bluuebunny/crossref_metadata_2025_split huggingface dataset:
Auricular pressure in the treatment of gallstones: A randomized, clinical trial of traditional chinese medicine
Authors: Wu Xiening 
Published: March 2007

Gallstones, which were diagnosed in 365 patients on the basis of symptoms, signs, ultrasound scanning and cholecystography were treated by compression of specific auricular points. The patients were predominantly women (76%) from 19 to 78 years of age. The stones were in the gallbladder in 326, in intrahepatic ducts in 20, in the common bile duct in 6 and at multiple sites in 14. An adhesive plaster with a seed of Semen vaccariae (an oblate spheroid 2 mm in diameter) fixed at its center was placed over the main auricular points which include the liver, gallbladder, bile duct and duodenum. The liver and gallbladder have corresponding points over the posterior surface of the ears, and compression of both the anterior and posterior points at the same time enhances the effect. Correct positioning over these points is of primary importance. If the individual ear varies in shape, then corresponding points can be taken. These seeds are chosen because of their hardness. Pressure was applied for 20 min thrice a day postprandially by the patients themselves, as shown by the doctor at the start, to one ear every other day and to the other ear on alternate days for 30 days. The seeds were changed by the physician every 3 days. All stools were collected by the patients and examined for expelled stones by the doctors. One hundred forty-four stone specimens were assayed for their cholesterol and bilirubin content, and 16 were examined by infra-red spectrophotography and scanning electron microscopy. After treatment, gallstones were demonstrated in the stool of 299 treated patients (82%) but in only 7 of the 47 controls cholagogue-treated patients (9%). These differences from the treated patients are highly significant statistically (p < 0.01). Reexamination with ultrasonography (except for 25 who were lost to follow-up)revealed the stones to be absent in 16 patients (5%), reduced in number to about half in 72 (20%). In 127, the number rermained the same (35%) and in 69, the number of gallstone increased (19%).
Stones were expelled more frequently from the common duct than from the gallbadder (p < 0.05). Multiple stones were expelled from the gallblader more frequently than single stones, and small stones (<0.5 cm) were expeleld more frequently than those > 1.0 cm. The explusion rate could be improved by prologing the treatment beyond 30 days.
Acinar redistribution and heterogeneity in transport of the organic cation rhodamine B in rat liver
Authors: Braakman Ineke , Groothuis Geny Martha Maria , Meijer Dirk Klaas Fokke 
Published: March 2007

We studied a possible acinar heterogeneity in the transport of organic cations, using rhodamine B as model compound. Employing perfusions of isolated rat livers in the ante- and retrograde mode and quantitative fluorescence microscopy, Zones 1 and 3 were shown to be equally efficient in taking up rhodamine B. Ten minutes after injection in an antegrade perfusion, 95% of the dose was localized in the portal half of the acinus. Fifty minutes later, however, the amount of rhodamine B in Zone 1 had been reduced to 23%; 30 and 31% were in Zones 2 and 3, respectively, and the medium concentration was doubled. Thus, unchanged rhodamine B appeared to be transported downstream within the liver, either via the medium or directly from cell to cell, finally resulting in a relatively higher rhodamine B concentration in Zone 3. To obtain additional data, we designed a perfusion setup in which the zones could be studied separately. In both zones, the amount excreted into the medium was about 30 times the amount excreted into bile. Intracellular sequestration of rhodamine B and the rate constant for sinusoidal secretion were higher in Zone 3, while the sinusoidal uptake rates were equal; biliary excretion was higher in Zone 1.
Acinar distribution changed with time because rhodamine B, primarily accumulated in Zone 1, was secreted into the sinusoids and taken up again by downstream cells. The finally higher rhodamine B concentration in Zone 3 was caused by a zonal heterogeneity in intracellular sequestration and sinusoidal secretion of rhodamine B.
Sinusoidal endothelial cells from guinea pig liver synthesize and secrete cellular fibronectin in vitro
Authors: Rieder Hartmut , Ramadori Giuliano , Dienes Hans-Peter , Büschenfelde Karl-Hermann Meyer Zum 
Published: March 2007

Endothelial liver cells were obtained from guinea pig by enzymatic digestion and centrifugal elutriation. Cells were cultured on gelatin and fibronectin pretreated culture vessels. Endothelial cells were characterized by phase-contrast microscopy, electron microscopy and the presence of Factor VIII-related antigen. Fibronectin secretion was determined in cell-free supernatants by a sensitive and specific ELISA and localized on fixed cultured cells by immunofluorescence. [35
S]Methionine endogeneously labeled fibronectin was immunoprecipitated from supernatants and cellular lysates and displayed on sodium dodecyl sulfate polyacrylamide slab gel electrophoresis.
After attachment to the culture vessel, one day after plating, endothelial cells start to produce fibronectin as measured by ELISA and demonstrated by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Secretion of fibronectin increases as cells proliferate to form a confluent monolayer. By immunofluorescence, fibronectin is visualized inside permeabilized cells and as a fibrillar network on the cell surface. Underneath the cell bodies, fibronectin-positive material is present as short strands. From supernatants and cellular lysates, fibronectin is immunoprecipitated with an apparent Mr of about 235,000 obviously larger than plasma fibronectin with an Mr of 220,000, which behaves electrophoretically like fibronectin isolated from early hepatocyte cultures. As endothelial cells incorporate [3H]fucose in fibronectin, whereas hepatocytes do not, we conclude that endothelial cells in contrast to hepatocytes produce cellular fibronectin. Endothelial cells, therefore, are probably the cellular source of the fibronectin present in the space of Disse. The significance of this finding with respect to fibrotic liver disease is discussed.
Establishment and characterization of a diethylnitrosamine-initiated woodchuck hepatocyte cell line
Authors: Lee Gang-Hong , Kawaguchi Tokuichi , Nomura Kimie , Kitagawa Tomoyuki 
Published: March 2007

Woodchucks free from woodchuck hepatitis virus were treated with diethylnitrosamine in vivo for 2 months, and then hepatocytes obtained by enzymatic perfusion were cultured with the hepatopromoter phenobarbital. This in vivo-in vitro procedure gave rise to proliferating epithelial cell foci, from one of which the presently described hepatocyte cell line (WLC-3) was established and characterized.
WLC-3 cells possess morphological and biochemical features of differentiated hepatocytes, including glucose-6-phosphatase activity and albumin production. Histopathological analysis of the tumor which developed transitorily in nude mouse subcutis after inoculation of the cell line revealed glandular structures comprising cells of hepatocellular-like morphology.
This is the first established woodchuck hepatocyte cell line free from woodchuck hepatitis virus and is therefore expected to be useful for studying the mode of gene expression and viral proliferation of woodchuck hepatitis virus and the mechanisms underlying woodchuck hepatitis virus-related hepatocarcinogenesis.
Chronic Delta Hepatitis: Detection of Hepatitis Delta Virus Antigen in Serum by Immunoblot and Correlation With Other Markers of Delta Viral Replication
Authors: Buti Maria , Esteban Rafael , Jardi Rosendo , Rodriguez-Frias Francisco , Casacuberta Jose , Esteban Juan Ignacio , Allende Elena , Guardia Jaime 
Published: March 2007

To investigate the presence of serum hepatitis delta virus antigen by immunoblot and its correlation with other markers of active viral replication (intrahepatic hepatitis D antigen, IgM antibody to hepatitis D and serum hepatitis D virus RNA), we studied serum samples from 50 patients with chronic hepatitis D virus infection (38 with and 12 without intrahepatic hepatitis D antigen). Of the 38 patients with intrahepatic hepatitis D antigen, 27 (71%) had antigen detectable in seurm by immunoblot, whereas only two were reactive by conventional enzyme–linked immunosorbent assay. Thirty–one (82%) patients were also positive for serum hepatitis D virus RNA by spot hybridization and 33 (87%) were positive for IgM anti–hepatitis D virus. All markers were simultaneously present in 24 patients. Circulating hepatitis D antigen was detected in one (8%), IgM antihepatitis D in seven (58%) and hepatitis D virus RNA in two (17%) of the 12 patients who had anti–hepatitis D in serum but not detectable hepatitis D antigen in liver. Hepatitis D antigen was not detected in serum of any of the 15 control patients.
The results suggest that serum hepatitis D antigen as detected by immunoblot and serum hepatitis D virus RNA are similar in sensitivity for detection of active hepatitis D virus replication during chronic infection and constitute useful, sensitive and noninvasive tests for the diagnosis and monitoring of chronic hepatitis D virus infection.
Interferon antibodies may negate the antiviral effects of recombinant α-interferon treatment in patients with chronic hepatitis B virus infection
Authors: Lok Anna Suk-Fong , Lai Ching-Lung , Leung Elsie Kit-Yee 
Published: March 2007

In a randomized controlled trial of recombinant α-2a interferon for chronic hepatitis B, interferon antibodies developed in 21 (39%) of 54 Chinese adults who received IFN. No correlation was observed between sex, age, pretreatment serum ALT level or liver histological findings and the development of interferon antibodies. Antibodies were significantly more likely to develop in patients who received lower doses (2.5 or 5 MU/m2) of α-2a interferon than in those who received a higher dose (10 MU/m2): 53% vs. 11% (p = 0.006).
The development of interferon antibodies appeared to reverse the initial antiviral response to treatment, with reappearance of hepatitis B virus DNA in serum in 12 patients and HBeAg in three patients. Sustained clearance of HBeAg was achieved in only one (5%) patient but was achieved in seven (21%) patients without interferon antibodies. The mere presence of interferon antibodies did not preclude an antiviral response to interferon therapy, but patients with high titer neutralizing antibodies were less likely to respond.
These findings suggest that interferon antibodies may negate the antiviral effects of α-2a interferon. A higher incidence of interferon antibodies in Chinese vs. white patients with chronic hepatitis B may contribute to the poorer antiviral response in Chinese patients. (HEPATOLOGY 1990;12:1266-1270).
Hepatitis C virus antibodies in chronic alcoholic patients: Association with severity of liver injury
Authors: Parés Albert , Barrera Josep María , Caballería Joan , Ercilla Guadalupe , Bruguera Miquel , Caballería Llorenç , Castillo Ricardo , Rodés Joan 
Published: March 2007

The prevalence of hepatitis C virus antibody and its relationship to the severity of liver disease in chronic alcoholic patients has been assessed, using a recently developed enzyme immunoassay and confirmed by a recombinant immunoblot assay, in 144 patients (mean age ± S.D. = 44.4 ± 11.3 yr) who had consumed >80 gm/day ethanol for >5 yr. Hepatic disease was evaluated by clinical and biochemical studies and by liver biopsy when appropriate. In addition, 76 liver biopsy specimens from these patients were analyzed to determine whether liver lesions were similar in alcoholic patients with and without hepatitis C virus antibodies.
According to clinical and histological features alcoholic patients were divided into five groups: normal liver (45 patients), fibrosteatosis (20 patients), alcoholic hepatitis (14 patients), cirrhosis (61 patients) and chronic hepatitis (4 patients). Hepatitis C virus antibodies were present in 35 alcoholic patients (24.3%). The prevalence of hepatitis C virus antibodies correlated with the severity of liver injury: 2.2% in patients without liver disease, 20% in those with fibrosteatosis, 21.4% in those with alcoholic hepatitis and 42.6% in those with cirrhosis. Hepatitis C virus antibodies were found in one of the four patients with chronic hepatitis (p < 0.001). Furthermore, patients positive for hepatitis C virus antibodies with normal liver or fibrosteatosis showed higher serum bilirubin and γ-globulin concentrations and lower aminopyrine breath test scores than did patients negative for hepatitis C virus antibodies with normal liver or fibrosteatosis. Similar differences between patients with and without hepatitis C virus antibodies were observed in patients with alcoholic hepatitis or cirrhosis. Histological features, except cells within sinusoids, were comparable in alcoholic patients with and without hepatitis C virus antibodies.
The increased prevalence of hepatitis C virus antibodies in alcoholic patients with severe liver injury and the impaired liver function in patients with these antibodies suggest that hepatitis C virus is involved in liver damage in chronic alcoholic patients (HEPATOLOGY 1990;12:1295-1299).
Hepatocyte swelling stimulates macromolecular synthesis
Authors: Wondergem Robert 
Published: March 2007

In hepatocytes from fasted rats, several amino acids are known to stimulate glycogen synthesis via activation of glycogen synthase. The hypothesis that an increase in cell volume resulting from amino acid uptake may be involved in the stimulation of glycogen synthesis is supported by the following observations. 1) The extent of stimulation of glycogen synthesis by both metabolizable and nonmetabolizable amino acids was directly proportional to their ability to increase cell volume, except for proline, which stimulated glycogen synthesis more than could be accounted for by the increase in cell volume. 2) Both cell swelling and stimulation of glycogen synthesis by amino acids were prevented when hepatocytes were incubated in hyperosmotic media containing sucrose or raffinose. 3) Increasing the cell volume by incubating hepatocytes in Na+-depleted media in the absence of amino acids also stimulated glycogen synthesis. 4) Stimulation of glycogen synthesis by Na+ depletion was prevented by restoring the normal osmolarity with sucrose, but not with choline chloride which, by itself, stimulated glycogen synthesis and increased cell volume.
It is concluded that stimulation of glycogen synthesis by amino acids is due, at least in part, to an increase in hepatocyte volume resulting from amino acid uptake, and that hepatocyte swelling per se stimulates glycogen synthesis.
Prophylactic sclerotherapy for esophageal varices: Long-term results of a single-center trial
Authors: Triger David R. , Smart Howard L. , Hosking Shorland W. , Johnson Alan G. 
Published: March 2007

Survival after prophylactic sclerotherapy was assessed in a single-center study involving 99 cirrhotic (41 alcoholic) patients enrolled over 8-yr. The wedged hepatic vein pressure gradient was measured; those with pressure ≥ 12 mm Hg were randomized to receive sclerotherapy or no treatment. The rest were not randomized. Patients in all three groups who bled were treated with emergency endoscopy and sclerotherapy. Stratification according to presence of ascites was also undertaken. Median follow-up was 61 mo (range = 14 to 107 mo). Survival among unrandomized patients was significantly longer than among randomized patients (p < 0.006), but there was no significant difference between those treated by sclerotherapy and the controls (p = 0.27). Alcoholic cirrhotic patients undergoing sclerotherapy had better 2-yr survival than did the controls (80% vs. 43%; p = 0.09), but this benefit was not sustained at 5 yr. Survival in the nonalcoholic patient groups was identical. Only 10 of 50 deaths were caused by variceal bleeding. Forty-eight percent of patients with large varices bled, compared with 20% of patients with small varices. Wedged hepatic vein pressure < 12 mm Hg accurately identified alcoholic patients at low risk of variceal bleeding but not nonalcoholic patients. Only four episodes of variceal bleeding were attributable to elective sclerotherapy.
We conclude that in our population, prophylactic sclerotherapy alone does not improve survival. The discrepancy in survival between alcoholic and nonalcoholic cirrhotic patients suggests that factors other than variceal hemorrhage may be responsible for the difference. (Hepatology 1991; 13:117-123).
Dual association of HLA DR2 and DR3 with primary sclerosing cholangitis
Authors: Donaldson Peter T. , Farrant Mark J. , Wilkinson Mark L. , Hayllar Karen , Portmann Bernard C. , Williams Roger 
Published: March 2007

Human leukocyte antigen typing was performed in 81 patients with primary sclerosing cholangitis to investigate reported associations between human leukocyte antigen type and this disease. The results showed a significant increase in the frequency of the antigens B8 and DR3 compared with controls (53% vs. 23%, p < 0.0005, and 56% vs. 21%, p < 0.0005). This was caused by a significant rise in the frequency of the human leukocyte antigen A1 B8 DR3 haplotype (32 of 81 patients, 40% vs. 12 of 100 patients, 12%, p < 0.0005). By contrast, a significant reduction was seen in the frequency of the antigens B44 and DR4 (12% vs. 31%, p < 0.005, and 12% vs. 34%, p p < 0.001, pc p < 0.011) because of the complete absence of the B44 DR4 haplotype in the patient group (p = 0.027, Fisher's exact test). When all the DR3-positive individuals (including the DR2/DR3 heterozygotes) were eliminated, a significant secondary association with DR2 was noted, 25 (69%) of 36 remaining patients being DR2-positive compared with 27 (34%) of 79 DR3 negative controls (p < 0.0005, pc p < 0.006). Only 9% of the patients were DR2-positive and DR3-positive. Kaplan-Meier analysis demonstrated that survival was not influenced by the presence of either haplotype nor by the individual antigens. Patients who were DR3-positive were first seen at a significantly younger age than those who were DR2-positive (mean ages = 33 yr and 44 yr, respectively, p p < 0.002, Student's t test).
These data suggest that both human leukocyte antigen DR2 and the haplotype A1 B8 DR3 are independent factors that influence the initiation of PSC but do not determine the course of the disease. Furthermore, DR2 and DR3 may identify two etiological subsets of PSC. (Hepatology 1991;13:129-133).
Lysosomal and endosomal heterogeneity in the liver: A comparison of the intracellular pathways of endocytosis in rat liver cells
Authors: Kindberg Grete M. , Tolleshaug Helge , Gjøen Tor , Berg Trond 
Published: March 2007

Air-filled albumin microspheres, asialoorosomucoid and formaldehyde-treated serum albumin are selectively taken up by endocytosis in rat liver Kupffer cells, parenchymal cells and endothelial cells, respectively. Intracellular transport and degradation of endocytosed material were studied by subcellular fractionation in sucrose and Nycodenz gradients after intravenous injection of the ligand. By using ligands labeled with 125I-tyramine—cellobiose, the subcellular distribution of labeled degradation products can be studied because they are trapped at the site of formation.
The results show that the kinetics of intracellular transport are different in hepatic parenchymal, endothelial and Kupffer cells. In endothelial cells, the ligand is associated with two types of endosomes during the first minutes after internalization and then is transferred rapidly to the lysosomes. In parenchymal cells, 125I-tyramine-cellobiose-asialoorosomucoid was located in a relatively slowly sedimenting vesicle during the first minute after internalization and subsequently in denser endosomes. Degradation of 125I-tyramine-cellobiose-asialoorosomucoid in parenchymal cells started later than that of 125I-tyramine-cellobiose-formaldehyde-treated serum albumin in endothelial cells. Furthermore, the ligand seemed to be transferred relatively slowly from endosomes to lysosomes, and most of the undegraded ligand was in the endosomes. The rate-limiting step of proteolysis in parenchymal cells is probably the transport from endosomes to lysosomes. In Kupffer cells, most 125I-tyramine-cellobiose-microspheres are found as undegraded material in very dense endosomes up to 3 hr after injection. After 20 hr, most of the ligand is degraded in lysosomes distributed at a lower density than the endosomes in Nycodenz and sucrose gradients. (Hepatology 1991;13:254-259).
Interferon-α receptor expression and regulation in chronic hepatitis B virus infection
Authors: Lau Johnson Y. N. , Sheron Nick , Morris Alan G. , Bomford Adrian B. , Alexander Graeme J. M. , Williams Roger 
Published: March 2007

Interferon-α elicits antiviral and immunoregulatory activities by binding to specific receptors on the cell surface. In this study, binding characteristics of interferon-α to peripheral blood mononuclear cells in patients with chronic hepatitis B virus infection were studied using radioiodinated recombinant interferon-α2b to determine interferon-α receptor numbers and dissociation constants. A single class of interferon-α receptor was demonstrated on peripheral blood mononuclear cells and mononuclear subsets. Peripheral blood mononuclear cells from patients with chronic hepatitis B virus infection (n = 20) and controls (n = 16) expressed a similar number of interferon-α receptors (484 ± 175 vs. 511 ± 168 sites/cell respectively, p = NS) with a similar dissociation constant (dissociation constant ± 0.2 to 0.7 nmol/L). Expression of interferon-α receptors was similar in monocyteenriched and lymphocyte-enriched fractions in both groups. Similar changes were observed in patients receiving α-interferon therapy. There was no correlation between interferon-α receptors expression and serum transaminase, serum HBsAg, serum HBV DNA, liver histological findings or the response to interferon-α therapy.
After incubation of lymphocytes in vitro with interferon-α
2b
(10 to 1,000 U/ml), interferon-α receptors number dropped by 42% to 80%, but this was associated with an increase in binding affinity (dissociation constant ≈ 0.05 to 0.15 nmol/L) in both patients and controls. There was significant delay in the initial phase of receptor recovery in the patients with chronic hepatitis B virus infection compared with normal controls (days 1 and 2, p <0.05).
These data indicate that interferon-α receptors are expressed and regulated normally in chronic hepatitis B virus infection and that the variable response to interferon-α therapy is not due to a variation in interferon-α receptor. The increase in binding affinity on interferon-α therapy may be one factor explaining why long-term interferon-α therapy is effective despite a decrease in receptor number. (Hepatology 1991;13:332-338).