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V Daniel

Publications and source records attributed to V Daniel.

At least 163 records · Page 9Linked to original sources
PubMed1971

Purification and in vitro transcription of a transfer RNA gene.

A gene specifying tyrosine transfer RNA has been purified and transcribed in vitro. The purification procedure made use of two specialized transducing phages carrying the tRNA(Tyr) gene of Escherichia coli inserted into their DNA in opposite orientations. The separated heavy strands of the two phages were annealed and the single-stranded tails of the resulting hybrid were removed by digestion with Neurospora endonuclease. The size of the purified double-stranded structures was determined by electron microscopy. These isolated duplexes served as template for the in vitro transcription of tRNA(Tyr)-like molecules.

Centrifugation, Density Gradient↗
PubMed1970

In vitro transcription of a transfer RNA gene.

The Escherichia coli tRNA(Tyr) gene carried by the varphi80psu(3) + transducing phage was transcribed in vitro by DNA-dependent RNA polymerase. The enzymatically synthesized tRNA(Tyr)-like polynucleotide chains were detected by competition with purified E. coli(32)P-tRNA(Tyr) for specific hybridization sites on varphi80psu(3) + DNA. Analysis by sucrose gradient centrifugation showed the tRNA(Tyr)-like chains to possess a heterogeneous distribution with respect to sedimentation coefficients, with a broad peak around 8 S. The presence of the termination factor rho during the transcription did not significantly reduce the average size of the in vitro synthesized tRNA(Tyr)-like chains.

Bacteriophages↗
PubMedDate not supplied

Hepatitis C-virus (HCV) antibodies in patients after kidney transplantation.

The hepatitis C-virus (HCV) is the main etiologic agent of posttransfusion hepatitis (PTH). Most patients depending on hemodialysis need transfusion of blood before kidney transplantation. Of 272 patients after kidney transplantation, 27 (10%) were found to be anti-HCV-ELISA-positive (HCV-Antibody-ELISA, Ortho Diagnostics). The antibodies could be neutralized by HCV C-100-3 antigen. Eight of 22 patients (36%) who had more than one kidney transplantation were classified anti-HCV positive [30% (8/27) of all anti-HCV positive patients]. The number of transfused blood units ranged from 0 to 99 BU. Receiving more than one kidney graft or the transfusion of more than 5 units of blood increased the risk for HCV infection 3.5 or 4.1 times, respectively, compared with one transplantation or less than 5 units of blood. No significant interactions were seen between these two variables. Of the anti-HCV positive patients, 48% were anti-HBc negative as well as HBs-antigen negative, 52% were anti-HBc positive.

Adult↗
PubMedDate not supplied

Sequential occurrence of IgM, IgM/IgG, and gp120-IgM/IgG complement complexes on CD4+ lymphocytes in relation to CD4+ blood lymphocyte depletion in HIV+ hemophilia patients: results of a 10-year study.

The concept of autoimmune mechanisms playing an integral role in the pathogenesis of HIV disease is rapidly gaining ground. In this study, we determined IgM and IgG antibodies, complement fragments and gp120 on the surface of CD4+ lymphocytes using double-fluorescence flow cytometry. Sequential analysis demonstrated an inverse relationship of autoantibodies and CD4+ lymphocyte counts in the peripheral blood. HIV+ patients without autoantibodies (16/104 = 15%) had the highest CD4+ blood cell counts (324 +/- 264/microliters; mean +/- SD). CD4+ counts were successively lower in patients with complement-fixing IgM (243 +/- 240/microliter), complement-fixing IgG and IgM (139 +/- 138/microliter), or gp120-IgM/IgG complement complexes on the surface of CD4+ cells (38 +/- 45/microliter, P = 0.03). Individual patient profiles show that IgM autoantibodies typically are formed early after HIV infection and appear to deplete CD4+ lymphocytes very slowly, whereas complement-fixing IgG autoantibodies are generated at a later stage and deplete CD4+ lymphocytes more efficiently. The presence of both soluble gp120 and complement-fixing autoantibodies on CD4+ lymphocytes is associated with very low CD4+ cell counts and coincides with progression to terminal disease. Early during HIV infection autoantibody production is rather unstable, but it becomes more stable with disease progression and persists in advanced stages of the disease. These data suggest that autoantibody formation against CD4+ lymphocytes is a pathogenic mechanism for CD4+ cell depletion.

Antigen-Antibody Complex↗