bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Randomized Clinical Trial of Supplementary Parenteral Nutrition in Jaundiced Alcoholic Cirrhotic Patients
Authors: Naveau Sylvie , Pelletier Gilles , Poynard Thierry , Attali Pierre , Poitrine Alain , Buffet Catherine , Etienne Jean-Pierre , Chaput Jean-Claude 
Published: March 2007

Between March 1982 and September 1983, 40 inpatients (25 men and 15 women, mean age 53 years) with alcoholic cirrhosis and total serum bilirubin ≥5 mg per dl were studied. Those with hepatocellular carcinoma, renal failure, hyponatremia, septicemia, spontaneous bacterial peritonitis, gastrointestinal bleeding, and hepatic coma were excluded. Patients were studied for 28 days. The two groups were offered an oral diet containing 40 kcal per kg per day. Patients in the supplementary parenteral nutrition group received 40 kcal per kg per day and 200 mg nitrogen per kg per day using a central catheter. The major endpoint was total serum bilirubin on Day 28.
On admission, serum bilirubin was not significantly different in the two groups: oral group, 12.5 ± 6.6 mg per dl; supplementary parenteral nutrition group, 12.3 ± 8.5 mg per dl. On Day 28, serum bilirubin was lower in the supplementary parenteral nutrition group (2.5 ± 1.4 mg per dl) than in the oral group (4.1 ± 2.2 mg per dl) (p < 0.02). Serum bilirubin was also lower in the supplementary parenteral nutrition group than in the oral group on Days 7, 14and 21 (p < 0.05). Analysis of covariance, considering serum bilirubin on admission and at randomization and time between admission and randomization, confirmed these results. On Day 28, anthropometric parameters, serum transferrin, prealbumin and retinol–binding protein were higherin the supplementary parenteral nutrition group, but the differences were not significant. Serum albumin was significantly lower in the supplementary parenteral nutrition group. The incidence of encephalopathy and sepsis was not significantly different between the two groups.
Strain-related patterns of biliary excretion and hepatic distribution of copper in the rat
Authors: Nederbragt Hubertus , Lagerwerf Aart J. 
Published: March 2007

Biliary copper excretion was studied in male, bilecannulated rats of the inbred strains Fischer, Brown Norway, WAG/Rij and Lewis. After intravenous injection of 10, 30 and 50 μg copper per 100 gm body weight, two patterns of copper excretion were observed; their profiles varied with the copper dose and the strain of the rats used. The lowest amounts of copper were excreted by Fischer rats, the highest by WAG/Rij rats; this was related to the effect of the copper dose on both patterns. The subcellular distribution of copper in the liver was studied in Fischer and Brown Norway rats after doses of 50, 100, and 200 μg per 100 gm body weight. Brown Norway rats accumulated more copper in the liver, although the copper concentration was the same in both strains 1 hr after injection of all doses. Fischer rats accumulated proportionally more copper in lysosomal and nuclear mitochondrial fractions whereas Brown Norway rats accumulated proportionally more copper in the cytosol.
Gel filtration of liver supernatants revealed that the amount of copper accumulating in the protein presumed to be metallothionein was 2 to 3 times higher in Brown Norway rats, whereas in the Fischer rats more copper eluted in the void volume fraction. We conclude that both biliary copper excretion and copper distribution in the liver are under genetic control. Because of its low copper excretion and reduced binding of copper to metallothionein the Fischer rat, compared to other strains, may be a suitable model for studying the involvement of the liver in copper intoxication.
Serum mitochondrial aspartate aminotransferase as a marker of chronic alcoholism: Diagnostic value and interpretation in a liver unit
Authors: Nalpas Bertrand , Vassault Anne , Charpin Serge , Lacour Bernard , Berthelot Pierre 
Published: March 2007

Serum mitochondrial aspartate aminotransferase activity was measured using an immunochemical method in 251 subjects, of whom 140 were chronic alcoholics. The alcoholic patients included 37 with normal liver routine tests (Group I), 61 with noncirrhotic alcoholic liver disease (Group II) and 42 with cirrhosis (Group III), of whom 21 had been abstainers for at least 2 months. All of the remaining 111 subjects were nonalcoholic: 61 had various types of liver disease (Group IV) and 50 were healthy controls. A second assay of serum mitochondrial aspartate aminotransferase activity was performed in 76 alcoholics after a period of abstinence of about 7 days. In addition, serial mitochondrial aspartate aminotransferase determinations were performed in four nonalcoholic volunteers prior to, during and following an alcohol bout.
Mean mitochondrial aspartate aminotransferase and mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio were significantly increased in the alcoholics whatever their liver status, with a sensitivity of the ratio of 81, 85 and 66% for Group I, Group II and the 21 drinkers of Group III, respectively. Only 1 of the 21 cirrhotic abstainers had an increased ratio. Among the 61 nonalcoholic patients with liver disease, 11 had an increased mitochondrial aspartate aminotransferase/total aspartate aminotransferase ratio, specificity of which was 82%. After drinking had been stopped for about 1 week, mitochondrial aspartate aminotransferase decreased by more than 50% and therefore appears as a reliable tool to assess abstinence. In the four cases of alcohol bouts, no significant modifications in mitochondrial aspartate aminotransferase serum values were observed, thus suggesting that mitochondrial aspartate aminotransferase is indeed a marker of chronic, but not of acute, alcohol intake.
Calcitonin gene-related peptide in the hepatic and splanchnic vascular systems of the rat
Authors: Sasaki Yutaka , Hayashi Norio , Kasahara Akinori , Matsuda Hiroyuki , Fusamoto Hideyuki , Sato Nobuhiro , Hillyard Carmel J. , Girgis Samia , Macintyre Iain , Emson Piers C. , Shiosaka Sadao , Tohyama Masaya , Shiotani Yahe , Kamada Takenobu 
Published: March 2007

The distribution and origin of calcitonin gene-related peptide immunoreactive structures in hepatic and splanchnic vasculature of the rat were investigated by the immunofluorescent technique. Calcitonin gene-related peptide immunoreactive fibers were dissociated from compact thick calcitonin gene-related peptide immunoreactive fiber bundles located around the hepatic and splanchnic vasculature, and reached the tunica adventitia of the vasculature. Some fibers penetrated further into the tunica media of the vasculature. In the tunica adventitia of the vasculature, calcitonin generelated peptide immunoreactive fibers formed a fine meshwork which could be traced to the branches and arterioles. In the liver, calcitonin gene-related peptide immunoreactive innervation extended from porta hepatis to portal triads, running with branches of the hepatic artery and portal vein. Some calcitonin generelated peptide immunoreactive fibers separated from thinner calcitonin gene-related peptide immunoreactive fiber bundles in portal triads and coursed into the immediately adjacent parenchyma. In the doral spinal ganglia (T8-10, L1), calcitonin gene-related peptide immunoreactive cells accounted for about 60% of the total number of ganglion cells. Bilateral vagotomy just below the diaphragm or bilateral transection of the greater splanchnic nerve resulted in a marked decrease of the number of calcitonin gene-related peptide immunoreactive fibers in the vasculature, whereas a combined operation was followed by the complete depletion of calcitonin gene-related peptide immunoreactive fibers. These results indicate that calcitonin gene-related peptide immunoreactive innervation in hepatic and splanchnic vasculature may have a dual origin.
In conclusion, the widespread distribution of calcitonin gene-related peptide immunoreactive fibers in the hepatic and splanchnic vasculature suggest that calcitonin gene-related peptide innervation may be involved in sensory transmission.
The mechanisms of iron uptake by fetal rat hepatocytes in culture
Authors: Trinder Deborah , Morgan Evan , Baker Erica 
Published: March 2007

The mechanisms of iron accumulation by cultured hepatocytes isolated from fetal rat liver (19 days gestation) were investigated using rat transferrin labeled with 125I and 59Fe. The rates of iron and transferrin internalization by the cells were measured by incubating the hepatocytes with the labeled transferrin at 37°C followed by treatment with pronase at 4°C to remove surface-bound transferrin and iron. Iron internalization increased linearly with time. Approximately 65% of the internalized iron was incorporated into ferritin. In contrast to iron, the rate of transferrin internalization was biphasic, with a rapid phase during the first 10 to 15 min and a second slower phase which becomes more apparent after that time. Iron and transferrin internalization were temperature-dependent. Chase experiments showed that the internalized transferrin donated all of its iron to the cell and was then released in a biphasic manner which was dependent on the time of preincubation with radiolabeled transferrin.
These experiments showed that iron uptake occurs by at least three processes. The first mechanism involves the specific receptor-mediated endocytosis of transferrin. Each cell has an average of 7.8 ± 1.0×105 (mean ± SE, n = 5) transferrin binding sites with an apparent association constant of 2.0 ± 0.4×106
M
−1. The second process is nonsaturable up to a transferrin concentration of at least 6 μM but like the specific process, also leads to accumulation of iron in excess of transferrin. It involves the endocytosis of transferrin mediated by 4.2×106 transferrin binding sites which have a K′a value of 2.6×105
M
−1. Third, fluid-phase endocytosis of transferrin occurs at a rate of 0.13×104 molecules per cell per min at 1.25 μM transferrin concentration. This rate is not sufficient to account for the additional iron accumulated by the cells by the second process.
Release of prostanoids into the portal and hepatic vein in patients with chronic liver disease
Authors: Wernze Heinrich , Tittor Wolfgang , Goerig Matthias 
Published: March 2007

Arterial and hepatovenous concentrations of circulating prostaglandin E2 and prostaglandin F2α, the stable metabolites of prostacyclin and thromboxane A2 were measured in patients with chronic liver disease and compared with those in control patients with coronary artery disease but without hepatic dysfunction. Specific radioimmunoassays were used after extraction on octadecyl C 18-silica gel columns and thin-layer chromatography. While low levels of all cyclooxygenase products were found in hepatic arterial blood in patients with proven cirrhosis (n = 10) and fibrosis (n = 8), significantly higher concentrations were detected in the hepatic vein. A similar concentration profile was observed in controls (n = 4). Thus, there is a marked but comparable release of prostanoids from the normal as well as the diseased liver. Hepatovenous prostaglandin E2 was 11.6-fold, prostaglandin F2α was 7.5-fold, prostacyclin was 12.2.-fold and thromboxane B2 was 3.9-fold above the level in the artery in both groups of patients. The hepatovenous concentrations of all arachinodate metabolites were unrelated to changes of liver morphology, biochemical abnormalities or the presence of ascites. No correlation could be demonstrated between hepatic venous pressure gradient and the concentration of prostanoids in the hepatic vein with the exception of thromboxane B2 (r = 0.55, p < 0.05). The occurrence of esophageal varices was not associated with a specific pattern of circulating prostanoids in the posthepatic vasculature. Moreover, the portal-venous concentrations of all prostanoids (five patients: two with fibrosis, three with cirrhosis) exceeded the level in the hepatic vein substantially.
While the functional significance of high levels of arachinodate metabolites in the hepatic and portal vein remains questionable, excessive release of prostanoids from the prehepatic splanchnic area occurs in advanced stages of chronic liver disease as well as in patients with minor morphological changes and apparently in healthy subjects, too. We suggest that the high content of prostanoids in the portal vein primarily reflects its predominant role in regulating gastrointestinal motility as well as in regulating splanchnic microcirculation.
Prognostic value of preoperatively obtained clinical and laboratory data in predicting survival following orthotopic liver transplantation
Authors: Cuervas-Mons Valentin , Millan Isabel , Gavaler Judith S. , Starzl Thomas E. , van Thiel David H. 
Published: March 2007

Twenty-seven clinical and laboratory data and the subsequent clinical course of 93 consecutive adult patients who underwent orthotopic liver transplantation for various chronic advanced liver diseases were analyzed retrospectively to assess the risk factors of early major bacterial infection and death after the procedure. Forty-one patients (44%) had early major bacterial infection during hospitalization for orthotopic liver transplantation. The mortality rate was 70.7% in patients with early major bacterial infection and was 7.7% in patients without early major bacterial infection (p < 0.001). Total serum bilirubin, total white blood cell count and polymorphonuclear cell count, IgG (all p < 0.05) and plasma creatinine level (p < 0.001) were higher in patients that developed early major bacterial infection than in those who did not. By step-wise discriminant analysis, the strongest risk factor for early major bacterial infection was the serum creatinine level, which achieved an accuracy of 69% for a creatinine level greater than 1.58 mg per dl.
Seven variables (ascites, hepatic encephalopathy, elevated white blood and polymorphonuclear cell count, decreased helper to suppressor T cell ratio and elevated plasma creatinine and bilirubin levels) were associated with a significant increased risk for death. A step-wise discriminant analysis of these seven factors resulted in the demonstration of serum creatinine as the greatest risk factor for mortality. A preoperative serum creatinine either less than or greater than 1.72 mg per dl accurately predicts survival or death, respectively, in 79% of cases. These data suggest that the baseline preoperative serum creatinine level provides the best indication of the short-term prognosis after liver transplantation than does any other preoperatively obtained index of the patient's status.
Zinc therapy of Wilson's disease: Two views
Authors: Brewer George J. , Scheinberg Herbert I. 
Published: March 2007

After initial promotion of copper excretion with D-penicillamine, the effect of oral zinc sulphate (3×150 mg/day, loading dose; 3×100 mg/day, maintenance dose) in two children with clinically stable Wilson's disease was evaluated after completion of three years' treatment. The course, judged by clinical, biochemical, and histological parameters was satisfactory in both. The urinary copper concentration reverted to less than 1.26 μmol/24 hours; and the serum copper concentration decreased further during zinc sulphate treatment. In one child the rise in 24 hour urinary copper excretion observed after a challenge dose of D-penicillamine (±20 mg/kg) remained constant throughout the period of observation while the liver copper content fell from 1460 μg/g dry weight to 890 μg/g dry weight. In the other patient, however, the liver copper content as well as the 24 hour urinary copper excretion increased after D-penicillamine challenge during the third year of treatment.
We conclude that zinc sulphate is a low toxic and well tolerated alternative for D-penicillamine. The dosage depends, however, on individual factors not yet well understood, and we recommend restriction of its use to patients who do not tolerate D-penicillamine well. We suggest monitoring of treatment with yearly D-penicillamine challenge and a liver biopsy if liver function deteriorates.
Emergency portacaval anastomosis (EPCA): The long-awaited trial
Authors: Conn Harold O. 
Published: March 2007

A prospective randomized trial was conducted in all comers with cirrhosis and bleeding varices comparing 1) emergency portacaval shunt (EPCS) performed within 8 hr of admission, with 2) emergency medical therapy (EMT) followed in 2-6 wks by elective portacaval shunt in survivors. All patients received identical supportive therapy initially, and the EMT group received vasopressin in continuous infusion and, if necessary, esophageal balloon tamponade to control varix bleeding. No patients refused to participate in the trial, and there were no escape or cross-over provisions in the protocol. Randomization resulted in 21 patients receiving EPCS and 22 patients receiving EMT. All patients were followed up for at least 3 yrs.
Mean age was 48 yrs in each group. Cirrhosis was caused by alcoholism in 95% of each group. On admission, there were similar incidences in the 2 groups of ascites (EPCS-52%, EMT-50%), jaundice (EPCS-48%, EMT-50%), encephalopathy (EPCS-33%, EMT-14%), severe muscle wasting (EPCS-48%, EMT-59%), hyperdynamic state (82% in both groups), SGOT ≥ 100 u (EPCS-33%, EMT-36%), ICG retention ≥ 50% (EPCS-24%, EMT-23%), and ingestion of alcohol within 7 d of bleeding (EPCS-62%, EMT-59%). Child's risk classes in the EPCS group were A-10%, B-38%, and C-52%, while in the EMT group they were A-41%, B-32%, and C-27%, suggesting that the EPCS group had somewhat more severe liver disease.
There were highly significant differences (p < 0.01) in the results obtained by the 2 forms of treatment. Bleeding was permanently controlled in 100% of patients who underwent EPCS, but in 45% who received EMT. Mean requirement for blood transfusion was 5.8 u in the EPCS group and 15.5 u in the EMT group. 81% of the EPCS patients survived to leave the hospital compared to 45% of the EMT group. The 3-yr survival rate was 67% following EPCS compared to 27% following the combination of EMT and elective shunt. It is concluded that EPCS is significantly more effective than EMT followed by elective shunt in the treatment of bleeding varices in alcoholic cirrhosis.
Regulation of low density lipoprotein receptor activity in primary cultures of human hepatocytes by serum lipoproteins
Authors: Havekes Louis M. , Verboom Hans , de Wit Elly , Yap Sing Hiem , Princen Hans M. G. 
Published: March 2007

The low density lipoprotein receptor activity was measured in primary cultures of human hepatocytes. The receptor-mediated association and degradation of low density lipoprotein increased gradually up to 140 and 190%, respectively, upon incubation of the cells with increasing amounts of whole serum (up to 100%). Preincubation of the cells with low density lipoprotein resulted in a weak downregulation of the receptor-mediated association of low density lipoprotein (only 35% reduction at 100 μg low density lipoprotein per ml). However, preincubation with high density lipoproteins with density between 1.16 and 1.20 gm per ml (heavy high density lipoprotein) resulted in a more than 2-fold stimulation of the receptor-mediated association of low density lipoprotein. This heavy high density lipoprotein-mediated stimulation could not be antagonized by a simultaneous addition of low density lipoprotein during that preincubation.
We conclude that, in primary cultures of human hepatocytes, the downregulation of the low density lipoprotein receptor activity by low density lipoprotein is weak and completely overruled by heavy high density lipoprotein. If these results for human hepatocytes in vitro hold true for hepatocytes in vivo, our results might explain why in vivo liver cells still display low density lipoprotein receptor activity notwithstanding the exposure of these cells to physiological concentrations of low density lipoprotein.
HLA antigens in patients with various courses after hepatitis B virus infection
Authors: Van Hattum Jan , Th. Schreuder Geziena M. , Schalm Solko W. 
Published: March 2007

The course after hepatitis B virus infection seems to be determined by the host's immune response, which in turn may be regulated by the major histocompatibility complex. In order to find a possible relationship between the course of disease and the phenotype frequency of HLA determinants, we studied 396 Dutch subjects of northern European local race. Six groups of individuals with various courses after hepatitis B virus infection were compared to healthy controls. The hepatitis B patients were grouped according to standard criteria: (i) 47 had recovered from acute symptomatic hepatitis B virus infection; (ii) 60 had recovered from asymptomatic hepatitis B virus infection; (iii) 26 were asymptomatic hepatitis B surface antigen carriers; (iv) 16 had chronic persistent hepatitis B; (v) 37 had chronic active hepatitis B, and (vi) 10 had chronic active hepatitis after elimination of hepatitis B antigens. Twenty-nine Class I and 13 Class II HLA antigens were assayed by standard microlymphocytotoxicity tests.
The phenotype frequency of the Class II antigen DQw1 appeared to be significantly lower in patients with chronic active hepatitis B virus infection. Some other HLA specificities showed deviations from control values, but they were not statistically significant after correction for the number of antigens tested.
In conclusion, we have found no evidence that the elimination of hepatitis B virus is related to HLA phenotype. DQw1, however, may affect the morphologic type of chronic hepatitis B infection, since its presence may protect against chronic active hepatitis.
Isolated rat hepatocyte couplets in short-term culture: Structural characteristics and plasma membrane reorganization
Authors: Gautam Anil , Ng Oi-Cheng , Boyer James L. 
Published: March 2007

Studies of canalicular bile secretion have been limited due to lack of direct access to the canalicular lumen. Isolated rat hepatocyte couplets, consisting of two hepatocytes enclosing a canalicular space, have been proposed as a primary secretory unit that may be useful for direct studies of unmodified canalicular bile secretion. The present study examines their structural characteristics and plasma membrane reorganization. The canalicular space of freshly isolated hepatocyte couplets is freely permeable to ruthenium red, but within 4 hr the junctional borders reseal in most couplets which then exclude ruthenium red from the luminal area. These resealed spaces expand in 61.8 ± 10% of couplets as secretion is elaborated and after 4 hr in monolayer culture, 12.7 ± 4.7% of the canalicular spaces are dilated to diameters greater than 3 μ. Normal-appearing microvilli line these canalicular membranes in the majority of dilated spaces as assessed by electron microscopy. Immediately after isolation, Mg++-ATPase, a histochemical marker for canalicular membranes, is located as a discrete band corresponding to the normal in vivo circumferential distribution of the canalicular membrane domain. However, this pattern of Mg++-ATP-ase staining rapidly diminishes and reorganizes at the remaining canalicular pole within several hours. This membrane reorganization is a microfilament-dependent process, since it is inhibited by cytochalasin D but not by colchicine, an inhibitor of microtubular function or cycloheximide, an inhibitor of new protein synthesis.
Thus, 3 to 4 hr after isolation, the isolated hepatocyte couplet has reorganized its canalicular membrane, retaining polarity of its excretory domain only at the remaining junctional contacts between adjacent hepatocytes. Secretion is elaborated into the ruthenium red impermeant canalicular lumen permitting direct studies of canalicular bile secretion by micropuncture, electrophysiologic and quantitative microscopic techniques.