Search PubMed⌕ Search

Biomedical subjects

J Fevery

Publications and source records attributed to J Fevery.

At least 181 records · Page 10Linked to original sources
PubMed1981

Human non-A, non-B hepatitis: ultrastructural alterations in hepatocytes.

Ultrastructural investigation of liver biopsies from two patients with non-A, non-B hepatitis revealed cytoplasmic and nuclear alterations in the hepatocytes. The lesions in both patients, one with acute and one with chronic hepatitis, were similar and distinct from those previously described in other forms of hepatitis. These findings are compared with the reported findings in chimpanzee liver after inoculation with non-A, non-B infective material. The intranuclear findings are similar to the aggregations of 20-27 nm particles described in some infected chimpanzees, and the cytoplasmic alterations seem to be similar to the cytoplasmic structures and tubular arrangements reported in other inoculated chimpanzees. A striking finding of this study is the presence of both alterations together in the same biopsy in two different patients, suggesting that they represent a different stage of viral infection or different parts of the viral agent. It still remains to be proved that the ultrastructural particles indeed contain antigen(s) of the non-A, non-B hepatitis virus. The nuclear and cytoplasmic alterations are, however, characteristic for non-A, non-B hepatitis and are useful as ultrastructural hallmarks of this form of hepatitis.

Adult↗
PubMed1981

Cholestatic action of somatostatin in the rat: effect on the different fractions of bile secretion.

Somatostatin was administered intravenously to male Wistar rats, recovered for 3 h from an anesthesia during which the common bile duct and jugular vein were cannulated. Different bile acid-secretory rates were obtained by infusion of saline, or of Na+-taurocholate (150 nmol/min/100 g body wt), or by 8-h bile depletion. At the dose of 2 micrograms/h/100 g body wt, somatostatin causes a prompt decrease of bile flow (about 30%) and of bile acid secretion (32%-47%). The bile acid-independent fraction of canalicular bile is more decreased than the one associated with bile acid secretion. The changes are dose dependent and show a saturation pattern, with half-maximal saturation already at 2.2 ng/min/100 g body wt. Despite this cholestasis, endogenous bilirubin secretion remained unchanged, pointing to different secretory mechanisms for bilirubin and bile acids. In the isolated and perfused liver, somatostatin displays an anticholeretic effect, proportional to the amount of Na+-taurocholate present in the system. Hepatic blood flow and O2 consumption remained constant during perfusion, and were not affected by somatostatin. The hepatic transport of bile acid, and the water and electrolyte secretion are directly affected by somatostatin, and the experimentally-induced cholestasis seems a new and suitable model for studying mechanisms of bile secretion.

Animals↗
PubMed1980

Glucuronidation of bilirubin and the occurrence of pigment gallstones in patients with chronic haemolytic diseases.

A group of thirty-seven patients with increased haem catabolism has been studied to gain insight in their bilirubin conjugating capacity. Bilirubin UDP-glucuronyl transferase activity (GlcATa) in the liver and bilirubin monoconjugates in bile were measured and the hepatic bilirubin clearance was calculated from the radio-chromium-survival data. In the present group, 41% of the patients clearly had a deficiency in bilirubin conjugation similar to what is classically found in Gilbert's syndrome. The association may facilitate detection of these patients as serum bilirubin levels were higher (65.8 microM +/- 19) (m +/- 1 SD) in the fifteen patients with associated Gilbert's syndrome versus thirteen having only haemolysis (43.6 microM +/- 15). A fair correlation was found between the percentage of monoconjugates in bile and the GlcATa levels in the liver as well as with the calculated hepatic bilirubin clearance, although some discrepancies exist. Using these determinations, a clearcut separation from normal values was not obtained, suggesting at least in the present group of patients that Gilbert' syndrome represents only one end of a continuum of bilirubin conjugation rates and not a separate entity. Pigment stones in the gall-bladder were documented in 51% of the patients and usually at an early age. There was no relationship towards sex, serum bilirubin, GlcATa in liver, total bilirubin or monoconjugates in bile. Age played some role as well as the type of haemolysis as all patients with congenital dyserythropoiesis (n = 4) or acquired haemolysis (n = 3) had lithiasis. Moderate chronic cholecystitis was present, whereas an accumulation of iron and bile pigment was evident in the liver.

Adolescent↗
PubMed1979

Stimulation by secretin of bilirubin UDP-glycosyltransferase activities and of cytochrome P-450 concentration in rat liver.

The activity of bilirubin UDP-glucuronyltransferase in liver tissue was increased 1.5-fold after 90 min of secretion administration (4 i.u./h per kg body wt.) in anaesthetized Wistar rats biopsied half-hourly over a period of 2 h. In unanaesthetized R/A Wistar rats, activities of liver enzymes were assayed after administration secretin for 1 h. Bilirubin UDP-glycosyltransferase activities and cytochrome P-450 concentration were increased, but p-nitrophenol UDP-glucuronyltransferase and UDP-glucose dehydrogenase activities remained unchanged.

Animals↗
PubMed1979

Gallbladder wall sonolucency in acute cholecystitis.

The usual ultrasound findings in acute cholecystitis include diffuse hyperreflective wall thickening, hazy wall delineation and gallbladder distension. In 11 patients with acute cholecystitis, an additional sign was seen consisting of a hyporeflective or sonolucent layer, continuous or interrupted, within the hyperreflective, thickened gallbladder wall. Anatomic-pathologic correlation, comparative CT scans and clinical follow-up studies showed subserosal edema and necrosis to be the most probable cause of this finding.

Acute Disease↗
PubMed1979

Hepatitis B core antigen immune complexes in the liver of hepatitis B patients.

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.

Antigen-Antibody Complex↗
PubMed1978

The fate of bilirubin-IXalpha glucuronide in cholestasis and during storage in vitro. Intramolecular rearrangement to positional isomers of glucuronic acid.

1. In aqueous solution above pH7 bilirubin-IXalpha 1-O-acylglucuronide rapidly isomerizes to the non-C-1 glucuronides by sequential migration of the bilirubin acyl group from position 1 to positions 2, 3 and 4 of the sugar moiety. The transformations are enhanced by increasing the pH. Compared with the rates at 37 degrees C the transformations are rather slow at 0 degrees C. Virtually complete inhibition is observed at values below pH6. The isomerization at 25 degrees C and pH 7.4 is not affected by the presence in the solutions of a molar excess of human serum albumin. 2. Isomerization in bile kept at 37 degrees C at pH7.7-7.8 is probably non-enzymic, as the rates of change are similar to those observed under comparable conditions for aqueous solutions of glucuronides of bilirubin-1Xalpha and of azodipyrrole. 3. Analysis without delay of normal biles of man and rats collected at 0 degrees C over a maximum period of 10 min shows that the bilirubin-IXalpha mono- and di-glucuronides consist exclusively of the 1-O-acyl isomers. 4. The mixtures of the four positional isomers of bilirubin-IXalpha glucuronide found in freshly collected biles of man and rats with cholestasis probably originate from initially synthesized 1-O-acylglucuronide by the same mechanism of sequential migration as has been observed in aqueous solutions of conjugated bilirubin-IXalpha.

Animals↗
PubMed1978

Gallbladder wall thickening: a new sign of gallbladder disease visualized by gray scale cholecystosonography.

The use of gray scale equipment in a prospective study of radiologically non-visualizing gallbladders, permitted detection of a new echographic aspect of gallbladder disease. Along with even, discrete bile thickening and the presence of sand-sized calculi, thickening of the gallbladder wall incholecystitis is another ultrasonographic sign of gallbladder disease that can be visualized successfully by gray scale ultrasound.

Cholecystography↗