Biomedical subjects

Y Xing

Publications and source records attributed to Y Xing.

61 records · Page 4Linked to original sources

PubMed1992

The human XIST gene: analysis of a 17 kb inactive X-specific RNA that contains conserved repeats and is highly localized within the nucleus.

X chromosome inactivation in mammalian females results in the cis-limited transcriptional inactivity of most of the genes on one X chromosome. The XIST gene is unique among X-linked genes in being expressed exclusively from the inactive X chromosome. Human XIST cDNAs containing at least eight exons and totaling 17 kb have been isolated and sequenced within the region on the X chromosome known to contain the X inactivation center. The XIST gene includes several tandem repeats, the most 5' of which are evolutionarily conserved. The gene does not contain any significant conserved ORFs and thus does not appear to encode a protein, suggesting that XIST may function as a structural RNA within the nucleus. Consistent with this, fluorescence in situ hybridization experiments demonstrate localization of XIST RNA within the nucleus to a position indistinguishable from the X inactivation-associated Barr body.

Base Sequence↗

PubMed1992

The Ribosomal Database Project.

The Ribosomal Database Project (RDP) complies ribosomal sequences and related data, and redistributes them in aligned and phylogenetically ordered form to its user community. It also offers various software packages for handling, analyzing and displaying sequences. In addition, the RDP offers (or will offer) certain analytic services. At present the project is in an intermediate stage of development.

Base Sequence↗

PubMed1992

Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

Tuberculosis remains one of the major infectious causes of morbidity and mortality in the world, yet the mechanisms by which macrophages defend against Mycobacterium tuberculosis have remained obscure. Results from this study show that murine macrophages, activated by interferon gamma, and lipopolysaccharide or tumor necrosis factor alpha, both growth inhibit and kill M. tuberculosis. This antimycobacterial effect, demonstrable both in murine macrophage cell lines and in peritoneal macrophages of BALB/c mice, is independent of the macrophage capacity to generate reactive oxygen intermediates (ROI). Both the ROI-deficient murine macrophage cell line D9, and its ROI-generating, parental line J774.16, expressed comparable antimycobacterial activity upon activation. In addition, the oxygen radical scavengers superoxide dismutase (SOD), catalase, mannitol, and diazabicyclooctane had no effect on the antimycobacterial activity of macrophages. These findings, together with the results showing the relative resistance of M. tuberculosis to enzymatically generated H2O2, suggest that ROI are unlikely to be significantly involved in killing M. tuberculosis. In contrast, the antimycobacterial activity of these macrophages strongly correlates with the induction of the L-arginine-dependent generation of reactive nitrogen intermediates (RNI). The effector molecule(s) that could participate in mediating this antimycobacterial function are toxic RNI, including NO, NO2, and HNO2, as demonstrated by the mycobacteriocidal effect of acidified NO2. The oxygen radical scavenger SOD adventitiously perturbs RNI production, and cannot be used to discriminate between cytocidal mechanisms involving ROI and RNI. Overall, our results provide support for the view that the L-arginine-dependent production of RNI is the principal effector mechanism in activated murine macrophages responsible for killing and growth inhibiting virulent M. tuberculosis.

Animals↗

PubMed1991

[Studies on the mutagenicity of vesnarinone].

The mutagenicity of domestic Vesnarinone (OPC-8212) was studied by Ames test, micronucleus test of NIH mouse bone marrow and chromosome aberration assay in CHL cells. Negative results were obtained, which suggested that OPC-8212 did not induce prokaryotic cell gene mutation or chromosome damage both in vitro and in vivo.

Animals↗

PubMed1991

Schistosoma mansoni and S. japonicum: decline of antibodies against diagnostic adult worm antigens (Sm31/32) following praziquantel treatment of mice.

Mice were infected with 10, 100 or 200 cercariae of Schistosoma mansoni or S. japonicum and treated between one and two months later with two doses of praziquantel. At this time, the animals had high levels of antibodies against the adult worm proteins Sm31/32 (schistosome cathepsin B and haemoglobinase). Antibody levels were followed up for about one more year by Western blots and ELISA using purified Sm31/32. Among the 34 surviving mice perfused at the end of the experiments, 14 had between 1 and 4 and one mouse had 8 residual stunted worms. In most mice without detectable worms, anti-Sm31/32 antibodies started to drop within a few months after therapy. In other animals of this group and in those harbouring residual worms, the decrease in titers was not observed or less pronounced. Thus, the presence of even one stunted worm was sufficient to induce continued high titres of antibodies. Decreasing levels of antibody against Sm31/32, however, reflected complete elimination of schistosomes.

Animals↗

PubMed1985

Physical and biological properties of cyclopolymers related to DIVEMA ("pyran copolymer").

A series of copolymers related in structure to the 1:2 alternating cyclocopolymer of divinyl ether and maleic anhydride (DIVEMA) have been shown to possess antitumor properties. The synthesis and structures of these copolymers are discussed, and their effectiveness as antitumor agents is presented. Certain of the copolymers have been prepared in controlled molecular weight ranges using chain transfer agents, and the resultant copolymers finally fractionated via use of solvent-nonsolvent systems. These samples of narrow molecular weight distribution have been evaluated for their antitumor properties and have been found to be quite effective.

Alkadienes↗

PubMedDate not supplied

Synthesis of 2,6-diazido-9-(beta-D-ribofuranosyl)purine 3',5'-bisphosphate: incorporation into transfer RNA and photochemical labeling of Escherichia coli ribosomes.

2,6-Diazido-9-(beta-D-ribofuranosyl)purine was prepared by the reaction of 2,6-dichloro-9-(beta-D-ribofuranosyl)purine with sodium azide. The nucleoside was bisphosphorylated with pyrophosphoryl chloride to form 2,6-diazido-9-(beta-D-ribofuranosyl)purine 3',5'-bisphosphate. This product was labeled with 32P using T4 polynucleotide kinase to exchange the 5' phosphate with the gamma phosphate of [gamma-32P]ATP. When yeast tRNA(Phe) containing 2,6-diazido-9-(beta-D-ribofuranosyl)purine at the 3' terminus was bound to the P site of the Escherichia coli ribosome in the presence of poly(U) and irradiated with 300-nm light, the photoreactive tRNA derivative became cross-linked exclusively to the 50S subunit. The label was attached to proteins L27 and L33 as well as to the 23S rRNA.

Adenosine↗