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Biomedical subjects

X Jin

Publications and source records attributed to X Jin.

188 records · Page 11Linked to original sources

Significance of seizures in very low-birthweight infants.

Of 506 very low-birthweight (VLBW) infants, the authors review data on 67 identified as having seizures. 29 survivors with seizures and 305 without were followed up at the ages of one, two and five years: statistical significance of psychological and mental impairment was evaluated. Impairment was higher in the seizure group at 66 per cent (15 per cent in non-seizure group) and 43 per cent of these were considered to be severely impaired. Infants with seizures occurring for more than seven days and lasting for more than five minutes had the poorest outcome, and infants with late onset had the best outcome. Analysis showed that 40 per cent of seizures were caused by birth asphyxia, and these were strongly prognostic, correlating with mortality and impairment rates. 60 per cent of the infants who died had the same cause for both their seizures and death, and for 57 per cent of these the cause was perinatal asphyxia. The poor outlook for the VLBW infants suggests that the seizures themselves are a serious neurological insult.

Female↗

Mutants of p53 gene presence in laryngeal carcinoma and adjacent histopathologically normal tissue.

Possible differences were analyzed between histopathological and molecular biological findings in laryngeal cancer tissue and its adjacent normal tissues. p53 gene mutations were detected in histopathologically normal tissue both within 0.5 cm of and more than 0.5 cm distant from the nearest cancerous tissue. Since the p53 mutation was common in both cancer tissue and adjacent normal tissue, the gene mutation may play an important role in laryngeal carcinogenesis. Radical excision of the tumor is defined by histopathological limits, but 'normal' tissue may nevertheless contain the gene mutation, giving rise to the danger of further cancer development. We suggest that the determination of the surgical margin should be based on a combination of histopathology and molecular biological findings.

Aged↗

Suppression activity of pro-apoptotic gene products in cancer cells, a potential application for cancer gene therapy.

Overexpression of anti-apoptotic Bcl-2 and Bcl-XL proteins may play a role in the development of resistance to cancer therapy. We examined the expression of these proteins in prostate, breast, and ovarian cancer cells. We found that some of these cancer cell lines expressed high levels of Bcl-XL or Bcl-2., In order to develop an effective strategy to overcome the potential inhibition of cancer therapy by Bcl-2 and Bcl-XL, we tested the inhibitory ability of several pro-apoptotic or tumor suppressor genes in these cells. The expression of these genes induced apoptosis or suppressed cell growth with variable efficiency in these cells. Harakiri (Hrk) appears to result in the greatest induction of apoptosis or inhibition of cell growth Mtd, bax and bcl-XS were also effective in inhibiting cell growth. Furthermore, transfection of Hrk, bax, or Mtd into these cells caused significantly less colony formation than in cells transfected with p53 or BRCA1. Therefore, these results suggest that Hrk, bax, and Mtd are potent therapeutic agents for cancers expressing high levels of Bcl-2 and Bcl-XL.

Apoptosis↗

Phenomenological theory on refrigeration effect of practical type-I superconductor.

In accordance with the phenomenological theory of thermodynamics, we discussed the Magnetocaloric effect of type-I superconductors, which are exposed to a varying magnetic field. It is concluded theoretically that the refrigeration effect is closely associated with demagnetization effect for practical specimens, which is different from the situation for ideal superconductor sample having no demagnetization effect. From the thermodynamic formulation of superconductivity, we deduced the integrating function of the thermal effect. By numerical calculation, we found a quantitative relation between the refrigeration effect and the demagnetizing factor which is determined by the shape of the sample.

Electric Conductivity↗

Resistance to p53-mediated growth suppression in human ovarian cancer cells retain endogenous wild-type p53.

Cancer cells containing mutated p53 are sensitive to the re-introduction of the wild-type (wt) p53. We sought to determine whether ovarian cancer cells that retain wt p53 are sensitive to the re-introduction of wt p53. Our results demonstrated that A2780 and PA-1 cells, which retain wt p53, are more resistant to apoptosis and growth suppression induced by exogenous expression of wt p53 than SKOV-3 and Caov-3 cells that contain mutated p53. All cell lines, except PA-1, showed induction of the p53-targeted genes. Further, inhibitors of p53-dependent apoptosis, mdm2 and Bcl-xL were not overexpressed in A2780 and PA-1 cells. These results suggest that one major defect in PA-1 cells is due to abrogation of induction of the p53-targets which is independent of mdm2 and Bcl-xL. Although A2780 cells showed induction of the p53-targeted genes, the cleavage of caspase-9 was undetectable. Therefore, p53-dependent apoptosis may be blocked upstream or at the caspase-9 level in A2780 cells.

Adenoviridae↗

Signal transduction in activated natural killer cells and natural killer cells inactivated with sensitive targets.

We have recently demonstrated that the activation of NK cells involves a protein-kinase-C (PKC)-dependent step as well as a phosphatidylinositol (PI)-linked signal transduction system. We have also shown that when NK cells are incubated with sensitive targets for up to 6 h they lose their lytic potential and require IL-2 to regain their lytic activity. PKC is involved in many cell processes such as the transduction of hormonal signals and the machinery of cellular secretion and is activated by diacylglycerol and by a number of phorbol esters, including phorbol myristic acid (PMA). To reinforce the role of PKC in NK-cell-mediated cytotoxicity, we first showed that NK-CMC is inhibited by two agents that inhibit PKC activation, staurosporine and sphingosine. Next, we showed that antibody-dependent cellular cytotoxicity of NK-resistant targets was PKC dependent and Ca2+ dependent. Further, we showed that PMA plus ionophore alone could induce NK killing of resistant targets and that this killing was PKC and Ca2+ dependent. Finally, we contrasted the role of PKC in these activated cells to the role of PKC in cells that have been inactivated with a sensitive target, K562. We showed that PKC is not required for the IL-2-dependent reactivation of NK cells but that Ca2+ is required. To further determine what event in signal transduction is inactivated by K562, we showed that inactivated NK cells do not turnover PI in response to K562 stimulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Inhibition of esophageal cancer proliferation by adenovirally mediated delivery of p16INK4.

We have been investigating the molecular basis of esophageal carcinogenesis in an attempt to develop gene therapy of established esophageal cancers and premalignant esophageal lesions. In this report we demonstrate the efficacy of adenovirally mediated p16 gene replacement in esophageal squamous cell cancers. Adenoviral p16 efficiently transduced epidermoid cancer cells containing p16 mutations, and expression of exogenous p16 in these cells correlated with G1 cell cycle arrest and profound growth inhibition. No effects were observed in esophageal adenocarcinoma cells due to extremely poor transduction of these cells by adenovirus. These results may have implications regarding the design of clinical trials using p16 gene replacement strategies for intervention in esophageal cancers.

Adenocarcinoma↗