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At least 397 records · Page 22Linked to original sources
PubMed1975

Psoriasis: a review. II.

Notwithstanding the intense interest in systemic cytotoxic therapy in recent years, the great majority in psoriatics are likely to go on needing topical therapy with tar, dithranol or corticosteroids, and a welcome trend is the spreading of interest in day care centres such as those in Paris (GRUPPER), Stockholm (THYRESSON), Stanford (FARBER) and San Francisco (CRAM) evolving from the out-patient regimes advocated by INGRAM in Leeds a generation ago.

Adrenal Cortex Hormones↗
PubMed1976

Anemia of azaribine in the treatment of psoriasis.

Azaribine is an effective agent in the treatment of psoriasis. In this investigation the extent of clinical dermatologic remission appeared to correlate with the degree of metabolic block induced by 6-azauridylic acid, as quantitated by the urinary excretion of orotic acid and orotidine, and the development of anemia. Following azaribine therapy there was a coordinate rise of the specific activities of erythrocyte orotate phosphoribosyltransferase and orotidine-5'-monophosphate decarboxylase. There was no correlation between the pretreatment activity of these enzymes and the clinical response to azaribine. The anemia of azaribine therapy was mile and of a megaloblastic type. Uridine effectively corrected the azaribine-induced anemia, but led to exacerbation of the patients' psoriasis. Following uridine therapy there was a reduction in the urinary excretion of orotic acid and orotidine, presumable reflecting end-product inhibition or repression of the first steps of a repeated pyrimidine biosynthesis.

Adult↗
PubMed1999

Potential carcinogenicity of the synthetic 1,3,6-triazine (6-azapyrimidine) nucleic acid analogues determined by DC polarography. II. Nucleosides of 6-azauracil.

The polarographic reduction of six synthetic 1,3,6-triazine (6-aza) nucleosides with 6-azauracil as the nucleoside base in the strictly anhydrous solutions was studied in the absence and presence of alpha-lipoic acid. The values of the half-wave potentials E1/2 and the parameter of potential carcinogenicity tg alpha were compared for six nucleosides of 6-azauracil and two nucleosides of 4-thio-6-azauracil. The current value of the first diffuse polarographic wave or a new diffuse polarographic wave belonging to the nucleoside-alpha-lipoic acid complex increased with the increase of the alpha-lipoic acid concentration for the all compounds only marginally. Although this diffuse current increase was linear and dependent on the alpha-lipoic acid concentration in anhydrous solutions, the determined index tg alpha values ranged between 0.027 and 0.114. This is an indication of a very low potential carcinogenicity of the all nucleoside analogues investigated.

Azauridine↗
PubMed1975

[Some properties of strains of the transmissible gastroenteritis virus of swine (TGE) isolated in Bulgaria].

Strains of the swine transmissive gastroenteritis (TGE) virus were isolated for the first time in Bulgaria in 1972. The dynamics was followed up of some strains' propagation in primary cell cultures of kidney tissue and subcultures of the thyroid of pigs. The intracellular virus reached highest titers at the 24--48th hour in the kidney cells, and at the 24--36th hour in the thyroid cells, while the extracellular virus was subjected to inactivation by the 2nd hour after infecting the cultures, by the 4--6th h its titer dropped up to 50 per cent of its initial value, and by the 24th h it was completely inactivated. The viability of the virus was tested after freeze-drying and after it had been stored at 4degreesC and--20degreesC. It was found that chloroform fully inactivates the virus at 4degreesC for 24 hours. The same results were obtained with the use of sodium desoxycholate. The strains isolated in this country form plaques, and with some strains the plaques are of a varying size. Halogenic desoxyuridines (IUDR, BUDR), as well as 8-azoridine do not suppress the multiplication of the tested TGE strains even in high concentrations. Inhibitory effect has 5-bromurazyl which in given concentrations affects the titer of the virus and the size of the plaques formed. Two Bulgarian and two reference strains have lowered their plaque-forming titer by 2 log after being treated with rifamycin-B or rifampicin.

Animals↗
PubMed1985

Deproteinization of influenza virus in the presence of rimantadine.

Virion deproteinization and viral RNA transport to the isolated cell nuclei have been studied in the presence of rimantadine with rimantadine-sensitive influenza viruses fowl plague (H7N7), A/Krasnodar/101/59 (H2N2) and rimantadine-resistant influenza strains (WSN/H1N1 and A/Krasnodar/101/59-R). Rimantadine failed to affect deproteinization during incubation with the isolated cellular plasma membranes as well as the transport to isolated cell nuclei of the viral RNA of either sensitive or resistant strains of influenza virus. Using photosensitive viruses (labelled with neutral red) rimantadine exerted dissimilar effects on deproteinization of the sensitive and resistant influenza virus strains. The possible effects of rimantadine on influenza virus deproteinization is discussed.

Adamantane↗
PubMedDate not supplied

Homocystinuria: pathogenetic mechanisms.

Homocystinuria with elevated plasma homocysteine and methionine levels is the result of deficient activity of cystathionine synthetase, the enzyme catalyzing conversion of homocysteine to cystathionine. It is inherited as an autosomal recessive trait with a worldwide distribution. The major clinical manifestations result from the elevated plasma homocysteine level. The excitotoxic effect of homocysteic acid accounts for mental retardation and seizures. Interference with collagen cross-linking by sulfhydryl groups of homocysteine causes ectopia lentis and skeletal deformities. Sulfation factor-like effects contribute to disruption of vascular endothelium, which is followed by platelet thrombosis and widespread arterial and venous occlusions. Low methionine homocystinuria, with deficient remethylation of homocysteine, results from deranged vitamin B(12) metabolism and from deficient 5,10-methylene-tetrahydrofolate reductase. Administration of azaribine produces homocystinuria by mechanism not yet elucidated.

Animals↗