bluuebunny/crossref_metadata_2025_split huggingface dataset:
Epiphenomenology and the gallbladder: Several examples
Authors: Charlson Mary E. 
Published: March 2007

It has been suggested that gallbladder removal may protect against subsequent development of myocardial infarction because of increased gastrointestinal cholesterol excretion resulting from increased enterohepatic cycling. To test this hypothesis, the authors used data from two large case-control studies of myocardial infarction--one conducted in 1976-1979 in 155 US hospitals and one conducted in 1980-1983 in 78 US hospitals. First, 550 female myocardial infarction cases were compared to 1,658 controls. Simultaneously adjusting for possible confounding variables using logistic regression, the odds ratio for development of a myocardial infarction subsequent to cholecystectomy was 0.8 (95% confidence interval, 0.5-1.1). Second, 1,511 male myocardial infarction cases were compared to 3,837 controls. With similar adjustments, the odds ratio was 0.8 (95% confidence interval, 0.5-1.2). The risk did not decline as the interval following cholecystectomy increased. The present data are compatible with a protective effect of cholecystectomy on the risk of subsequent myocardial infarction, but they are not conclusive.
This study was undertaken to assess possible modifications of the proliferative activity of co-Ionic mucosa, which could be related to a suggested cancer-promoting role of cholecystectomy. The mitotic index (number of mitoses per 1000 gland cells) was evaluated in the colonic mucosa of 14 healthy subjects, 11 patients with cholelithiasis, before and 6 months after surgery, and 10 patients who had undergone cholecystectomy 2 or more years previously. The mitotic index of cholecystectomized patients was significantly higher than controls. It rose significantly within 6 months of cholecystectomy. The mitotic index of patients with cholelithiasis before surgery was similar to controls. These data suggest that cholecystectomy is followed by an enhancement in the proliferative activity of the colonic mucosa, which could play a cancer-promoting role.
Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid
Authors: Moroni Flavio , Riggio Oliviero , Carlà Vincenzo , Festuccia Vittorio , Ghinelli Florio , Marino Ignazio R. , Merli Manuela , Natali Laura , Pedretti Giovanni , Fiaccadori Franco , Capocaccia Livio 
Published: March 2007

The aim of the study was to verify the role of γ-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic γ-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid γ-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symtoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy.
The mean plasma and cerebrospinal fluid γ-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the γ-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of γ-aminobutyric acid in the pathogenesis of hepatic encephalopathy.
Procollagen III peptide (PIIIP): Can it reflect hepatic fibrosis?
Authors: Alcorn Joseph , Chojkier Mario 
Published: March 2007

Immunolocalization of type III collagen and procollagen in cirrhotic human liver was studied using monoclonal antibody specific for the helical determinant of type III collagen extracted from human placenta. Deparaffinized, trypsin-treated cirrhotic liver sections from 8 autopsy cases were examined by the unlabeled peroxidase-antiperoxidase and immunofluorescence techniques. These techniques revealed the localization of this epitope shared by type III collagen and procollagen not only in the extracellular matrix of hepatocytes and sinusoidal cells but also in the cytoplasm. In hepatocellular carcinoma concurrent with cirrhosis, neoplastic cells were shown to react with this antibody as well.
These results are consistent with data obtained using antiserum specific for bovine type III procollagen aminopeptide which appeared in our previous report.
Electropermeabilization: Getting inside the cell to study autophagy
Authors: Yamazaki Kiyoshi , Larusso Nicholas F. 
Published: March 2007

Electropermeabilisation—i.e. subjecting cells to a short series of high-voltage pulses—has been used to make isolated rat hepatocytes transiently permeable to small molecules. The permeabilised cells can be loaded with [14C]sucrose at 0°C and resealed by a brief incubation at 37°C. The electrical treatment does not impair cellular function, since autophagic sequestration of sucrose occurs at the same rate as in untreated cells. The latter are permeable to sucrose immediately after isolation, due to the presence of hyperpermeable surface blebs similar to those formed in response to electrical treatment.
In order to separate [14C]sucrose-sequestering organelles from cytosol, the cells are broken up by electrodisruption—i.e. a single high-voltage pulse given in a non-ionic medium (isotonic sucrose)— and the resulting cell corpses are sedimented through a dense metrizamide/sucrose cushion to form a cytosol-free pellet containing intact lyso-somes. Since mitochondria also take up sucrose, the radioactivity in autophagosomes/lysosomes must be selectively extracted with a low concentration of digitonin.
The resulting procedure provides a specific bioassay of autophagic sequestration. The sequestration is virtually completely inhibited by the autophagy inhibitor 3-methyladenine, and at temperatures below 20°C. The sequestration step is energy-dependent, and can probably account for the known energy requirement of autophagic-lysosomal protein degradation.
Emergency liver transplantation in fulminant hepatitis
Authors: Lorber Marc I. 
Published: March 2007

Seven patients with hepatitis delta virus (HDV) cirrhosis underwent liver transplantation. In every case the HDV infection was florid but accompanied by an inactive hepatitis B virus (HBV) infection. The patients were given anti-HB surface antigen (HBsAg) serum globulins and HBV vaccine. Two patients cleared the HBsAg and the HDV, and are alive and well 14 and 15 months, respectively, after transplantation. HDV infection recurred in the other five patients: hepatitis developed in three, another died, and the fifth was re-transplanted for causes unrelated to viral hepatitis (reinfection was shown by the presence of HD antigen in the graft). Liver transplantation is feasible in patients with HDV disease but involves a high risk of HDV reinfection that cannot be predicted by the virological pattern of the native HBV infection or prevented by conventional HBV prophylaxis.
Orthotopic liver transplantation was done in 17 patients with fulminant hepatitis. The cause of the liver disease was infection with hepatitis B virus, or co-infection with hepatitis B virus and hepatitis D virus, or infection with hepatitis A virus in 6 patients; drug hepatotoxicity in 5; and indeterminate in 6. Grafts from incompatible blood groups, steatotic grafts, or reduced-size grafts were used in 5, 4, and 4 patients, respectively. Of the 17 patients, 5 died: 2 of early liver failure due to the poor quality of the graft, 1 presumably of accidentally transmitted acute infection with the human immunodeficiency virus, and 2 of decerebration occurring during or immediately after surgery. The 12 other patients were alive 2 to 15 months after transplantation.
The ischemic liver—do not resuscitate too much
Authors: Isaacson Yisrael , Van Thiel David H. 
Published: March 2007

The interest in liver transplantation has focused more attention on the mechanisms of injury during hepatic ischemia, preservation, and reperfusion. Although the human liver has been successfully maintained under hypothermic conditions for up to 10 hours, organ preservation remains the major obstacle to liver transplantation.
With tissue ischemia, cell respiration and oxidative phosphorylation cease, with a decline in high-energy phosphates including adenosine triphosphate (ATP). If oxygen and substrate are made available within a certain period of time, energy stores are regenerated and cells live. However, with irreversible ischemia, ATP stores cannot be regenerated despite the restoration of blood flow, and the cells consequently die. When ATP-MgCl2 has been given by intravenous infusion, animal survival has been improved in shock, and renal function and histology have been maintained after renal ischemia. The mechanism responsible for this beneficial effect of ATP-MgCl2 has not been defined, but it is generally presumed that ATP preserves sublethally injured cells by enhancing their repair and recovery after ischemic injury.
Although reperfusion is necessary to prevent cell death, it is not without hazard. During the period of ischemia, ATP is broken down to adenosine monophosphate, adenosine, inosine, and finally to hypoxanthine, which can be irreversibly converted by xanthine oxidase to xanthine. The introduction of oxygen into this reaction by reperfusion results in the production of the free radicals superoxide (02 ) and hydrogen peroxide (H2O2), which are mediators of tissue injury, probably by lipid peroxidation. Protection from these oxidative effects can be achieved by dismutation of superoxide to H2O2 by the enzyme superoxide dismutase (SOD) and reduction of H2O2 by catalase.
Thallium-201 per rectum for the diagnosis of cirrhosis in patients with asymptomatic chronic hepatitis
Authors: D’Arienzo Agesilao , Celentano Luigi , Scuotto Alessandro , Di Siervi Pasqualina , Lombardi Vinicio , Squame Giovanni , Mazzacca Gabriele 
Published: March 2007

In normal subjects, thallium-201, administered per rectum, is taken up mainly by the liver (heart/liver ratio in normal subjects: 0.04 to 0.12). It has been claimed that an increased heart/liver ratio is suggestive of portal-caval shunting and portal hypertension. To evaluate the possibility of using thallium-201 as a test to diagnose cirrhosis, we administered this substance per rectum to 33 patients with biochemical evidence, but no clinical symptoms, of liver disease. Laparoscopy and liver biopsy revealed chronic active hepatitis without cirrhosis in 18 patients, and chronic active hepatitis with cirrhosis in the others. The results of conventional liver function tests were similar in both groups. A significant difference, however, was found between the means of fasting serum bile acid concentrations (9.8 ± 3.2 and 18.3 ± 4.2 μM per liter) in chronic active hepatitis without cirrhosis and cirrhotic patients, and between the means of the heart/liver ratios 20 min after thallium-201 administration (heart/liver: 0.09 ± 0.03 and 0.54 ± 0.13, respectively). Unlike the serum bile acid concentration which gave some overlapping values, the thallium-201 test clearly distinguished the chronic active hepatitis without cirrhosis group from the cirrhotics.
In the cirrhotic group, there was a significant correlation between the heart/liver ratio and signs of portal hypertension such as esophageal varices, increased diameter of the vena porta and hypersplenism.
The thallium-201 test is therefore useful in discriminating between chronic active hepatitis with and without cirrhosis in clinically asymptomatic subjects with biochemical evidence of moderate liver function impairment. A heart/liver uptake ratio much higher than normal (above 0.30) strongly suggests the development of hepatic cirrhosis.
Regulation of the hepatic transferrin receptor in hereditary hemochromatosis†
Authors: Lombard Martin , Bomford Adrian , Hynes Miriam , Naoumov Nikolai V. , Roberts Stephanie , Crowe John , Williams Roger 
Published: March 2007

The liver is the main site of iron accumulation and pathologic sequelae in hereditary hemochromatosis. Whether this is a result solely of inappropriately increased absorption of iron by the gastrointestinal tract or a more generalized regulatory failure of iron balance is unknown. Using immunohistochemical techniques, we have examined the effects of therapeutic changes in liver iron stores on the expression of the hepatic trans-ferrin receptor in hereditary hemochromatosis. Ten patients with untreated hereditary hemochromatosis had no detectable staining for transferrin receptor in their liver biopsies. All had increased hepatic ferritin (mean = 19.9 μg per mg protein, range = 1 to 31.7 μg per mg protein) and hepatic iron levels (mean = 36.2 μg per mg protein, range = 3.6 to 69.9 μg per mg protein). In contrast, hepatocyte transferrin receptor was detected in seven patients in whom hepatic iron stores were markedly depleted by venesection (hepatic ferritin mean = 0.32 μg per mg protein, range = 0.16 to 0.53 μg per mg protein; hepatic iron mean = 0.98 μg per mg protein, range = 0.3 to 2.1 μg per mg protein). Sequential data from one patient confirmed the reexpression of receptor in response to therapeutic iron depletion, whereas data from another patient studied during treatment illustrated a reciprocal relationship between liver tissue distribution of iron and expression of transferrin receptor.
The finding that appropriate physiologic regulation of the hepatic transferrin receptor operates in hereditary hemochromatosis does not support the concept of a generalized defect in receptor-mediated uptake of trans-ferrin-bound iron.
Immunization of newborns of HBsag- positive mothers: A successful first step in control of hepatitis B virus in Taiwan
Authors: McMahon Brian J. 
Published: March 2007

To combat hepatitis B virus (HBV) infection in Taiwan, a mass immunoprophylaxis program was launched on July 1, 1984, aiming first at prevention of chronic HBV carriage from perinatal mother-to-infant infection. In the first 15-month period, 352721 (78%) of 450585 pregnant women were screened for hepatitis B surface antigen (HBsAg); HBsAg was present in 62359 (18%), with 50% of them categorized as highly infectious. Infants born to HBsAg-positive women were given 5 μg of a plasma-derived hepatitis B vaccine at ages 1, 5, and 9 weeks, with a booster at age 12 months. Infants of highly infectious carrier mothers recived an additional 0.5 mL of hepatitis B immune globulin within 24 hours after birth. The coverage rate of the hepatitis B immune globulin was 77% in 27375 infants born to highly infectious mothers, and that of the first, second, third, and the fourth doses of vaccine was 88%, 86%, 84%, and 71%, respectively, in infants of 55620 carrier mothers. The reported untoward reactions to immunization were negligible. We conclude that a mass hepatitis B vaccination program is feasible in hyperendemic areas such as Taiwan; this should be a significant step toward the effective control of HBV infection in these areas.
To evaluate the efficacy of the mass hepatitis B vaccination program in Taiwan in interrupting perinatal hepatitis B virus transmission, 3464 randomly selected 18-month-old infant vaccinees born to hepatitis B surface antigen-carrier mothers were recruited from 9697 eligible infants during a six-month period of the program. They were divided into ten groups according to maternal in-fectivity and compliance with the vaccination schedule. Serum samples were tested for hepatitis B surface antigen, antibody to hepatitis B surface antigen, and antibody to hepatitis B core antigen. In 786 infants who had highly infectious mothers and who received hepatitis B immune globulin and vaccine on schedule, the protective efficacy was about 85%. The efficacy seemed to be slightly lower in those immunized off schedule. Overall, 11% of infants still carried hepatitis B surface antigen, and 81% of the infants had antibody to hepatitis B surface antigen that exceeded 10 mlU/ mL in more than 90% of them. The geometric mean titers of antibody to hepatitis B surface antigen were more than 200 mlU/mL in every group of infants. We conclude that the mass vaccination program is efficacious in preventing perinatal hepatitis B virus transmission and the chronic carrier state; most infant vaccinees have adequate levels of protective antibody at 18 months of age. This program is extremely significant in the control of hepatitis B virus infection in Taiwan.
Primary sclerosing cholangitis: Natural history, prognostic factors and survival analysis
Authors: Wiesner Russell H. , Grambsch Patricia M. , Dickson Rolland E. , Ludwig Jurgen , Maccarty Robert L. , Hunter Ellen B. , Fleming Thomas R. , Fisher Lloyd D. , Beaver Sandra J. , Larusso Nicholas F. 
Published: March 2007

The natural history of primary sclerosing cholangitis was assessed in 174 patients; 37 were asymptomatic and 137 had symptoms related to underlying liver disease. At the time of diagnosis, the mean age was 39.9 years, 66% of the primary sclerosing cholangitis patients were male and 71% had associated inflammatory bowel disease, most commonly chronic ulcerative colitis. Longterm follow-up (mean: 6.0 years; range: 2.7 to 15.5 years) was available in all patients. During follow-up, 59 (34%) of the patients died: 55 in the symptomatic group and four in the asymptomatic group. Median survival from the time of diagnosis of primary sclerosing cholangitis at the Mayo Clinic was 11.9 years. Survival in the asymptomatic group was significantly decreased compared with that in a control population matched for age, race and sex. Multivariate analysis (Cox proportional hazards regression modeling) revealed that age, serum bilirubin concentration, blood hemoglobin concentration, presence or absence of inflammatory bowel disease and histologic stage on liver biopsy were independent predictors of high risk of dying.
The development of a multivariate statistical survival model is a major step in identifying individual primary sclerosing cholangitis patients at low, moderate and high risk of dying. Such models will be useful for stratifying patients in therapeutic trials, in patient counseling and in patient selection and timing of liver transplantation.
Diverticular Bile Duct Lesion in Chronic Active Hepatitis
Authors: Vyberg Mogens 
Published: March 2007

Liver needle biopsies from patients with non–A, non–B chronic active hepatitis and so–called abnormal bile duct epithelium were studied with a three–dimensional method. Photographs of bile duct structures in serial sections were transferred to acrylic plates. Five bile duct lesions of a not previously described diverticular type were revealed. The diverticuli were of varying shape with a diameter of 30 to 110 μ and a length of 75 to 150μm budding from small (12 to 25μm), slightly ectatic bile ducts. The diverticular epithelium was disordered. Some cells appeared as bile duct cells, but most were larger, with rounded nuclei, prominent nucleoli and abundant eosinophilic cytoplasm, sometimes with periodic acid–Schiff–positive, diastase–resistant granules. The lesions were only partly surrounded by a basement membrane. They were all embedded in a tight mononuclear inflammatory infiltrate associated with pronounced periportal piecemeal necrosis. In two cases, a germinal center was adjacent to the epithelium.
The pathogenesis of the diverticular bile duct lesion is unknown, but the diverticuli probably represent Hering ducts and groups of periportal liver cells which have escaped the piecemeal necrosis.
Orthotopic Liver Transplantation and the Cytosolic Estrogen–Androgen Receptor Status of the Liver: the Influence of the Sex of the Donor
Authors: Kahn Delawir , Zeng Qihua , Makowka Leonard , Murase Noriko , Nakajima Yasuaki , Eagon Patricia K. , Francavilla Antonio , Starzl Thomas E. , van Thiel David H. 
Published: March 2007

Mammalian liver is known to contain cytosolic receptors for both estrogens and androgens. Furthermore, certain mammalian hepatic functions are known to display a sexual dimorphism. However, in clinical liver transplantation, the sex of the donor is not taken into consideration in selection of the donor. In this study, the effect of liver transplantation on the estrogen and androgen receptor content of the liver was determined.
Adult male and female rats were subjected to orthotopic liver transplantation, using donors form both the same and the opposite sex as the recipient. The animals were killed on the tenth postoperative day, and the livers were assayed to determine their cytosolic estrogen and androgen receptor content.
Transplantation of a liver from a male donor into a male recipient, from a male donor into female recipient and from a female donor into a male recipient produced similar changes in the number of cytosolic estrogen and androgen receptors in hepatic cytosol. In all three situations, the estrogen receptor content in the cytosol of the transplanted liver was the same as that found in an unoperated male liver, and the cytosolic content of the androgen receptor was the same as that of an unoperated female liver. After transplantation of the liver from a female donor into a female recipient, the estrogen and androgen receptor content in the cytosol of the transplanted liver was the same as that of an unoperated female. A consistent finding in this study was a reduction in the cytosolic androgen receptor activity of the transplanted liver when a male was either the recipient or donor. This reduction was maximal at 10 days posttransplantation. At 40 days following transplantation, a partial recovery in the androgen receptor acitivy of hepatic cytosol had occurred. These studies demonstrate that orthotopic liver transplantation changes the cytosolic content of both the estrogen and androgen receptors of the liver, and their ratios may have important effects during the immediate postoperative period and profound long–term consequences relative to gender differences in hepatic function.
A Multicenter, Randomized, Double–Blind Trial of Somatostatin in the Management of Acute Hemorrhage From Esophageal Varices
Authors: Valenzuela Jorge E. , Schubert Timothy , Fogel Ronald M. , Strong Richard M. , Levine Joel , Mills Peter R. , Fabry Thomas L. , Taylor Linda W. , Conn Harold O. , Posillico James T. 
Published: March 2007

A prospective, randomized, placebo–controlled, double–blind, multicenter clinical trial of intravenous somatostatin (Stilamin®; Serono Laboratories, Inc., Randolph, MA) was performed in 102 patients with actively bleeding esophageal varices from August, 1985, to November, 1986. Patients had major hemorrhage indicated by hematemesis or melena and evidence of significant blood loss. For entry, patients had to have endoscopic demonstration of active bleeding from esophageal varices or stigmata of recent hemorrhage and bright red blood in the gastric aspirate with no other source of bleeding found. Randomized patients received identical appearing somatostatin or placebo for a 30–hr study period. Those given somatostatin received a 250–μg bolus and a 250–μg per hr infusion with repeat bolus and doubling of the infusion if the bleeding was not controlled. In retrospect, 18 patients could not be evaluated.
Of the 84 evaluable patients, 48 received somatostatin and 36 placebo. They were comparable in age, gender, severity of liver disease and history of variceal bleeding. Transfusion requirements were similar in both groups. Bleeding stopped for 12 consecutive hr during 30 hr of the study period in 31 (65%) of the somatostatin group vs. 30 (83%) of the placebo group (p = 0.06). The median time to cessation of bleeding was 2 hr in the placebo group and 3 hr in the somatostatin group. Deaths following the study period were nine (25%) in the placebo group and 15 (31%) in the somatostatin group. Within the limitations of the present study, we conclude that somatostatin was ineffective in the management of active bleeding of esophageal varices.