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Biomedical subjects

P Czygan

Publications and source records attributed to P Czygan.

At least 19 recordsLinked to original sources
PubMed1987

Chronic ursodeoxycholic acid- and chenodeoxycholic acid-feeding-induced changes of colon mucosal cell proliferation in rats.

Hyperproliferation has been suggested to play a major role in bile acid-dependent colorectal tumor promotion. Effects of chronic feeding of chenodeoxycholic acid (CDC) and ursodeoxycholic acid (UDC) were tested on cell proliferation in the colon of male noninbred Wistar rats. By use of a dynamic method measuring actual rates of cell production, proliferation was modulated by both bile acids only in the proximal part of the colon. UDC feeding produced mild hyperproliferation of basal crypt cells (cell position 5-8: 7.6 +/- 2.0 vs. 3.5 +/- 1.3 cells/1,000 cells/hr--P less than .05; cell position 9-12: 18.1 +/- 10.7 vs. 10.3 +/- 2.9--P less than .05; cell position 13-16: 18.1 +/- 8.9 vs. 9.1 +/- 2.3--P less than .05). This finding reflected a characteristic compensatory response to superficial cell damage. However, CDC application did not effect cell regeneration in this crypt area but led to a striking drop of cell renewal in higher crypt cell positions (positions greater than or equal to 17), where no proliferation was detectable. These data suggest that CDC exerts its tumor-promoting effect by other means than hyperproliferation.

Animals↗
PubMed1986

Isomers of bilirubin glucuronide in serum and bile before and after relief of common duct obstruction.

Isomers of bilirubin glucuronide with the bilirubin acyl group attached to the C1-, C2-, C3- and C4-positions of the glucuronyl residue are present in bile of patients with extrahepatic cholestasis, whereas in normal bile only C1-isomers are found. In the present study, these bilirubin glucuronide isomers, and the fractions of unconjugated bilirubin, and bilirubin mono- and diconjugates were determined in serum and bile of 8 patients before and after relief of common duct obstruction by endoscopic papillotomy. Before papillotomy we found 39.6% C1-isomers (median value), 22.2% C2-isomers, 19.3% C3-isomers and 11.4% C4-isomers in the bile. The values in serum before papillotomy were comparable. Twenty-four hours after papillotomy, the level of C1-isomers in bile increased significantly to 56.3% (P less than 0.05) with a concomitant decrease of the non-C1-isomers. In contrast, in serum the isomers of bilirubin glucuronide did not change significantly at 24 h after papillotomy. Before papillotomy, the fraction of unconjugated bilirubin in bile was 3.6% of the total, with 15.8% bilirubin monoconjugates and 75.5% bilirubin disconjugates. After papillotomy, unconjugated bilirubin decreased to 1.6% (n.s.) and bilirubin monoconjugates to 11.9% (n.s.), while bilirubin diconjugates increased to 86.1% (P less than 0.05). In serum, the elevated fractions of bilirubin diconjugates and monoconjugates decreased from 38.4 to 32.2% (P less than 0.05) and from 29.6 to 23.4% (n.s.), respectively. In parallel, the fraction of unconjugated bilirubin in serum increased from 24.1 to 37.0% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

[Frequency of delta infections in Heidelberg].

The frequency of delta infection was studied in sera of 203 patients with acute hepatitis B, further 461 hepatitis B virus surface antigen-(HBsAg)-positive patients and 117 HBsAg-negative controls by determination of anti-delta by a competitive enzyme immunoassay. Sera have been collected since 1974. None of the sera of acute hepatitis B was anti-delta-positive whereas seven of the HBsAg-positive carriers were anti-delta-positive. Two of the anti-delta-positive patients had chronic hepatitis, four had liver cirrhosis. One of the anti-delta-positive patients with liver cirrhosis died of liver failure. Risk factors included Italian origin and parenteral routes of infection. All sera of 19 relatives of three anti-delta-positive index cases remained anti-delta-negative.

Antibodies, Viral↗
PubMed1985

Different effects of dietary chenodeoxycholic acid and ursodeoxycholic acid on colonic adenylate cyclase in the rat.

The oral administration of dietary chenodeoxycholic acid (1%), but not of ursodeoxycholic acid (1%), to male Sprague Dawley rats results in a significant increase in the colonic adenylate cyclase activity without any influence on the colonic cyclic-AMP phosphodiesterase activity. No effect of chronic bile acid feeding on the response of colonic adenylate cyclase to prostaglandin E2 and vasoactive intestinal peptide is observed. These data emphasize a dependence of the cyclic-AMP adenylate cyclase activation on the chemical structure of the bile acid. This may be of pathophysiologic relevance with respect to the frequently observed diarrhea as a side effect of oral chenodeoxycholic, but not ursodeoxycholic acid therapy for cholesterol gallstone dissolution in man.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Duodenal gamma-glutamyltransferase activity in human biopsies: effect of chronic ethanol consumption and duodenal morphology.

Gamma-glutamyltransferase activity was determined in duodenal biopsies, and in the sera of forty-six non-alcoholic and eighteen alcoholic patients with a daily alcohol consumption of more than 80 g. Additionally, duodenal morphology was examined in biopsy material obtained at the same time. In both alcoholics (P less than 0.05) and in non-alcoholics (P less than 0.001) the duodenal gamma-glutamyltransferase activity revealed a significant positive correlation with duodenal villus length. In addition, alcoholics exhibited a significant decrease in duodenal villus length (338 +/- 13 vs. 363 +/- 13 microns, P less than 0.01), and a significant increase in duodenal gamma-glutamyltransferase activity (13.0 +/- 1.4 vs. 8.4 +/- 0.6 mU mg-1 protein, P less than 0.01) when compared to controls. No significant correlation was found between duodenal and serum gamma-glutamyltransferase activity in alcoholics and non-alcoholics. During follow up of two patients, duodenal gamma-glutamyltransferase activity decreased and duodenal villus length increased after withdrawing alcohol. These data underline the damaging effect of alcohol on the duodenal mucosa and demonstrate that chronic alcohol intake reversibly effects duodenal gamma-glutamyltransferase. In addition, the small intestine appears of minor importance as an origin for the elevated serum gamma-glutamyltransferase activities seen in the alcoholic.

Adult↗
PubMed1985

[Integrated and nonintegrated hepatitis B virus DNA in liver tissue].

Liver tissue was taken in eight patients with virus hepatitis B and one patient with liver carcinoma by biopsy, as well as in seven other patients at post mortem. HBV-DNA was measured in these tissue specimens by hybridization. In four out of eight patients who had had biopsy, HBV-DNA could be found; in two patients it was present in integrated form. The same was true for the tumor tissue stemming from the patient with liver carcinoma. In five out of eight liver tissue specimens taken at post mortem HBV-DNA could be demonstrated as well; it was integrated into the host genom in two cases. It may be important to find out in patients with chronic hepatitis virus infection, if HBV-DNA is present in free or integrated form before antiviral treatment is considered.

Adult↗
PubMed1985

Stimulation of chemically induced rectal carcinogenesis by chronic ethanol ingestion.

The effect of chronic ethanol administration on 1, 2-dimethylhydrazine-induced rectal carcinogenesis was investigated in 32 paired male Sprague-Dawley rats fed a nutritionally-adequate liquid diet containing 36% of the total calories as either ethanol or isocaloric carbohydrates. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs 6; P less than 0.02), whereas no cocarcinogenic effect of ethanol was observed in other parts of the intestine. Alcohol did not influence tumor size or histopathology. A 47% increase in the activity of mucosal alcohol dehydrogenase in the distal colorectal region was found between chronically-ethanol-fed rats and pair-fed controls (0.241 +/- 0.019 vs 0.164 +/- 0.020 mumol/mg of protein/hr; P less than 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Faecal bile acids, however, do not play a role as promotors of rectal carcinogenesis under the present experimental conditions. The results give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.

Adenocarcinoma↗
PubMed1985

Determination of HBV DNA by a simplified method of spot hybridization.

Molecular hybridization was employed to detect HBV DNA in sera of patients with acute or chronic hepatitis, by a simplified version of the spot hybridization technique. HBV DNA was found in 21 out of 50 sera obtained in acute hepatitis B. Determination of HBV DNA was negative in sera of patients with hepatitis A, Epstein-Bar virus infections or other HBsAg-negative liver diseases. There was no cross-hybridization between HBV DNA and sera of patients with non-A, non-B hepatitis.

Acute Disease↗
PubMed1985

Determination of HBV DNA in serum in a case of needlestick hepatitis.

HBV DNA in serum was determined by modified spot hybridization. A nurse of the dialysis staff was inoculated via needlestick with blood of a HBsAg-positive hemodialysis patient, who had 2000 pg HBV DNA per milliliter serum. After insufficient passive immunization the nurse developed transient anicteric hepatitis B. HBV DNA was positive in sera of the recipient before and at the beginning of the elevation of transaminases.

Adult↗
PubMed1984

[Anti-HBc IgM in acute and chronic hepatitis B virus infection].

Hepatitis B core antigen (HBcAg) synthesized in E. coli was used for determination of immunoglobulin M class-specific antibodies against HBcAg. It was found that 98% of cases with acute hepatitis B surface antigen (HBsAg) positive hepatitis type B were anti-HBc immunoglobulin M (IgM) positive. Atypical hepatitis B was detected in 33% of anti-HBc-positive HBsAg-negative cases with acute hepatitis. Anti-HBc IgM was positive for 6 months in acute resolving hepatitis type B, whereas cases resulting in chronic hepatitis B remained anti-HBc IgM-positive for up to 900 days. Chronic HBsAg carriers with severe liver disease had anti-HBc IgM more often than individuals with minor liver damage; 83% of HBsAg-positive liver cirrhoses, 63% of chronic aggressive hepatitis, 50% of HBsAg-positive liver carcinoma, but only 17% of chronic persistent hepatitis or 7% of healthy blood donors were anti-HBc IgM-positive. Determination of anti-HBc IgM is useful in detecting atypical hepatitis B virus infections without HBsAg in serum and, with some restrictions, in discriminating acute and chronic hepatitis type B.

Acute Disease↗
PubMed1984

Detection of hepatitis B viral DNA in sera positive for antibody to delta antigen.

Hepatitis B virus (HBV) DNA was detected in 17 sera positive for antibody to delta antigen (anti-delta). Six sera from two patients were positive for HBV DNA. Analysis by the Southern blot technique showed identity between HBV DNA in anti-delta-positive and anti-delta-negative sera. These results show that anti-delta-positive sera contain HBV DNA, although these sera were also positive for antibodies to hepatitis B e antigen.

DNA, Viral↗
PubMed1984

HBV-DNA in sera of patients with HBsAg-positive primary liver cell carcinoma.

Sera of ten patients with HBsAg-positive primary liver carcinoma were tested for anti-HBc-IgM and HBV-DNA. Five patients were positive for anti-HBc-IgM and six for HBV-DNA. There was no correlation between the presence of anti-HBc-IgM and HBV-DNA. Our study suggests that complete viral replication exists in some HBsAg-positive primary liver carcinomas.

Aged↗
PubMed1984

Enhancement of 1,2-dimethylhydrazine-induced rectal carcinogenesis following chronic ethanol consumption in the rat.

The incidence, distribution, size, and histopathology of grossly visible intestinal tumors induced by the parenteral administration of 1,2-dimethylhydrazine dihydrochloride were examined in 32 paired rats fed a nutritionally adequate liquid diet containing 36% of total calories either as ethanol or isocaloric carbohydrates. The liquid diets were begun 4 wk before the first of four weekly injections of 1,2-dimethylhydrazine dihydrochloride. At the time of the subcutaneous application of the procarcinogen, liquid diets were omitted for 3 wk, and were replaced by a standard laboratory diet. This feeding schedule was repeated four times, and after 32 wk the animals were killed. Chronic ethanol ingestion increased the total number of rectal tumors significantly (17 vs. 6, p less than 0.02). However, alcohol had no effect on tumor size or histopathology. Chronic ethanol ingestion did not exhibit any cocarcinogenic effect in tissues other than the rectum. A 47% increase in the activity of mucosal alcohol dehydrogenase in the distal colorectum was found between chronically ethanol-fed rats and pair-fed controls (0.241 +/- 0.019 vs. 0.164 +/- 0.020 mumol X mg protein-1 X h-1, p less than 0.01). This could in part explain the cocarcinogenic effect of alcohol in this tissue. Fecal bile acids, however, do not play a role as promoters of rectal cancer under the present experimental conditions. The data give experimental support to the epidemiologic findings of an increased incidence of rectal cancer in the alcoholic.

Adenocarcinoma↗
PubMed1983

Colonic cyclic AMP metabolism following chronic ethanol consumption in the rat: effect of hormonal secretagogues.

The colonic cyclic AMP system is known to be involved in intestinal secretion and can be stimulated by a variety of gastrointestinal hormones including prostaglandins. We have investigated the effect of chronic ethanol ingestion on the activity of the key enzymes in cyclic AMP metabolism--adenylate cyclase and cyclic AMP phosphodiesterase--in the colonic mucosa of the rat. Chronic ethanol consumption by feeding a nutritionally adequate liquid diet enhanced basal colonic adenylate cyclase activity significantly by 168% (p less than 0.01), but had no effect on colonic low Km cyclic AMP phosphodiesterase activity. In addition, various hormonal secretagogues were used to stimulate colonic adenylate cyclase. Colonic adenylate cyclase exhibited a significantly greater sensitivity and efficacy to prostaglandins and vasoactive intestinal peptide after chronic ethanol ingestion. Since increased intestinal cyclic AMP production due to an increased activity of intestinal adenylate cyclase is known to promote intestinal secretion of water and electrolytes, the frequently observed diarrhea in alcoholics may be explained at least in part by an enhanced production of colonic cyclic AMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Effect of chronic ethanol ingestion on the cyclic AMP system of the upper gastrointestinal tract in the rat.

Chronic ethanol consumption significantly increases gastric adenylate cyclase (AC) activity (p less than 0.05) without influencing low Km 3',5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase (PD) activity in the rat. On the other hand, in the duodenum and upper part of the jejunum, chronic ethanol feeding leads to a significant decrease of adenylate cyclase activity (p less than 0.02) and, again, does not affect low Km cAMP phosphodiesterase activity. In addition, the effect of various hormonal secretagoques on small intestinal adenylate cyclase activity was investigated. Prostaglandin I2 and D2, as well as glucagon, do not stimulate AC at all. However, small intestinal adenylate cyclase exhibits a lower sensitivity to prostaglandin E2 and vasoactive intestinal peptide (VIP), and a lower efficacy to VIP after chronic ethanol consumption when compared to controls. The decrease of both basal and stimulated AC activity following ethanol ingestion in the upper small intestine may be due to membrane alterations and tissue damage caused by ethanol. The ethanol-induced increase in gastric AC may be of relevance with respect to an increased acid secretion observed after alcohol administration.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Hepatic secretion of bilirubin and biliary lipids in patients with alcoholic cirrhosis of the liver.

In patients with cirrhosis of the liver elevated bilirubin concentrations in the plasma could be the result of decreased bilirubin excretion or an overproduction of bilirubin with insufficient excretion of the increased amounts of bilirubin. Under steady state conditions with constant serum bilirubin concentrations bilirubin synthesis equals biliary and urinary bilirubin excretion. In the present study in 10 healthy volunteers and 11 patients with alcoholic cirrhosis of the liver and serum bilirubin concentrations of 7.0 +/- 1.9 mg/dl the biliary excretion of bilirubin was studied by the intestinal perfusion method and compared with the excretion of bile lipids. Biliary excretion of bilirubin in the cirrhotics was 38.7 +/- 8.8 mumol/h, the 10 healthy controls excreted 17.9 +/- 0.9 mumol/h bilirubin. Only minor amounts of bilirubin were excreted in urine. In 4 of the 11 cirrhotics 51Cr-red blood cell half-lives were studied revealing ongoing hemolysis. Bilirubin production calculated from red cell life span was identical to biliary excretion of bilirubin with an error less than 5%. The data indicate that in patients with alcoholic cirrhosis of the liver serum concentrations of bilirubin may be elevated due to overproduction of bilirubin and a concomitant decrease of the biliary transport capacity of bilirubin.

Adult↗