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Biomedical subjects

O Bernard

Publications and source records attributed to O Bernard.

At least 289 records · Page 16Linked to original sources
PubMedDate not supplied

Pigment gallstones of the common bile duct in infancy.

Ten infants of less than 6 months of age presented with cholestatic jaundice and gallstones. Jaundice occurred after a lag period, and sepsis was present in three children. Ultrasound examination showed dilatation of intrahepatic and extrahepatic bile ducts in eight patients and detected cholelithiasis in three. Percutaneous transhepatic cholangiography and/or surgery allowed separation of the patients into two groups: (i) six children with lithiasis in the distal common bile duct, and (ii) four children with lithiasis associated with bile duct perforation at the junction between the cystic and common bile ducts with gallstones probably secondary to bile stasis and infection. Surgical treatment was confined to removal of calculi and drainage in eight children; biliary reconstructive surgery was necessary in the other two who had serious biliary duct lesions. No recurrence was observed after 1 to 7 years. The pigmentary nature of cholelithiasis was established by stone morphology in all cases, and by bile and stone analysis in several cases.

Bile↗
PubMedDate not supplied

Anti-liver-kidney microsome antibody is a marker for the rat hepatocyte endoplasmic reticulum.

Human sera, containing anti-liver-kidney microsome antibody as demonstrated by indirect immunofluorescence, were obtained from a subgroup of young patients with autoimmune chronic hepatitis. The anti-liver-kidney microsome antibody-positive sera were used to study the localization of the liver-kidney microsome antigen in hepatocytes. Immunoblot analysis of microsomal subfractions, lysosomal membranes, plasma membranes, mitochondria and purified ribosomes obtained from rat liver demonstrated that this antibody recognizes a protein of 50 kD present only in endoplasmic reticulum membranes. Immunogold labeling of ultrathin frozen sections and immunoperoxidase staining of 11 to 15 micron cryostat sections were used to detect the liver-kidney microsome antigen in rat liver tissue. The anti-liver-kidney microsome antibody binds to antigenic domains on the cytoplasmic face of smooth and rough endoplasmic reticulum membranes of hepatocytes. No labeling was observed of the Golgi apparatus, peroxisomes, mitochondria, lysosomes, nuclei or plasma membranes. Not only was the antigen recognized by the anti-liver-kidney microsome antibody specific for endoplasmic reticulum membranes, but it was also specific for the endoplasmic reticulum of hepatocytes only, since no labeling was observed in any organelle of Kupffer or endothelial cells. Therefore, the anti-liver-kidney microsome antibody can be considered as a marker for endoplasmic reticulum in rat hepatocytes.

Antigens↗
PubMedDate not supplied

Chronic active hepatitis associated with antiliver/kidney microsome antibody type 1: a second type of "autoimmune" hepatitis.

Sixty-five patients with histologically proven chronic active hepatitis of unknown cause but associated with the antiliver/kidney microsome antibody type 1, confirmed by immunofluorescence and immunoprecipitation, were selected as forming a special entity. This disease was found to be rare with a prevalence of 5/1,000,000. The female to male ratio was 8:1. The condition occurred at all ages but was most common between the ages of 2 and 14 years. In 22 of the 65 cases, the hepatitis was associated with an autoimmune disease, most commonly insulin-dependent diabetes, autoimmune thyroid disease and vitiligo. The same autoimmune diseases were present in first-degree relatives from seven families. In 36 cases, the onset of disease resembled acute viral hepatitis. Serum biochemical tests showed marked elevation in aminotransaminases and hypergammaglobulinemia. Paradoxically, serum and salivary IgA levels were often normal or low. Histologic findings were multifocal hepatic necrosis with bridging in the acute stage, and aggressive hepatitis with mononuclear cell infiltration or macronodular cirrhosis in the late stages. Serologically, apart from the presence of antiliver/kidney microsome antibody type 1, the disease was characterized by the absence of antiactin, antimitochondria and antinucleus antibodies; however, organ-specific autoantibodies were often present. The clinical course was usually severe: six patients in the acute stage presented with fulminant hepatitis, and all, except two, other patients progressed to cirrhosis. Prolonged treatment with corticosteroids and immunosuppressants was usually effective in rendering the cirrhosis inactive. The cumulative survival rate was 51% at 14 years. We propose to call this entity "anti-LKM1 chronic active hepatitis" or "autoimmune hepatitis type II" to differentiate it from classical "lupoid hepatitis" or autoimmune hepatitis type I.

Autoantibodies↗
PubMedDate not supplied

Pharmacokinetics of tacrolimus (FK506) in paediatric liver transplant recipients.

The pharmacokinetics of intravenous and oral tacrolimus was assessed in paediatric liver transplant patients at two centers in Europe. Sixteen patients, age 0.7 to 13 years, participated in the study; 12 patients were evaluable for intravenous pharmacokinetics, and 16 for oral. Intravenous tacrolimus was given as a continuous 24 h infusion (mean 0.037+/-0.013 mg/kg/day), and oral tacrolimus was given in 2 doses per day (mean 0.152+/-0.015 mg/kg). Whole blood samples for the intravenous pharmacokinetic profile were taken before initiation of the first infusion, 4, 8, 12 and 24 h post-infusion, and every 24 h thereafter until intravenous administration was discontinued. During the 12 h wash-out period between intravenous and oral administration, samples were taken every 3 h. Samples for the oral pharmacokinetic profile were taken immediately before the first oral dose and 0.5, 0.75, 1, 2, 2.5, 3, 4, 6, 8, 10 and 12 h post-administration. Non-compartmental procedures were used to characterise the pharmacokinetic parameters. Mean estimates for clearance and terminal half-life were 2.3+/-1.2 ml/min/kg and 11.5+/-3.8 h, respectively, following intravenous tacrolimus. The mean bioavailability of oral tacrolimus was 25+/-20%. A strong correlation was observed between AUC and trough whole blood levels of tacrolimus (r=0.90). The clearance was approximately 2-fold higher than that previously observed in adults; this could explain the higher dosage requirements in children.

Administration, Oral↗
PubMedDate not supplied

LIM-kinase1.

LIM-kinase1 (LIMK1) is a serine-only protein kinase that contains LIM and PDZ protein-protein interaction domains which is highly expressed in neurons. Overexpression of LIMK1 in cultured cells results in accumulation of filamentous (F-) actin. LIMK1 phosphorylates cofilin, an actin depolymerisation factor, which is then unable to bind and depolymerise F-actin. Rac-GTP enhances phosphorylation of LIMK1 and cofilin, which leads to accumulation of F-actin, while Rac-GDP and PMA reduce these effects. LIMK1 is therefore a key component of a signal transduction network that connects extracellular stimuli to changes in cytoskeletal structure. Control of cell morphology and mobility via LIMK1 activity may provide novel approaches to cancer therapy.

Humans↗
PubMedDate not supplied

Detection of anti-endoplasmic reticulum antibody-positive autoimmune hepatitis in children, using an ELISA technique.

Anti-endoplasmic reticulum antibody positive autoimmune hepatitis in children is characterized by the recognition of a single 50,000 MW protein of the endoplasmic reticulum in liver microsomal fractions by their sera. We have developed an enzyme-linked immunosorbent assay technique with rat liver microsomal preparations as the antigen to be used for detection of this disease. Titers obtained may be useful in following the course of the disease and as an aid in determining when therapy can be discontinued. The technique is rapid, sensitive, reproducible, and simple to perform and is easier to manipulate than immunofluorescence or radioimmunoassay techniques.

Animals↗
PubMedDate not supplied

Time to exhaustion at VO2max and lactate steady state velocity in sub elite long-distance runners.

The aim of the present study was to estimate the importance of lactate steady state velocity (WCL) of the running velocity at maximal oxygen uptake (Va max) and its time to exhaustion (Tlim), in the performance of a half marathon stated by the velocity over 21.1 km sustained by the runners during 1 h 12 min +/- 2 min 27 s. The population consisting of ten sub-elite male long distance runners (32 +/- 4 years old) was homogeneous with regard to their velocities on 21 km (V21 = 17.5 +/- 0.88 km.h-1, coefficient of variation, CV = 5%) and their aerobic maximal speed (Va max) (21.6 +/- 1.2 km.h-1, CV 6%). The fractional utilization of VO2max on 21 km was calculated from their own running economy (oxygen consumed per kilo of body mass and kilometer run (194 +/- 74 ml.kg-1.km-1). V21 represented 83 +/- 5% VO2max (VO2max = 68.1 +/- 4.1 ml.kg-1.min-1) and 81 +/- 3.3% Va max. The velocity corresponding to lactate steady state and called "lactate steady state velocity" (WCL) was measured according to a protocol proposed by CHASSAIN (1986). The subjects ran twenty minutes at a constant velocity representing 70-75% and 85-90% VO2max. Lactatemia was measured at the fifth (Lact 5) and the twentieth minute (Lact 20). Lactate slope was measured for two running velocities in order to determine the velocity (WCL) corresponding to lactate steady state, i.e. the lactate slope is equal to zero.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Course of chronic hepatitis related to B virus in children. Study of serum viral DNA].

Nineteen children with chronic hepatitis related to the hepatitis B virus were followed for an average of 6 years. The determination of the hepatitis B virus DNA in the serum allowed us to know the state of viral replication. Thus three groups of patients could be defined: the first in which replication remained active during the total period of follow-up; the second in which the extinction of replication was observed; the third in which replication was inactive from the beginning of the serological follow-up. Symptoms, high levels of aminotransferases and histologically aggressive lesions, sometimes with cirrhosis, were more frequent in the presence of viral DNA. During the decrease of the replication, a clear-cut and time-limited increase of serum-aminotransferase levels was often noted. After the disappearance of hepatitis B virus DNA in the serum, clinical signs could be found only in children with cirrhosis or hepatocellular carcinoma. Four cases of hepatitis with initial aggressive lesions led to persistent chronic hepatitis without viral DNA in the serum. In all but one of the patients who started with an aggressive form, viral DNA disappeared in the serum. This loss occurred later and only in 2 patients of 5 who presented initially with chronic persistent hepatitis. Thus a long period of follow-up in childhood chronic hepatitis related to B virus shows frequent inactivation of viral replication. This evolution seemed to occur earlier when the initial histological lesions were aggressive as if this aggressiveness favored the elimination of the virus and the presence of specific antibodies in the serum.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Portal hypertension in children. Hemorrhagic risk and measures for prevention (author's transl)].

The retrospective analysis of 201 children who presented with portal hypertension and were investigated by esophageal endoscopy provides the following results : 1) esophageal varices were present in 90% of the children examined; 2) the hemorrhagic risk is much higher in children with extra hepatic portal obstruction (gastrointestinal bleeding occurred in 80% of these children) than in children with intrahepatic or postsinusoidal portal hypertension (29%); 3) endoscopic signs of major portal hypertension such as tension of varices and/or congestion of the esophageal mucosa were present in virtually all children who experienced one or more episodes of gastrointestinal bleeding; 4) esophageal or gastric lesions not related to varices were responsible for bleeding in 6 children; 5) gastric varices were present in 21 of 105 children in whom a thorough gastric endoscopy was carried out; 6) partial or complete regression of varices occurred in 11 of 27 children in whom several endoscopies were performed with a follow-up of 9 months to 6 years; complete regression occurred only when varices were of small size; 7) measures used to prevent gastrointestinal bleeding in children with varices often failed when endoscopic signs of major portal hypertension were present. These results confirm the major importance of eso-gastric endoscopy in the investigation of children with portal hypertension and suggest that porto-systemic surgical shunts should be considered in children who experience at least one spontaneous episode of gastrointestinal bleeding provided the responsibility of varices is ascertained by endoscopy.

Child↗
PubMedDate not supplied

[Early gastro-intestinal bleeding in children with portal hypertension (author's transl)].

From the retrospective study of 47 children who presented with portal hypertension and gastro-intestinal bleeding before 3 years of age, the following conclusions can be drawn: 1) The cause of portal hypertension was extrahepatic portal obstruction in 35 children, cirrhosis in 10 and congenital hepatic fibrosis in 2. 2) Endoscopic signs of major portal hypertension were present in 26 of 27 children in whom a thorough endoscopic examination was carried out. 3) Most children experienced several episodes of bleeding. One or several hematemeses occurred in 36 children, one or several episodes of melaena in 23, one or several proctorrhagia in 5 and anemia alone in 2. Two children with liver failure died during a gastrointestinal bleeding episode. 4) Transthoracic direct ligation of esophageal varices was performed in 8 children ; all but one experienced one or more episodes of bleeding within one year after surgery. One child died during one of these episodes. 5) A surgical portosystemic shunt was carried out in 37 rated on before the age of 3. Shunts were successful in 7 of 11 children who were ope children. Patency of the shunt was demonstrated in 32. These results show that early shunt surgery can provide a permanent solution to the life-threatening problems of gastrointestinal bleeding in young children with portal hypertensions.

Age Factors↗