Generalized BCG tuberculosis.
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Biomedical subjects
Publications and source records attributed to V D Patil.
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We have studied the oligomerization reactions of the 2-methylimidazolide derivatives of 3-isoisoguanosine 5'-phosphate (2) and 3-isoxanthosine 5'-phosphate (5) in the presence of a variety of homopolynucleotide templates. In no case did we observe a substantial template-facilitated production of long oligomers. Polyuridylic acid directed the synthesis of low molecular-weight products from both monomers. Polycytidylic acid, polyadenylic acid, polyinosinic acid, and polyguanylic acid were ineffective as templates in the systems that we investigated.
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3-beta-D-Ribofuranosylhypoxanthine, 3-beta-D-ribofuranosyl-1,6-dihydro-3H-purin-6-one, C10H12-N4O5, Mr = 268.23, monoclinic, P2(1), a = 6.503 (1), b = 24.007 (6), c = 7.392 (2) A, beta = 106.53 (2) degrees, V = 1106.3 (9) A3, Z = 4, Dx = 1.610 g cm-3, lambda(Mo K alpha) = 0.71073 A, mu = 1.23 cm-1, F(000) = 560, T = 299 K, R = 0.048 and wR = 0.043 for 1602 observed reflections. There are two crystallographically independent molecules in the structure; in both of them the 6-oxo, 7H tautomer is the predominant form. The bond lengths and angles of the two molecules are almost identical and the hypoxanthine moiety is almost planar. The torsional angles of the glycosidic linkage O(4')-C(1')-N(3)-C(4) are -159.3 and -148.8 degrees, both in the anti range. The sugar puckers are 4T3 (C4'-exo/C3'-endo), with P = 46.35 degrees and tau m = 42.30 degrees, and 2E (C2'-endo), with P = 157.24 degrees and tau m = 41.32 degrees. All N and O atoms except N(3) and O(4') participate in a three-dimensional hydrogen-bonding system.
Two children with extensive respiratory diphtheria developed haemorrhagic manifestations. A leukaemoid blood picture with prolonged bleeding time and normal platelet count was noted in both cases. One child developed ventricular tachycardia. Both of them died. Toxic vasculitis as a possible cause for bleeding has been proposed.
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The title nucleoside 5 was prepared by a condensation of the silylated heterocycle thieno[2,3-d]pyrimidin-4-one (1) with 1-O-acetyl-2,3,5-tri-O-benzoyl-beta-D-ribofuranose (2a) in the presence of a Lewis acid or with 2,3,5-tri-O-acetyl-D-ribofuranosyl bromide (2b) in the presence of mercuric oxide and mercuric bromide. The site of ribosylation and anomeric configuration of this nucleoside were established by 1H NMR. The synthesis of 3-beta-D-ribofuranosylpyrrolo[2,3-d]pyrimidin-4-one (8), 1-phenyl-5-beta-D-ribofuranosylpyrazolo[3,4-d]pyrimidin-4-one (9), 5-methyl-3-beta-D-ribofuranosylthieno[2,3-d]pyrimidin-4-one (10), and 2-methyl-6-beta-D-ribofuranosyltriazolo[5,4-d]pyrimidin-7-one (11) is also described. The title compound inhibited the growth of murine L-1210 leukemic cells in vitro with an ID50 of 3 X 10(-5)M. The growth inhibition could not be prevented by uridine, cytidine, thymidine, deoxycytidine, cytosine, hypoxanthine, or uridine and hypoxanthine together. On the other hand, inhibition of adenosine kinase by 10(-7) M 5-iodotubercidin prevented the cytotoxic effect. Also a subline of L-1210 cells resistant to several cytotoxic adenosine analogues was also resistant to this nucleoside. Thus it appears that this compound 5 may act as an adenosine analogue.
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Five cases of fulminant diphtheritic myocarditis are described. Among them, three had extensive faucial diphtheria. Two had minor ECG abnormalities like low voltage QRS complexes. One of the three cases of severe diphtheria had atrioventricular dissociation, one developed LBBB leading to complete heart block, and the last one had ventricular tachycardia. Three of the five children died; all of them had major ECG abnormalities. Prognosis was also related to SGOT levels.