the present study, we selected the tumour necrosis factor‐α, interleukin‐2 and interleukin‐3 genes as potential cytokine genes to induce antitumour effects. We constructed retroviral vectors carrying these cytokine genes under the control of the murine albumin enhancer and promoter and retrovirally transduced these genes into hepatoma and non‐hepatoma cell lines. Strong expression of the cytokine genes was induced in transduced hepatoma cells, while no evident expression was detected in transduced non‐hepatoma cells. These results demonstrate the hepatoma‐specific expression of cytokine genes and imply the feasibility of in vivo gene transfer into hepatomas without affecting any other tissues. Furthermore, these cytokine genes were expressed much more intensively when they were derived from the albumin enhancer and promoter than when derived from the simian virus 40 early region promoter. These results indicate that transcriptional regulatory sequences specific for the target tissues could be preferable to viral promoters for the gene therapy of cancer.