bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corticosteroid therapy of alcoholic hepatitis: How many studies will it take?
Authors: Reynolds Telfer B. 
Published: March 2007

Study Objective:
To determine the efficacy of a corticosteroid in reducing the short-term mortality of patients with 8evere alcoholic hepatitis.

Design:
Randomized, double-blind, placebo-controlled multicenter trial.

Setting:
Four university teaching hospitals.

Patients:
We enrolled 66 patients with alcoholic hepatitis and either spontaneous hepatic encephalopathy or a discriminant function value greater than 32, calculated using the formula: 4.6(prothrombin time -control time) + serum bilirubin [in pmoUL]/17.1. Fifty-nine patients (89%)completed the study. Two patients withdrew from the trial. The other 64 patients were hospitalized for the duration of the trial: however, treatment was discontinued in 5 patients because of potential drug toxicity.

Interventions:
Patients were randomly assigned to receive either methylprednisolone (32 mg) or placebo within 7 days of admission. Treatment was given for 28 days. The doses were then tapered over 2 weeks and discontinued.

Measurements and Main Results:
The endpoint of the study was death. Of the 31 recipients of placebo, 11 (35%)died within 28 days of randomization compared with 2 (6%)of the 36 patients given methylprednisolone (p = 0.006). The 95% CI for the difference in mortality was 12% to 70%. In the patients with spontaneous hepatic encephalopathy at entry, 9 of 19 recipients of placebo died (47%)compared with 1 (7%)of the 14 patients given methylprednisolone (p = 0.02). The 95% CI for the difference in mortality was 14% to 66%. The Cox proportional hazards regression model showed the advantage of methylprednisolone over placebo after adjustment for other potentidy important prognostic variables (p = 0.004).

Conclusions:
Methylprednisolone therapy decreases short-term mortality in patients with severe alcoholic hepatitis manifested either by spontaneous hepatic encephalopathy or a markedly elevated discriminant function value.
Monomicrobial nonneutrocytic bacterascites: A variant of spontaneous bacterial peritonitis
Authors: Runyon Bruce A. 
Published: March 2007

Spontaneous bacterial peritonitis is diagnosed when (a) the ascitic fluid culture is positive, (b) the ascitic fluid neutrophil count is ≥ 250 cells/mm3 and (c) there is no evident intraabdominal surgically treatable source for infection. Few details are available regarding the variant of ascitic fluid infection in which the culture grows bacteria (pure growth of a single type of organism), but the neutrophil count is <250 cells/mm3. In this prospective study of 138 episodes of culture-positive spontaneously infected ascites detected in 105 patients, 44 (31.9%) were episodes of “monomicrobial nonneutrocytic bacterascites” compared with 94 (68.1%) episodes of spontaneous bacterial peritonitis. Seventeen patients had both types of infection. The infection-related mortality and hospitalization mortality were similar between the two groups. Patients with bacterascites appeared to have less severe liver disease. In 62% of bacterascites episodes in which a second paracentesis was performed before any treatment the fluid spontaneously became sterile without development of ascitic fluid neutrocytosis. Thirty-eight percent of patients with bacterascites (who underwent a second paracentesis before treatment was started) progressed to spontaneous bacterial peritonitis—sometimes within a few hours. The concentration of the chemoattractant C5a was not decreased in the ascitic fluid of the bacterascites patients; this excludes ascitic fluid C5a deficiency as the explanation of the lack of neutrocytosis.
Monomicrobial nonneutrocytic bacterascites is a common variant of ascitic fluid infection that may resolve without treatment or may progress to spontaneous bacterial peritonitis. (HEPATOLOGY 1990;12:710-715).
Calcium absorption in bone disease associated with chronic cholestasis during childhood†
Authors: Bucuvalas John C. , Heubi James E. , Specker Bonny L. , Gregg Deborah J. , Yergey Alfred L. , Vieira Nancy E. 
Published: March 2007

Fractional absorption of calcium was determined in 9 children aged 4.9 to 16.9 yr with chronic cholestatic liver disease to determine the role of calcium malabsorption in the development of metabolic bone disease. Radiological evidence of rickets was absent in all patients, but bone density, measured by single beam photon absorptiometry of the distal radius, was reduced in eight of nine subjects. Serum calcium and phosphorus concentrations were normal in all except one subject. Serum 25-hydroxyvitamin D concentration was decreased compared with controls in only one of nine patients, but serum 1,25-dihydroxyvitamin D concentrations were diminished in seven of nine subjects. In all subjects, dietary calcium and phosphorus intakes were greater than 80% of the RDA. Fractional absorption of calcium, determined by oral and intravenous administration of stable calcium isotopes, was similar in cholestatic compared with control subjects (37.1% ± 12.5% vs. 34.0% ± 16.4%). In the cholestatic subjects, calcium absorption correlated with serum 1,25-dihydroxyvitamin D (r = 0.871, p < 0.002) but not 25-hydroxyvitamin D concentrations. Calcium balance, assessed by the duplicate diet method, was positive in four of five subjects. Anthropometric measurements were performed to examine the relationship between nutritional status and bone mineral content. Heights of all subjects were less than or equal to the 10th percentile and fat stores and somatic protein stores were less than the 25th percentile in six of nine subjects.
We conclude that factors other than calcium malabsorption and decreased serum 25-hydroxyvitamin D concentration contribute to diminished bone mass in children with cholestatic liver disease. (HEPATOLOGY 1990;12:1200-1205).
Hepatobiliary effects of morphine are mediated in the brain
Authors: Hurwitz Aryeh , Looney Greg , Sullins Mark , Ben-Zvi Zvi 
Published: March 2007

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component.
When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 × 10—3 mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice.
These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit. Hepatobiliary effects of morphine are mediated by interaction with opiate receptors in the brain. (HEPATOLOGY 1990;12:1406-1412).
New insights into canalicular organic anion secretion
Authors: Moseley Richard H. 
Published: March 2007

The effect of partial and complete dissipation of the membrane potential and partial depletion of cellular ATP content on the efflux of dinitrophenyl-glutathione and oxidized glutathione was examined in hepatocytes isolated from normal and mutant (TR−) rats exhibiting defective organic anion transport. Whereas alterations in the membrane potential difference had no effect on the initial efflux rate of dinitrophenyl-glutathione and oxidized glutathione, depletion of cellular ATP inhibited dinitrophenyl-glutathione and oxidized glutathione efflux and a linear relationship between the cellular ATP content and the initial efflux rate of dinitrophenyl-glutathione was observed in normal isolated rat hepatocytes. In contrast, depletion of cellular ATP content had no significant effect on the slower rate of dinitrophenyl-glutathione efflux from TR− rat hepatocytes. These findings implicate an ATP-dependent hepatic transport system for oxidized glutathione and glutathione conjugates that is absent in TR− mutants.
Fluorescence image analysis reveals normal secretion of a fluorescent bile acid fluorescein isothiocyanate glycocholate into the canalicular lumen of isolated normal and TR− mutant rat hepatocyte couplets, but negligible canalicular accumulation of a non-bileacid organic anion (carboxydichlorofluorescein diacetate) in TR− hepatocyte couplets. Canalicular membrane vesicles derived from normal rats exhibited saturable temperature- and ATP-dependent transport of sulfobromophthalein and sulfobromophthalein-glutathione that was absent in canalicular membrane vesicles from TR− rats. However, ATP-dependent daunomycin transport, reflecting transport mediated by the multidrug resistance gene product, p-glycoprotein, was present in canalicular membrane vesicles from both normal and TR− rats. Canalicular membrane vesicles from normal and TR− rats contained equal amounts of p-glycoprotein on immunoblots. These studies demonstrate that the conjugated hyperbilirubinemia in TR− mutant rats is the result of a functional absence of an ATP-dependent organic anion transport system on the canalicular membrane.
High doses of recombinant α-interferon or γ-interferon for chronic hepatitis C: A randomized, controlled trial
Authors: Sáez-royuela Federico , Porres Juan Carlos , Moreno Alberto , Castillo Inmaculada , Martinez Gracia , Galiana Fernando , Carreño Vicente 
Published: March 2007

Chronic hepatitis C is often a progressive liver disease for which there is no satisfactory treatment. We studied the efficacy of recombinant α-interferon or γ-interferon in the treatment of this disease in comparison with a control group. Thirty patients were randomly assigned to three groups. Ten patients received 7.5 MU α-interferon/m2 body surface three times weekly for 3 mo, then 5 MU/m2 for 3 mo and 2.5 MU/m2 for 6 mo. Ten patients were treated with γ-interferon at a dose of 2 MU/m2 for 6 mo and the other 10 served as controls without treatment.
The mean serum ALT levels and liver histological findings improved significantly only in the patients treated with α-interferon. No changes were observed in patients treated with γ-interferon or in controls. Five of 10 patients treated with α-interferon had complete responses (mean ALT normal during therapy). After treatment ALT returned to pretreatment levels in two of 5 patients. The long-term response rate after α-interferon therapy was 30% at 18 mo. We conclude that α-interferon is effective in controlling disease activity in a portion of patients with chronic hepatitis C. High doses of α-interferon do not appear to add further benefit in the response rate or relapse rate. γ-Interferon therapy is ineffective. (Hepatology 1991;13:327-331).
Hepatitis B virus replication modulates pathogenesis of hepatitis D virus in chronic hepatitis D
Authors: Smedile Antonina , Rosina Floriano , Saracco Giorgio , Chiaberge Elisabetta , Lattore Valter , Fabino Antonina , Brunetto Maurizia R. , Verme Giorgio , Rizzetto Mario , Bonino Ferruccio 
Published: March 2007

Hepatitis D virus and hepatitis B virus nucleic acids were detected by Northern and Southern blot hybridlzation in the sera and livers of 85 chronic carriers of HBsAg and anti-hepatitis D followed up for a mean of 10 yr. We identified three subsets of patients: 13 with hepatitis D virus and hepatitis B virus viremia, 53 with serum hepatitis D virus RNA, but without hepatitis B virus DNA and 19 negative for both nucleic acids.
Genomic and subgenomic forms of hepatitis D virus RNA were detected only in patients with hepatitis D virus and hepatitis B virus viremia. Histological findings and disease activity at admission were comparable in the three groups of patients, but the outcome was significantly worse in patients with active replication of both viruses; two of them died of terminal liver failure and hepatocellular carcinoma developed in two; the remaining patients had an uneventful course. These results suggest that active hepatitis B virus replication represents an important previously unrecognized determinant of severe liver damage in patients with chronic hepatitis D virus infection. Since hepatitis B virus provides the means for hepatitis D virus secretion and release from infected cells, active hepatitis B virus multiplication favoring the spread of hepatitis D virus from cell to cell may increase the pathogenetic potential of the defective agent. (Hepatology 1991;13:413-416.)
Laparoscopic cholecystectomy: What is really known about it?
Authors: Gumucio Jorge J. , Malet Peter F. 
Published: March 2007

Endoscopic intra abdominal surgery yet routinely used for gynecologic operations can be extended for performing cholecystectomy in uncomplicated cholelithiasis.
With the available but not yet completely satisfactory endoscopic instruments, 330 patients underwent coelioscopic cholecystectomy with few and only benign complications. The main advantages are the cosmetic aspect and strength of scars, moderation of post-operative pain and short hospital stay.
Determination of hepatitis B virus DNA in serum using the polymerase chain reaction: Clinical significance and correlation with serological and biochemical markers
Authors: Baker Bennie L. , Di Bisceglie Adrian M. , Kaneko Shuichi , Miller Roger , Feinstone Stephen M. , Waggoner Jeanne G. , Hoofnagle Jay H. 
Published: March 2007

Sera from 98 patients with various stages of chronic hepatitis B virus infection were studied to determine the clinical significance of hepatitis B virus DNA in serum detected by the polymerase chain reaction. Patients were divided into three groups according to their HBsAg and HBeAg status. Group I (n = 31) had detectable HBsAg and HBeAg, group II (n = 46) had HBsAg but not HBeAg and group III (n = 21) consisted of patients who were once chronic hepatitis B virus carriers but had lost HBsAg during follow-up.
Group I patients usually had significant liver disease (raised serum aminotransferases), had higher titers of HBsAg and had been infected with hepatitis B virus for a shorter period than patients in the other two groups. All patients in group I had hepatitis B virus DNA detectable by polymerase chain reaction and 94% had sufficient hepatitis B virus DNA present for detection by dot-blot hybridization. Group II patients had lower mean serum aminotransferase activities and titers of HBsAg than those in group I. Serum hepatitis B virus DNA was detectable by polymerase chain reaction in 78% but in only 30% of group II patients by dot-blot hybridization. Group II patients who did not have hepatitis B virus DNA detectable by polymerase chain reaction had mean serum aminotransferase levels within the normal range and had a younger mean age than those with hepatitis B virus DNA. Group III patients generally had no evidence of active liver disease. Of five patients in this group seropositive for hepatitis B virus DNA by polymerase chain reaction on initial testing, all eventually became negative for hepatitis B virus DNA on subsequent testing. There was a tendency for those patients in group III with hepatitis B virus DNA detectable by polymerase chain reaction to have elevated serum aminotransferase levels (40% vs. 25%); however, these differences were not statistically significant.
Taken together, these data show that the presence of hepatitis B virus DNA in serum as detected by polymerase chain reaction appears to be a good marker of the level of viremia, can be correlated with aminotransferase levels and parallels the presence of HBsAg in serum. (Hepatology 1991;13:632-636.)
Inhibition by colchicine of biliary secretion of diethylmaleate in the rat: Evidence for microtubule-dependent vesicular transport
Authors: Dumont Micheline , D’Hont Scorinnem , Durand-Schneider Anne-Marie , Legrand-Defretin Véronique , Feldmann Gérard , Erlinger Serge 
Published: March 2007

It has been proposed that a microtubule-dependent transport of vesicles derived from the Golgi apparatus may play a role in biliary secretion of bile salts and other cholephilic anions. To test this hypothesis, we examined the influence of colchicine and vinblastine, two microtubule inhibitors, on diethylmaleate-induced bile flow and on the biliary secretion of diethylmaleate, an organic anion whose glutathione conjugates may be secreted into bile through the Golgi apparatus and Golgi-derived vesicles. Rats were pretreated with colchicine or vinblastine, and diethylmaleate was injected intraperitoneally at doses of 28 to 400 μmol/100 gm body wt. Basal bile flow was unaffected by colchicine or vinblastine. In contrast, diethylmaleate-induced bile flow and the secretion into bile of diethylmaleate conjugates (estimated by the cation-anion gap in bile) were significantly lower in colchicine-treated and vinblastine-treated animals than in controls. Diethylmaleate-induced bile flow was reduced in proportion to diethylmaleate conjugate secretion. A linear relationship was seen between bile flow and biliary output of diethylmaleate conjugates: this relationship was similar in colchicine-treated or vinblastine-treated animals and in controls. At electron microscopy, diethylmaleate had induced distension of the Golgi saccules of the hepatocytes.
In conclusion, colchicine and vinblastine inhibited the secretion into bile of diethylmaleate conjugates and diethylmaleate-induced bile flow. These results support the view that microtubule-dependent transport of Golgi-derived vesicles is involved in the biliary secretion of diethylmaleate and, perhaps, other cholephilic organic anions. (HEPATOLOGY 1991;14:10-15.)
Clinical significance of two forms of IgM antibody to hepatitis delta virus
Authors: Jardi Rosendo , Buti Maria , Rodriguez-Frias Francisco , Garcia-Lafuente Ana , Sjogren Maria H. , Esteban Rafael , Guardia Jaime 
Published: March 2007

Separation of 7-8 S and 19 S forms of serum IgM antibodies to the hepatitis delta virus by rate-zonal centrifugation was carried out on serum from 24 patients with hepatitis delta virus infection: 4 patients with acute, self-limited hepatitis; 5 patients with hepatitis delta virus superinfection progressing to chronicity; and 15 patients with chronic hepatitis delta virus.
The high molecular weight IgM form (19 S) was predominantly detected in acute hepatitis delta virus cases, whereas the low molecular weight (7 S) form was found in chronic hepatitis delta virus cases. The serological profile of these two forms of IgM antibody to hepatitis delta virus was investigated in serial samples from five patients with acute hepatitis delta virus superinfection that evolved to chronic hepatitis delta virus. We found that, in the acute stage of the disease, the 19 S form was predominant, whereas 6 mo later a predominance of 7-8 S IgM was observed. These results suggest that IgM antibody to hepatitis delta virus antibody forms are different in acute and chronic hepatitis delta virus infection and that their detection only helps in differentiating an acute infection from a chronic infection but not a hepatitis delta virus—hepatitis B virus.-HBV coinfection from hepatitis delta virus superinfection in the acute stage of the disease. (HEPATOLOGY 1991;14:25-28.)
Interpenetrating polymer networks containing gelatin modified with PEGylated RGD and soluble KGF: Synthesis, characterization, and application in in vivo critical dermal wound
Authors: Waldeck Heather , Chung Amy S. , Kao Weiyuan John 
Published: March 2007

AbstractThe purpose of this study was to evaluate the biocompatibility and the efficacy in wound healing of a gelatin‐based interpenetrating polymer network (IPN) containing poly(ethylene glycol) (PEG)‐ylated RGD and soluble KGF‐1 (RGD‐IPN+KGF). IPNs were applied to full‐thickness wounds on a rat model. Wound healing was assessed through histological grading of the host response and percent area contraction at 2 days, 1 week, 2 weeks, and 3 weeks. A control IPN containing unmodified gelatin (unmod‐IPN) and a conventional clinical bandage were applied to similar wounds and also evaluated. During the first week of healing, the unmod‐IPN and conventional dressing wound showed a greater amount of contraction than that of RGD‐IPN+KGF. However, by 3 weeks the extent of wound contraction was comparable between treatments. The RGD‐IPN+KGF treated wound demonstrated lower macrophage and fibroblast densities at 3 weeks as compared to unmod‐IPN treated wounds. RGD‐IPN+KGF acted as a tissue scaffold while preventing the entry of foreign bodies, advantages not seen with the conventional dressing. The extent of cellularity and extracellular matrix organization was higher for wounds healed with RGD‐IPN+KGF than those healed with unmod‐IPN. These results indicate that both soluble and immobilized bioactive factors can be incorporated into our IPN platform to enhance the rate and the quality of dermal wound healing. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res 2007
Effect of solvent content on resin hybridization in wet dentin bonding
Authors: Wang Yong , Spencer Paulette , Yao Xiaomei , Brenda Bohaty 
Published: March 2007

AbstractWith wet bonding techniques, the channels between the demineralized dentin collagen fibrils are filled with debris, solvent, and water. Commercial adhesives include solvents such as ethanol or acetone to facilitate resin‐infiltration into this wet substrate. Under in vivo conditions, the solvent may be diluted because of repeated exposure of the material to the atmosphere, or concentrated because of separation of the bonding liquids into layers within the bottle. The purpose of this study was to investigate the effect of different concentrations of ethanol (10–50%) on infiltration of the adhesive resin and collagen fibril encapsulation in the adhesive/dentin interface using light microscopy, micro‐Raman spectroscopy, and scanning electron microscopy. The results indicated that under wet bonding conditions the hybridization process was highly sensitive to the initial solvent concentration in the adhesive system. The staining and scanning electron microscopy results showed that the quality of the interfacial hybrid layer was poor at the lower (10%) or higher (50%) ethanol content. Micro‐Raman analysis indicated that there was a distinct difference in the degree of adhesive penetration among adhesives containing different concentrations of ethanol. Adhesives containing 10 or 50% ethanol did not realize effective penetration; the penetration of the adhesive monomers increased dramatically when the initial ethanol content was 30%. The amount of solvents are essential for achieving effective bonding to dentin. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007