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Biomedical subjects

R A Sharma

Publications and source records attributed to R A Sharma.

At least 19 recordsLinked to original sources
PubMed1997

Pharmacological investigation of Cassia italica.

In the present study, the ethanolic extract of the whole plant parts (root, stem leaves and pods) of Cassia italica (Mill.) Lam. ex F.W. Ander (Leguminosae) was investigated for bioactivities: namely anti-inflammatory, antipyretic, analgesic and prostaglandin (PG) release by rat peritoneal leucocytes, antineoplastic and antiviral. In rats, the extracts reduced carrageenin-induced paw swelling (100 mg/kg bw-31%) and fever (100 mg/kg bw-37%). The extract showed weak effect on writhing induced by acetic acid. A dose-dependent inhibition of PG release effect was observed using rat peritoneal leucocytes.

Animals↗
PubMed1995

Dacryocystitis.

Explore the source record for details and available documents.

Adolescent↗
PubMed1993

Role of arthrography in non-traumatic painful wrist.

The arthrographic examination was carried out in 25 patients with non-traumatic painful wrist of more than 6 weeks duration. Plain x-rays were non-contributory in making any diagnosis in 20 cases. Arthrography was performed even when plain x-rays were normal and it revealed the soft tissue abnormalities and early phases of cartilage destruction not visible on routine roentgenograms. The extent of synovial involvement demonstrated on arthrography proved useful when synovectomy was planned. After operation pain and swelling disappeared and functions of the joint improved considerably.

Arthritis, Rheumatoid↗
PubMed1987

Acetylenic nucleosides. 4. 1-beta-D-arabinofuranosyl-5-ethynylcytosine. Improved synthesis and evaluation of biochemical and antiviral properties.

5-Ethynyl-1-beta-D-arabinofuranosylcytosine (EAC) was prepared from 1-(2,3,5-tri-O-acetyl-beta-D-arabinofuranosyl)cytosine by iodination followed by coupling with (trimethylsilyl)acetylene and deblocking. At 50 microM, EAC was found to inhibit the in vitro replication of herpes simplex virus type 1 and type 2 by greater than 99%. EAC also showed activity against a strain of HSV-1 resistant to (E)-5-(2-bromovinyl)-2'-deoxyuridine which has an alteration of the virus-induced thymidine kinase (TK). At 100 microM, EAC did not inhibit the in vitro growth of leukemia L1210 and HeLa cells. EAC was resistant to the action of dCR-CR deaminase, its rate of deamination being approximately 2% that of dCR. The compound was a poor substrate for dCR kinase, but it was phosphorylated by HSV-1- and HSV-2-induced TKs at 50% and 30%, respectively, the rate of thymidine.

Antiviral Agents↗
PubMed1987

Demonstration of viral thymidine kinase inhibitor and its effect on deoxynucleotide metabolism in cells infected with herpes simplex virus.

The thymidine analog 5'-ethynylthymidine was a potent inhibitor of herpes simplex virus type 1 (strain KOS)-induced thymidine kinase with a Ki value of 0.09 microM. 5'-Ethynylthymidine was less inhibitory against herpes simplex virus type 2 (strain 333)-induced thymidine kinase with a Ki of 0.38 microM and showed no inhibition against human cytosolic thymidine kinase under the conditions tested. The compound was effective against the altered thymidine kinase induced by acyclovir- and bromovinyldeoxyuridine-resistant virus variants. At 100 microM 5'-ethynylthymidine, the cellular pool size of dTTP in herpes simplex virus type 1-infected cells was 5% that of infected cells receiving no drug treatment, while there was no significant effect on the pool sizes of dATP, dGTP, and dCTP. There was a positive correlation between dTTP pools and the intracellular thymidine kinase activity of herpes simplex virus type 1-infected cells. When tested alone, 5'-ethynylthymidine exhibited no antiviral activity, but it antagonized the antiviral efficacy of five compounds which require viral thymidine kinase for their action.

Antiviral Agents↗
PubMed1984

Acetylenic nucleosides. 3. Synthesis and biological activities of some 5-ethynylpyrimidine nucleosides.

Iodination of 1-(2,3,5-tri-O-acetyl-beta-D-arabinofuranosyl)uracil furnished the 5-iodo derivative (Ib), which, on treatment with (trimethylsilyl)acetylene in the presence of catalytic amounts of (Ph3P)2PdCl2/CuI and subsequent deblocking, afforded 1-beta-D-arabinofuranosyl-5-ethynyluracil (Ie). Condensation of the trimethylsilyl derivative of 5-(dibromovinyl)uracil with 3-O-acetyl-5-O-benzoyl-2-deoxy-2-azido-D-arabinofuranosyl chloride, followed by treatment with phenyllithium, gave 1-(2-deoxy-2-azido-beta-D-arabinofuranosyl)-5-ethynyluracil (IIb). Condensation of 3-O-acetyl-5-O-benzoyl-2-deoxy-2-fluoro-D-arabinofuranosyl bromide with the trimethylsilyl derivative of 5-ethynylcytosine and subsequent removal of the protecting groups furnished 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-ethynylcytosine (IIIb). The structural assignment for IIb and IIIb was made by NMR and ORD spectra. Compounds Ie and IIIb inhibited the growth of leukemia L-1210 cells in culture by 50% at concentrations of 1.7 X 10(-5) and 6 X 10(-5) M, respectively. In addition, Ie and IIIb inhibited the replication of herpes simplex virus type I by 90% at concentrations of 2.8 X 10(-5) and 5 X 10(-5) M, respectively. Compound IIb did not show any antileukemic or antiherpes activity.

Acetylation↗
PubMed1976

Antiviral action and cellular toxicity of four thymidine analogues: 5-ethyl-,5-vinyl-, 5-propyl-, and 5-allyl-2'- deoxyuridine.

5-Ethyl-, 5-vinyl-, 5-propyl-, and 5-allyl-2'-deoxyuridine (dUrd) had antiviral activity against herpes simplex type 1 and type 2 grown in HeLa TK(-) cells, in the order 5-vinyl-dUrd, 5-ethyl-dUrd, 5-propyl-dUrd, 5-allyl-dUrd, but they were inactive against a TK(-) mutant of herpes simplex type 1. The antiviral activity of these compounds could be partially reversed by thymidine. Except for 5-vinyl-dUrd, they were not toxic to WI-38 and HeLa TK(-) cells at a concentration of 25 muM. All four analogues inhibited the growth of herpes simplex type 1-transformed HeLa TK(-) cells at a concentration of 1 muM.

Antineoplastic Agents↗
PubMed1975

Synthesis and biological activity of 4-beta-Iribofuranosyl-1,3-dihydroxybenzene ("1,3-dideazauridine").

In view of the marked antitumor activity of 3-deazauridine, the synthesis of 4-(beta-D-ribofuranosyl)-1,3-dihydroxybenzene (1,3-dideazauridine) and its dibenzyl derivative was carried out. 4-Bromo-1,3-dihydroxybenzene was converted to its dibenzyl derivative, which, upon reaction with n-butyllithium followed by treatment with anhydrous cadmium chloride, gave bis(1,3-dibenzyloxyphenyl-4)cadmium. Condensation of this intermediate with 2,3,5-tri-O-benzoyl-D-ribofuranosyl chloride in refluxing toluene, and subsequent removal of the protecting benzoyl groups, afforded 4-(beta-D-ribofuranosyl)-1,3-dibenzyloxybenzene which, upon catalytic hydrogenation over Pd/C, furnished the desired 4-(beta-D-ribofuranosyl)-1,3-dihydroxybenzene. The beta configuration at the anomeric center was established by NMR and hydrogen bonding studies. 4-(Beta-D-ribofuranosyl)-1,3-dibenzyloxybenzene inhibited the growth of leukemia L1210 cells by 50% at 7 x 10(-6) M, and that of mammary carcinoma TA3 cells at 5 x 10(-5) M. Dideazauridine itself was less active, inhibiting the leukemia L1210 but not the TA3 cells at 1 x 10(-4) M, but the compound was significantly active against herpes simplex (type I) virus in vitro.

3-Deazauridine↗
PubMed1975

Preparation and biological activity of some aminoacyl and peptidyl derivatives of 2'-amino-2'-deoxyuridine.

Several aminoacyl and peptidyl derivatives of 2'-amino-2'-deoxyuridine have been synthesized. 2'-Amino-2'-deoxyuridine (I) and 2'-N-glycyl-2'-amino-2'-deoxyuridine (IIIa) were condensed with N-Cbz blocked p-nitrophenyl esters of the appropriate amino acids to afford the protected aminoacyl and peptidyl nucleosides. Removal of the protecting groups gave the title compounds in good yields. The biological effects of these derivatives are discussed.

Deoxyuridine↗