bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of Hepatitis B Virus DNA in Hepatocellular Carcinomas in Japan
Authors: Hino Okio , Kitagawa Tomoyuki , Koike Katsuro , Kobayashi Midori , Hara Mitsuru , Mori Wataru , Nakashima Toshiro , Hattori Nobu , Sugano Haruo 
Published: August 2008

Hepatitis B virus (HBV) DNA in hepatocellular carcinoma (HCC) and/or cirrhotic livers of Japanese patients in Japan was investigated by molecular hybridization utilizing a 32P-labeled cloned HBV DNA of adr subtype. Among 24 HCC cases, 9 (37.5%) were positive for serum HBsAg and 10 (41.7%), including 2 cases which were negative for serum HBV markers, were positive for tissue HBsAg in noncancerous portions of the liver. In the latter 10 cases, integrated HBV DNA was detected in HCC. The restriction pattern of integrated viral DNA was different from one case to another. In the noncancerous portion of these 10 HCC cases, free (3/10), random integration (2/10), or clonal integration (1/10) of viral DNA was demonstrated; no hybridization was detected in the remaining 14 HCC cases, either in cancerous or noncancerous portions.
Of 6 cases of liver cirrhosis, 2 were positive for serum and histochemical HBsAg; viral DNA was in free state. Viral DNA was not detected in pancreatic tissue in 5 HBsAg-positive cases.
The present results are in agreement with previous reports indicating a high frequency of integrated viral DNA in HBV-associated HCC and heterogeneity in the mode of integration. Our results differ in finding no HBV DNA in HCC cases not associated with HBV markers and in finding clonal populations of hepatocytes with integrated HBV DNA less frequently in the noncancerous portion of the liver of HBsAg carriers.
Renal Kallikrein Excretion in Cirrhotics with Ascites: Relationship to Renal Hemodynamics†
Authors: Pérez-Ayuso Rosa M. , Arroyo Vicente , Camps Jordi , Rimola Antoni , Costa Josep , Gaya Joan , Rivera Francisca , Rodes Joan 
Published: August 2008

To investigate if the renal kallikrein-kinin system may be involved in the homeostasis of renal perfusion in cirrhosis, urinary kallikrein activity was measured in 11 normal subjects, 31 cirrhotics with ascites and preserved rena plasma flow (548.2 ± 32.2 ml per min) and glomerular filtration rate (85.8 ± 3.4 ml per min), and 18 cirrhotics with functional renal failure (renal plasma flow: 229.9 ± 23.4 ml per min; glomerular filtration rate: 34.9 ± 3.3 ml per min). Plasma renin activity, plasma norepinephrine concentration and the urinary excretion of prostaglandin E2 were also measured in these subjects.
Cirrhotics without renal failure showed a significantly higher renin (4.9 ± 1.1 ng per ml per hr), norepinephrine (458.2 ± 50.4 pg per ml), urinary kallikrein (15.4 ± 1.8 pkat per min) and urinary prostaglandin E2 (0.52 ± 0.08 ng per min) than did normal subjects (1.08 ± 0.1 ng per ml per hr, 218.1 ± 18.2 pg per ml; 8.4 ± 1.4 pkat per min and 0.24 ± 0.02 ng per min, respectively). Cirrhotics with renal failure showed a significantly higher renin (16.1 ± 3.4 ng per ml per hr) and norepinephrine (739.4 ± 79.2 pg per ml), and a significantly lower urinary kallikrein (5.2 ± 0.6 pkat per min) and urinary prostaglandin E2 (0.15 ± 0.02 ng per min) than did normal subjects and cirrhotics without renal failure. Glomerular filtration rate correlated (p < 0.001) with urinary kallikrein (r = 0.53), urinary prostaglandin E2 (r = 0.55), plasma renin (r = -0.41) and norepinephrine (r = -0.44).
These results suggest that renal kallikrein-kinin system may be involved in maintenance of renal blood flow in cirrhosis with ascites, and that functional renal failure in these patients could be a consequence of impaired renal production of kallikrein and prostaglandins in the setting of activation of the renin-angiotensin and sympathetic nervous systems.
Mechanisms of the Impaired Diuretic and Natriuretic Responses to a Sustained and Moderate Saline Infusion in Rats with Experimental Cirrhosis
Authors: López-Novoa José M. , Santos Juan C. , Caramelo Carlos , Fernandez-Muñoz Dolores , Blanchart Alicia , Hernando Luis 
Published: August 2008

Kidney function and tubular handling of water and sodium by superficial nephrons, packed cell volume, total plasma proteins and albumin distribution space were studied in control and cirrhotic rats before and after a moderate and sustained saline infusion (3% body weight per 30 min + reposition of urinary losses). Tubular fluid samples were obtained from late proximal, early distal and late distal convolutions of superficial nephrons using micropuncture. Protein distribution was assessed by intravenous injection of 0.5 μCi of (125I)-albumin. In basal conditions, both groups of rats showed similar glomerular filtration rate and renal plasma flow, but cirrhotic animals had lower sodium excretion (fractional excretion of sodium = 0.04 ± 0.01% vs. 0.22 ± 0.02%, p < 0.05) and urinary volume (4.31 ± 0.41 vs. 7.57 ± 0.53 μ1 per min; p < 0.05). After saline infusion, total plasma proteins decreased more in cirrhotic than in control rats (-−18.5 ± 2.7 vs. -12.9 ± 2.2%, p < 0.05). The opposite was observed for albumin distribution space (34.5 ± 6.1 vs. 22.1 ± 3.5%, p < 0.05). Fractional sodium excretion increased to 2.98 ± 0.15% in control rats but only to 0.61 ± 0.080% in cirrhotic rats. The ratio single nephron glomerular filtration rate/glomerular filtration rate increased from 19.6 ± 0.7 to 21.2 ± 1.0 (x10−6, p < 0.005) in control animals but did not change in cirrhotic rats. These animals were unable to decrease adequately fractional fluid reabsorption in the proximal tubule and the loop of Henle.
The results suggest that the lack of adequate diuresis and natriuresis after saline infusion in cirrhotic rats depends on lower plasma volume expansion by extravasation of high protein content fluid, lack of intrarenal glomerular filtration rate redistribution, and inadequate decrease in proximal and Henle's loop fluid reabsorption.
Comparison of Intravenous Somatostatin and Vasopressin Infusions in Treatment of Acute Variceal Hemorrhage†
Authors: Kravetz David , Bosch Jaime , Terés Josep , Bruix Jordi , Rimola Antoni , Rodés Juan 
Published: August 2008

The present trial compared the effectiveness and complications of intravenous somatostatin and vasopressin in treatment of variceal bleeding. Sixty-one cirrhotic patients with endoscopically proven active variceal bleeding were included. Both drugs were given as continuous intravenous infusions for 48 hr. Thirty patients received somatostatin (250 #ig per hr after a bolus of 50 ng) and 31 vasopressin (0.4 units per min).
Initial control of bleeding was achieved in 26 (87%) patients receiving somatostatin and in 23 (74%) of those treated with vasopressin.
However, 10 patients [not significant statistically] in the somatostatin group and 5 in the vasopressin group rebled during treatment, after a mean of 15 and 20 hr, respectively. Therefore, complete control of bleeding during the 48 hr of therapy was achieved in 16 (53%) patients treated with somatostatin and in 18 (58%) of those receiving vasopressin. Mortality during hospitalization was similar in both groups (somatostatin 47%, vasopressin 45%).
Differences were observed in complications associated with each therapy. Vasopressin produced major complications in 8 patients (left ventricular failure in 4 and severe abdominal pain requiring drug withdrawal in 4), and minor complications in 14; somatostatin infusion produced minor complications in 3 patients (p < 0.01). In addition, the serum sodium concentration was significantly reduced by vasopressin (from 134.3 ± 1.6 to 128.3 ± 1.4 mEq per liter, p < 0.001) but not by somatostatin (134.6 ± 1.1 vs. 133.2 ± 1.1 mEq per liter).
This study shows that somatostatin is as effective as vasopressin in controlling variceal hemorrhage, but has a much lower rate of complications.
Effect of Albumin Binding on Extraction of Sulfobromophthalein by Perfused Elasmobranch Liver: Evidence for Dissociation-Limited Uptake
Authors: Weisiger Richard A. , Zacks Charles M. , Smith Neil D. , Boyer James L. 
Published: August 2008

We investigated the role of serum albumin in the hepatic uptake of organic anions by determining the effect of added bovine albumin on sulfobromophthalein (BSP) uptake in skates, an animal which naturally lacks this protein. A single-pass perfused liver model was used to determine steady-state net uptake rates as the BSP or BSP and albumin concentrations were systematically varied. Results indicated that two different steps in the uptake process are capable of limiting the uptake rate depending on the albumin and BSP concentrations selected. At higher rates of uptake corresponding to higher BSP concentrations (up to 112 μM), saturation kinetics were observed as the BSP concentration was varied, with apparent Kra and Vmax values which were independent of the albumin concentration (0.05 to 0.75%). These data suggest that under these conditions uptake is limited by a saturable step intrinsic to the liver. In contrast, for lower BSP concentrations and albumin concentrations below about 0.5%, a different kinetic pattern was seen which suggested that the rate-limiting step in uptake was transfer of BSP from albumin to the liver. The latter data were found to be consistent with a model in which the limiting step in the transfer process is spontaneous dissociation of the BSP from binding sites on albumin within the sinusoid.
These results suggest that skate liver clears BSP from albumin solutions by a two-step mechanism in which dissociation from albumin is followed by a saturable process consistent with carrier-mediated transport. The albumin concentration and uptake velocity are important factors in determining which of these steps limits the uptake rate. Clearance is efficient and irreversible even though elasmobranch liver lacks high-affinity cytosolic binding proteins for BSP, and elasmobranch plasma does not normally contain albumin.
Plasma Lipoprotein and Apolipoprotein Profile in Alcoholic Patients with and without Liver Disease: On the Relative Roles of Alcohol and Liver Injury
Authors: Duhamel Gilles , Nalpas Bertrand , Goldstein Sonia , Laplaud Michel P. , Berthelot Pierre , Chapman John M. 
Published: August 2008

In the present study, we report on alterations in plasma lipid, lipoprotein and apolipoprotein patterns in three separate populations of alcoholic patients, one without liver damage (Group I), a second presenting steatosis or mild alcoholic hepatitis or both (Group II) and a third with alcoholic cirrhosis (Group III), using a healthy, normolipidemic, nonalcoholic group as controls (Group C). Total plasma cholesterol levels were elevated in Groups II and III when compared with Groups I and C, while the ratio of esterified to free cholesterol was considerably lower in Group III than in the other groups. Plasma apo-AI levels were higher in Groups I and II than in Group C, but varied over a wide range in Group III. Apo-AII was present at higher concentrations in Groups I and II than in both Groups III and C. In contrast, no significant differences were detected in total apo-B levels, irrespective of the group. Modifications in the chemical composition of plasma lipoproteins primarily concerned a reduction in the cholesteryl ester content of low-density lipoproteins (LDL) and high-density lipoprotein (HDL) in Group III, this being compensated by a reciprocal increase in triglyceride. In addition, Group III lipoproteins, with the exception of HDL3 (density 1.100 to 1.140 gm per ml), exhibited a greater content of phospholipids than those of corresponding density from patients in Groups I and II. No significant differences were found in very low-density lipoprotein concentrations, while LDL levels increased in parallel with the severity of liver injury. In Groups I and II, HDL2 concentrations were elevated relative to Group C, while HDL3 decreased in parallel with the degree of impairment of liver function and thus from Group C to Group III. Such opposing tendencies led to an HDL2:HDL3 ratio which was more than 5-fold higher than normal in Group III.
The distribution of apoprotein B in the ultracentrifugal subfractions revealed no significant modification between the different groups. By contrast, in Groups I and II, apo-AI and apo-AII levels increased consequent to higher concentrations of HDL2. Our data suggest that abnormal HDL particles preferentially enriched in apo-AII and possibly apo-AI were present in Group I, while the lowest levels of both apo-AI and apo-AII were seen in Group III.
No simple association is evident between a well-defined plasma lipid, lipoprotein and/or apolipoprotein profile and chronic alcoholism in the presence or absence of liver injury. Nonetheless, our findings suggest that measurement of the absolute concentrations and ratio of HDL2 and HDL3, as well as of the levels and ratio of apo-AI and apo-AII in these subclasses, may permit differentiation of certain of the subpopulations of chronic alcoholics described herein.
Evidence for Valine Intolerance in Patients with Cirrhosis
Authors: Schauder Peter , SchrÖDer Karsten , Herbertz Lothar , Langer Klaus , Langenbeck Ulrich 
Published: August 2008

Valine (62.5 mg per kg), leucine (70 mg per kg) and equal amounts of the calcium salts of the corresponding keto acids, i.e., α1-ketoisovaleric acid (KIVA) and α1-ketoisocaproic acid (KICA) were orally administered to patients with cirrhosis and to control subjects.Valine or leucine ingestion increased serum valine and leucine levels and the corresponding keto acids, KIVA and KICA, in cirrhotics and controls. KIVA or KICA ingestion increased serum KIVA and KICA concentrations within a few minutes associated with a rise in valine and leucine.
In cirrhotics, administration of valine or KIVA resulted in significantly higher serum valine or KIVA concentrations than in control subjects. The clearance of valine and KIVA from blood was also delayed in cirrhotic patients. No such differences were observed after leucine or KICA ingestion.
It is suggested that cirrhotics have a diminished tolerance for valine. Since the tolerance for KIVA, but not KICA, is also impaired, it appears that cirrhotics have a derangement in one or more metabolic steps distal to the branched-chain keto acid dehydrogenase.
Ultrastructural Liver Pathology in Patients with Minimal Liver Disease and α1-Antitrypsin Deficiency: A Comparison Between Heterozygous and Homozygous Patients
Authors: Hultcrantz Rolf , Mengarelli Silva 
Published: August 2008

A light and electron microscopic investigation of liver tissue from three homozygous (Pi-type ZZ) and three heterozygous (Pi-type MZ) α1-antitrypsin deficiency patients is presented. All had slightly elevated levels of serum amino transferases as the only signs of liver damage. Light microscopical investigation showed minor periportal fibrosis and periodic acid-Schiff-positive globules in the homozygous patients, but no specific findings besides fatty changes were seen in the heterozygous patients.
Electron microscopical investigation was performed on periportal and centrilobular areas separately. In the three homozygous patients, dilatation of endoplasmic reticulum was found in many periportal liver parenchymal cells. In these cells, a marked increase in peroxisomes was also noted and in some instances they showed signs of cell necrosis. Evidence of Rupffer cell heterophagy of such cells was also found, thus indicating that they had died. Only in one liver parenchymal cell from one of the three heterozygous patients was evidence of a dilated endoplasmic reticulum found. No increase in peroxisomes was found and no apparent signs of liver cell necrosis were noted. An increased amount of lipofuscin-like material in the lysosomes was encountered in liver cells both from patients with homozygous and heterozygous ai-antitrypsin deficiency.
Based on these findings, it is suggested that cell death occurs in cells with a dilatation of the endoplasmic reticulum. If these findings are important for the pathogenesis in liver disease in α1-antitrypsin deficiency, the present study suggests that the risk to develop liver disease is less in heterozygous patients since, with one exception, alterations of the same nature were not found in their hepatocytes.
Close Association Between Basal Cell Layer Antibodies and Hepatitis B Virus-Associated Chronic Delta Infection
Authors: Zauli Daniela , Fusconi Marco , Crespi Cristina , Bianchi Francesco B. , Craxi Antonio , Pisi Emilio 
Published: August 2008

Antibodies reacting in immunofluorescence with the basal cell layer of rat forestomach (BCLA) have been detected in 36 of 121 (30%) hepatitis B virus (HBV)-mediated chronic liver disease (CLD), in 1 of 30 (3%) HBV-negative CLD, in 3 of 36 (8%) alcoholic liver disease (with no correlation with serum HBV markers), in 1 of 25 (4%) primary biliary cirrhosis, in none of 19 HBV-related HBsAg-negative CLD and 60 healthy blood donors. Of 352 hospitalized patients with miscellaneous diseases (including immunological conditions), the antibodies were found in four (1%).
In the 36 BCLA positive cases from HBV-mediated CLD, evidence of chronic delta infection was found in 34. The overall prevalence of BCLA in 68 delta cases was 50% (58% in chronic active hepatitis, 46% in cirrhosis), and in 28 delta negative cases was 4% (p < 0.00002).
BCLA of delta cases were mainly of the IgG class (38 of 41 sera), and high titers (up to 40,960) were found in the majority (66% >1:640).
The high titer BCLA has to be considered a marker of chronic delta infection in HBV cases.
Detection of Reovirus Type 3 in the Porta Hepatis of an Infant with Extrahepatic Biliary Atresia: Ultrastructural and Immunocytochemical Study
Authors: Morecki Rachel , Glaser Joy H. , Johnson Anne B. , Kress Yvonne 
Published: August 2008

This report describes immunocytochemical and ultrastructural methods which led to the identification of Reovirus type 3 (Reo-3) in the porta hepatis of a patient with extrahepatic biliary atresia. The study indicates that Reo-3 antigenic sites are demonstrable by the avidin-biotinylated complex peroxidase method following formalin fixation and paraffin embedding, but are destroyed by freezing and thawing prior to fixation. Deparaffinization of the block and subsequent rembed-ding in epon-araldite did not alter immunoperoxidase staining. This procedure offered the advantage of higher light microscopic resolution of semithin (1 jtm) sections and assisted in the selection of specific areas for ultrastructural studies.
Localization of Reo-3 in extrahepatic biliary atresia was confined to a biliary remnant in which there were acutely inflammed, partially necrotic microscopic ducts. Electron microscopic examination of the immunoreactive sites revealed virus-like particles similar in appearance to Reo-3 particles in infected tissue culture cells. The observations presented here support previously reported serologic data which have shown an association between Reo-3 infection and extrahepatic biliary atresia.
Effect of model selection on computed water balance components
Authors: Jhorar Raj Kumar , Smit A. A. M. F. R. , Roest C. W. J. 
Published: August 2008

AbstractSoil water flow modelling approaches as used in four selected on‐farm water management models, namely CROPWAT, FAIDS, CERES and SWAP, are compared through numerical experiments. The soil water simulation approaches used in the first three models are reformulated to incorporate an evapotranspiration process similar to that used in SWAP. Computations are carried out for three soil types, representing sandy loam, loam and sandy clay loam. The reformulated models are calibrated against simulation results obtained with SWAP. All the modelling approaches predict nearly equal estimates of cumulative actual evapotranspiration for a wheat crop. When compared with SWAP simulation results, the CERES type approach outperformed the other two approaches in respect of estimated cumulative deep percolation losses. A new criterion is proposed to interpret simulation results under deep water table conditions to suggest appropriate depth of water application. The resulting recommendations for irrigation planning suggest that any of the modelling approaches may be used to suggest practical irrigation considered in the present study. Copyright © 2008 John Wiley & Sons, Ltd.
Role of musculature during defecation in a particle‐feeding arachnid, Archegozetes longisetosus (Acari, Oribatida)
Authors: Heethoff Michael , Norton Roy A. 
Published: August 2008

AbstractMost extant Chelicerata are characterized by external digestion and the ingestion of fluid food. Exceptions include the marine taxa, most Opiliones, and the mite groups Opilioacarida (Parasitiformes) and Sarcoptiformes (Acariformes), which ingest particulate food. This leads to different physiological and morphological adaptations for food processing, including the production and extrusion of solid fecal pellets, which are rather large in sarcoptiform mites. Few studies have investigated the defecation of such large fecal pellets, and available information is contradictory. We use a combination of non invasive microscopical techniques and in vivo examination to investigate the complex functional morphology of the anal region of the oribatid mite Archegozetes longisetosus Aoki. The opening of the anus is at least initiated by indirect muscular action via an increase of hemolymph pressure, through the action of dorsoventral muscles (dvm). Extrusion of the fecal pellet is accomplished by the prerectal muscle collar, with full opening of the anus and rotation and bowing of the plates probably resulting from pressure of the pellet. The sequential nature of these actions was demonstrated by many observations in which the anus opened only partially; these were concomitant with dmv contraction but pellets were not being extruded. All muscles directly connected to the anal and adanal regions assist in keeping the anus closed; they are antagonists to hydrostatic forces that are necessary for normal activity. Based on the literature, no obvious similarities were noted with defecation musculature in other particle‐feeding chelicerates, but most muscles can be homologized with those of more specialized oribatid mites. The function of the outer anal muscles has been modified in both Euphthiracaridae and Brachypylina to assist in providing general hemolymph pressure. J. Morphol., 2009. © 2008 Wiley‐Liss, Inc.
Postoperative residual disease evaluation in the locoregional treatment of peritoneal surface malignancy
Authors: González‐Moreno Santiago , Kusamura Shigeki , Baratti Dario , Deraco Marcello 
Published: August 2008

AbstractBackgroundThe maximum size of the residual lesions left behind after cytoreductive surgery for peritoneal surface malignancy has consistently been shown to be the main prognostic factor in this setting. However, a uniform assessment method and categorization for this paramount prognostic indicator is lacking.MethodsIn order to achieve a consensus among experts, the Delphi methodology was employed. Conflicting points were identified and related multiple choice questions were circulated among a panel of experts on peritoneal surface oncology. Two rounds of web‐based voting were carried out.ResultsThe completeness of cytoreduction (CC) Score described by Sugarbaker was considered the current best classification for residual disease size. The experienced surgeon's naked‐eye estimation was considered the ideal method to assess residual disease size. There was agreement that the definition of CC‐0 or R0 cytoreduction needs further specification. A redefinition of “completeness of cytoreduction” according to disease process was favored by the experts but not favored for the type of intraperitoneal chemotherapy employed.ConclusionsFollowing the experts' consensus, it is recommended that the CC score be used to categorize residual disease after cytoreductive surgery for peritoneal surface malignancy. Pending issues for further consensus development in this area have been identified. J. Surg. Oncol. 2008;98:237–241. © 2008 Wiley‐Liss, Inc.