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Biomedical subjects

B Kommerell

Publications and source records attributed to B Kommerell.

At least 145 records · Page 8Linked to original sources
PubMed1978

[Successful gastric ulcer treatment of a patient with primary hyperparathyroidism with cimetidine (author's transl)].

Case report on the successful gastric ulcer treatment of a patient with primary hyperparathyroidism with the H2-receptor antagonist cimetidine. After four weeks of therapy with 0.8 g/d cimetidine stomal ulcerations were seen by x-rays and endoscopy to be healed. The patient was discharged on a regimen of 400 mg daily of oral cimetidine. Peptic ulcer did not recur after 1/2 year of treatment with this H2-receptor antagonist, although the signs of primary hyperparathyroidism were still present.

Aged↗
PubMed1978

Effects of prostaglandins and their methylated analogues upon human adenylate cyclase in the upper gastrointestinal tract.

The effects of prostaglandin E2, prostaglandin A2 and their methylated analogues upon the adenylate cyclase in human gastric mucosa were studied. PG E2 and 16,16-dimethyl-PG E2 stimulated the enzyme activity to a greater degree than PG A2 and 16,16-dimethyl-PG A2. 16,16-dimethyl-PG E2 was less potent in activating the enzyme system than its parent compound. The results suggest that the more pronounced antisecretory activity of 16,16-dimethyl-PG E2 is due to its greater resistance against enzymatic degradation.

Adenylyl Cyclases↗
PubMed1978

Inhibition of human colonic adenylate cyclase by RMI 12330 A.

RMI 12330 A, a compound of the lactamamide series, is a potent inhibitor of vasoactive intestinal polypeptide(VIP)- and prostaglandin (PG)-stimulated colonic secretion in the rat. This substance was tested on the adenylate cyclase system in human colonic mucosa. RMI 12330 A inhibited PGE2-, 16,16-dimethyl-PGE2- as well as VIP-sensitive adenylate cyclases in a dose-related manner. Half-maximal inhibition of hormone-stimulated enzyme activities occurred at a lactamimide concentration of about 0.15 mM. Lactamimide inhibition was non-competitive. Our results are compatible with the concept of RMI 12330 A acting as an inhibitor of colonic secretion via inhibition of hormone-sensitive adenylate cyclase. Since basal, NaF- and guanylyl-imidodiphosphate-stimulated enzyme activities were also affected by this compound, we may conclude that RMI 12330 A is a non-specific inhibitor of the human colonic adenylate cyclase system.

Adenylyl Cyclases↗
PubMed1978

Prostacyclin: a potent activator of human colonic adenylate cyclase activity.

Prostacyclin and its stable catabolite 6-keto-prostaglandin F1 alpha were tested on the human colonic mucosal adenylate cyclase which represents the key enzyme in the secretory process in this organ. Prostacyclin was able to activate dose-dependently the human cyclase system. Saturating concentrations of prostacyclin and 6-keto-prostaglandin F1 alpha (each 0.28 mM) increased the enzyme activity 2.5-fold and only 1.4-fold, respectively. The presence of prostacyclin receptor sites in human colonic mucosa suggests a physiological role of this novel prostaglandin in human colonic function.

Adenylyl Cyclases↗
PubMed1978

Pool size, synthesis, and turnover of sulfated and nonsulfated cholic acid and chenodeoxycholic acid in patients with cirrhosis of the liver.

In 5 patients with cirrhosis of the liver sulfated and nonsulfated [14C]cholic acid and [14C]chenodeoxycholic acid were administered intravenously and the specific activity curves were determined. Specific activities declined exponentially and pool sizes, synthesis rates, and turnover rates of bile acids were calculated on the basis of a one-pool system. The biological half-life of cholic acid was 4.3 +/- 1.6 days (mean +/- SEM) and of chenodeoxycholic acid was 2.8 +/- 1.2 days. The half-life of cholic acid sulfate was 0.7 +/- 0.5 day and of chenodeoxycholic acid sulfate was 0.8 +/- 0.5 day. The pool size of cholic acid was 513 +/- 103 mg, of chenodeoxycholic acid, 477 +/- 77 mg, of cholic acid sulfate, 4.7 +/- 1.0 mg, and of chenodeoxycholic acid sulfate, 38.7 +/- 4.0 mg. The daily synthesis of cholic acid was 90 +/- 14 mg, of chenodeoxycholic acid, 118 +/- 6 mg, of cholic acid sulfate, 7.2 +/- 2.1 mg, and of chenodeoxycholic acid sulfate was 32.6 +/- 3.2 mg. The data indicate that sulfate esters of bile acids are significantly more rapidly excreted than are unsulfated bile acids. More than one-fourth of the chenodeoxycholic acid but less than one-tenth of the cholic acid formed was sulfated. The preferential sulfation of chenodeoxycholic acid is responsible for the more rapid turnover of chenodeoxycholic acid in comparison to cholic acid. Sulfation enhances the excretion and thereby prevents the accumulation of hepatotoxic concentrations of chenodeoxycholic acid in patients with cirrhosis of the liver.

Alkaline Phosphatase↗
PubMed1977

[Biosynthesis of insulin. The Ferdinand-Bertram-Award lecture (author's transl)].

EEG recordings were done 1-3 months before and up to 5 years after shunt operations in 20 men and 7 women (aged 16 to 69 years) with liver cirrhosis, most of them of alcoholic aetiology, and with oesophageal bleeding. The EEG diagnosed encephalopathies before there were any clinical suspicions. Pre-operatively half of the patients (14) had EEG changes indicating encephalopathy. In only four patients who before operation had a normal EEG were there post-operative EEG changes indicating encephalopathy. In the other nine patients the EEG was normal before and after shunt operation. The abnormal EEGs which occurred post-operatively or got worse generally returned to pre-operative levels within 3-4 weeks. These studies indicate that in patients with pre-operative encephalopathy there is no improvement in the EEG after shunt operation. On the other hand, if pre-operatively there are no significant cerebral abnormalities, post-operative changes of encephalopathy are rare (14.8%).

Amino Acid Sequence↗
PubMed1977

[Treatment of intrahepatic cholesterol stones by chenodeoxycholic acid (author's transl)].

Intrahepatic gallstones were demonstrated by operative cholangiography in two men, aged 34 and 46 years, respectively. The cholesterol stones were dissolved in both patients within eight and two months, respectively, by retrograde instillation of chendeoxycholic acid via a T-drain. Additional endoscopic papillotomy was performed because of a papillary stenosis in one instance, and extrahepatic occlusion during treatment in the other. During treatment there was a rise of transaminases of 5-fold levels, of gamma-glutamyl transferase up to 10-fold of normal. Since chenodeoxycholic-acid instillations both patients have been receiving the drug orally to prevent recurrence of gallstones. So far all biochemical values are within the normal range, the patients are without symptoms and have a normal exercise tolerance.

Adult↗
PubMed1977

Antibodies against the hepatitis B surface antigen in diabetics.

The frequency of antibodies to the hepatitis B surface antigen was determined in 406 diabetics in two study series separated in time (1971-1972 and 1974-1975). In the 1971-1972 series, the antibody frequency in insulin and orally treated patients was significantly higher, and the incidence of hepatitis was also greater. The decline in the antibody frequency in the 1974-1975 series is primarily attributed to improved hygienic measures. Anti-HBs was more frequently demonstrable in insulin-dependent diabetics than in orally treated patients. Since the duration of diabetes was about three times as long in this treatment group and the frequency of metabolic checks twice as great, the raised antibody frequency in insulin-injecting diabetics was attributed to greater exposure to the virus.

Administration, Oral↗
PubMed1976

[The e antigen].

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Acute Disease↗
PubMed1976

Induction and activation of rat liver microsomal bile salt glucuronyltransferase.

In vivo induction and in vitro activation of the recently described bile salt glucuronyltransferase were investigated in rat. A radioactive assay for the determination of glucuronyltransferase activity was used. 14C-Labeled bile salts served as substrates, and the glucuronides were separated by thin layer chromatography. Lithocholate glucuronyltransferase activity was determined in liver microsomes of phenobarbital- and 3-methylcholanthrene-treated rats and of untreated controls. Pretreatment with phenobarbital induced lithocholate glucuronyltransferase activity to 150.5% of controls. In contrast, 3-methylcholanthrene treatment decreased activity to 29.6% of controls. In vivo activation of lithocholate glucuronyltransferase by Triton X-100 was observed in controls and in the 3-methylcholanthrene group, but not in the phenobarbital group. Substrate activation of the enzyme by lithocholate was demonstrated in microsomes of untreated controls. Pretreatment with 3-methylcholanthrene, but not phenobarbital, increased the latency of lithocholate glucuronyltransferase. The results indicate that rat liver microsomal bile salt glucuronyltransferase activity is increased by in vivo induction with phenobarbital and by in vitro activation with detergents like Triton X-100. The induction of bile salt glucuronide formation by phenobarbital is most likely one of the factors contributing to the increased biliary and fecal excretion of bile salts in patients with cholestasis following phenobarbital therapy.

Animals↗