[Indirect measurement of blood pressure in resting and exercising subjects by analysis of Korotkov sound pattern].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B Bertram.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The problem of iatrogenic carcinogenesis is treated with special reference to dermatological dispensings. The problem of arsenic as a drug, of cytostatic drugs, antimycotic drugs and external dispensings is discussed. The chance to induce cancer by medical treatment in dermatology is considered to be very low since arsenic has been eliminated.
Explore the source record for details and available documents.
The extent of ethylation of guanine in 7 N and O 6 position in rat liver DNA was studied after chronic feeding with unlabelled nitrosodiethylamine followed by a single application of the 14C labelled drug. Disulfiram inhibits the alkylation of rat liver DNA. It was also shown that a discontinuous dosage of disulfiram protects against the alkylating effect of 14C nitrosodiethylamine only for a distinct period of time.
Male Sprague-Dawley rats received 30 mg/kg body wt. (group I) or 15 mg/kg (group II) di(N-nitroso)-perhydropyrimidine (DNPP) by the intraperitoneal route once a week for life. The DNPP treatment significantly reduced the life expectancy in both groups. DNPP induced tumors of the esophagus (27% incidence in group I, 33% in group II) and possibly also of the liver (4% incidence in group I, 8% in group II).
After subcutaneous administration of dipropylnitrosamine (DPN) to Syrian hamsters, gas-liquid chromatographic analysis of the 16-h urine revealed the DPN metabolites, 2-hydroxypropyl-, 2-oxopropyl-, and methylpropylnitrosamines. In a related series of experiments, hamsters received equimolar doses of the above compounds and of N-nitrosobis(2-hydroxypropyl)-amine (BHP) and 2,2'-dimethyldipropylnitrosamine (DMDPN). The metabolites as well as BHP and DMDPN had a weaker effect than did DPN on the rate and/or latency of respiratory tumors. In the respiratory tract, the segmental tumor distribution and histological types varied according to the compounds. The metabolites of DPN induced additional tumors in the digestive tract. These experiments do not support the concept that the beta-oxidized metabolites of DPN are the proximate carcinogens of the parent compound.
The relative abilities of liver, kidney and lung fractions from untreated or phenobarbitone-pretreated rats and hamsters to convert N,N-di-n-propylnitrosamine and several beta-oxidized synthetic putative intermediates into mutagens was quantitatively compared in a tissue-mediated mutagenicity assay with S. typhimurium TA 1530 in vitro. With one exception, namely, N,N-di(2-acetoxy-n-propyl)nitrosamine, liver was the most active tissue from hamsters; in rats also, only liver fractions were able to activate some nitroso-compounds to mutagens. The highest enzyme-mediated mutagenicities were observed with N-2-hydroxy-n-propyl-N-n-propylnitrosamine, N,N-di-n-propylnitrosamine and N,N-di(2-acetoxy-n-propyl)nitrosamine. Hamster lung tissue converted N,N-di-n-propylnitrosamine, N-2-hydroxy-n-propyl-N-n-propylnitrosamine and N,N-di(2-acetoxy-n-propyl)nitrosamine into mutagens; activity with the latter compound was greater with lung tissue than with liver tissue when untreated animals were used. N-methyl-N-n-propylnitrosamine was mutagenic in the presence of hamster liver fraction but less so than N,N-di-n-propylnitrosamine. The results of the mutagenicity assays using various tissues are qualitatively compared to sites of tumour formation in rats and hamsters by these N-nitrosamines.
The synthesis of N, N'-dinitrosopiperazine and N-nitrosopiperazine, both 14C-labelled in the 2-and 5-position is described. After i.p. application of 10 mg/69.5 muCi/kg[2, 5-14C]-N, N'-dinitrosopiperazine to rats no labelled 7-methylguanine was detected in the liver RNA; 1% of the radioactivity was exhaled as 14CO2, 1% excreted via the bile and about 40% excreted in the urine. Two of the urine metabolites were identified as 3-hydroxynitrosopyrrolidine and 1-nitrosopiperazinone-(3).
After i. p. application of 6 mg/30 muCi/kg 2,5- and 3,4--14C-nitrosopyrrolidine about 20% of the radioactivity is exhaled as 14-CO2 and about 7% is found in the urine. One of the urinary metabolites was identified by thin layer chromatography, combined GC/MS spectrometry and ultraviolet absorption as 3-hydroxy-1-nitrosopyrrolidine.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Retinal vessel diameter is an important parameter in blood flow analysis. Despite modern digital image technology, most clinical studies investigate diameters subjectively using projected fundus slides or negatives. In the present study we used a technique to examine vessel diameters by digital image analysis of color fundus slides. We investigated in a retrospective manner diameter changes in twenty diabetic patients before and after panretinal laser coagulation. MATERIAL AND METHODS: Color fundus slides were digitized by a new high resolution scanning device. The resulting images consisted in three channels (red, green, blue). Since vessel contrast was the highest in the green channel, we assessed grey value profiles perpendicular to the vessels in the green channel. Diameters were measured at the half-height of the profile. RESULTS: After panretinal laser coagulation, average venous diameter was decreased, whereas arterial diameter remained unchanged. There was no significant relation between the diameter change and the number of laser burns or the presence of neovascularization. CONCLUSIONS: Splitting digitized images into color planes enables objective measurements of retinal diameters in conventional color slides.
New water soluble derivatives of oxysterols--the phosphodiesters of oxysterols and of nucleosides--have been synthesized. In vitro, these compounds share the biological properties of their parent oxysterols. Furthermore, they display anticancer activity when injected i.p. in mice bearing experimental tumors. The pharmacokinetic study described here proved that the water-soluble derivatives of oxysterols act as prodrugs releasing free oxysterol in the blood, the liver and the kidney after i.p. or i.v. injection in rats. The hydro-solubility of such compounds as well as their slow metabolism into the active principle could account for their biological activity and make them suitable as new therapeutic agents.
Several agents with anticarcinogenic potential such as diethyldithiocarbamate (DDTC), lactose-DDTC, proline-dithiocarbamate (PDTC), its dimer proline-thiuramdisulfide (PTDS) and 4-carboxy-piperazine-TDS (4-pip-TDS) were investigated for their influence on the metabolism and the detoxication of aflatoxin B1 (AFB1) in vitro and in vivo. Aflatoxins are a group of mycotoxins produced by aspergillus species and are among the most important risk factors for hepatocellular carcinoma in certain areas of the world. AFB1 metabolism measured by the formation of tris-diol adducts showed that the thiuramdisulfides 4-carboxy-piperazine-TDS and PTDS were better inhibitors in vitro than the corresponding dithiocarbamates. Ex vivo studies in rats showed that dithiocarbamates (DTCs) including sugar linked lactose-DDTC decreased the formation of tris-diol adducts. Among the dithiocarbamates administered, DDTC showed a 40% inhibition whereas the other compounds showed only marginal effects. In vivo experiments on the formation of glutathione-adducts derived from AFB1-endo- and exo-epoxides showed that lactose-DDTC enhanced the formation of AFB1-GSH adducts, whereas PDTC, 4-pip-TDS, PTDS and DDTC displayed inhibitory effects. We conclude that DTCs may be promising agents in the chemoprevention of liver carcinogenesis caused by AFB1.