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Biomedical subjects

Y Cui

Publications and source records attributed to Y Cui.

312 records · Page 18Linked to original sources
PubMedDate not supplied

Phosphatidic acid-mediated regulation of neutrophil plasma membrane CD45-phosphotyrosine phosphatase.

CD45-phosphotyrosine phosphatase (PTPase) constitutes the major portion of thr PTPase activity within plasma membranes of neutrophilic leukocytes, where it regulates signals leading to functional activation. We have previously demonstrated that the catalytic component of neutrophil plasma membrane CD45-PTPASE is regulated by a cytosolic inactivator which itself is attenuated upon cellular stimulation, allowing enzyme translocated from granule stores to express full activity. The present study investigated mechanisms of cytosolic inactivator attenuation. Preincubation of plasma membranes of stimulated neutrophils with cytosol from resting cells resulted in a rapid loss of membrane-associated PTPase activity. Phosphatidic acid had no direct effect on plasma membrane PTPase activity but blunted in a dose dependent manner the effects of the PTPase inactivator. Inactivator attenuation was not observed with equivalent concentrations of either diacylglycerol or lysophosphatidic acid. Optimal attenuation of inactivator activity was obtained with long chain, soluble ligands, such as dicapryl phosphatidic acid. Inhibitors of neutrophil plasma membrane ecto-phosphatidic acid phosphohydrolase did not block inactivator attenuation, suggesting that phosphatidic acid and not one of its metabolites was the entity responsible. In conclusion, neutrophil plasma membrane PTPase is dynamically regulated by a cytosolic inactivator, the inhibition of which may potentiate the effects of PTPase translocated during cellular stimulation. Phosphatidic acid generated as a consequence of cellular stimulation may mediate this inhibition and thereby regulate the effects of tyrosine kinases activated during the initial phases of cell stimulation.

Cell Membrane↗
PubMedDate not supplied

Chromosome 18 suppresses prostate cancer metastases.

Loss of heterozygosity and allelic imbalance data has shown that there are two distinct regions of loss on chromosome 18q associated with the progression of prostate cancer (CaP). To investigate the functional significance of chromosome 18q loci in CaP, we utilized the technique of microcell-mediated chromosome transfer to introduce an intact chromosome 18 into the human prostate cancer cell line, PC-3. Three of the resulting hybrid lines were compared to the PC-3 cells in vitro and in vivo. The hybrid cell lines, containing an intact copy of the introduced chromosome 18, exhibited a substantial reduction in anchorage-dependent and independent growth in vitro. These hybrid cell lines also made smaller tumors in nude mice following subcutaneous injection compared to PC-3 cells. Because tumor growth was not completely eliminated by introduction of chromosome 18, we assessed the ability of the hybrids to metastasize to bone after intra-cardiac inoculation in a nude mouse model. Mice inoculated with PC-3 hybrids containing intact copies of chromosome 18 had significantly fewer bone metastases and dramatically improved survival compared to PC-3 cells. In addition, the introduction of chromosome 18 significantly reduced tumor burden in extraskeletal sites. This was not because of differences in growth rates because mice bearing hybrids were monitored for metastases over twice as long as mice bearing PC-3 cells. Taken together, these data suggest that chromosome 18 has a functional role in CaP to suppress growth and metastases. Identification of the responsible gene(s) may lead to molecular targets for drug discovery.

Agar↗
PubMedDate not supplied

Esophagogastric anastomoses in rats--an experimental model.

Esophagectomy with esophagogastric anastomosis is not uncommonly complicated by anastomotic dehiscence. Although this is a major problem in clinical esophageal surgery, laboratory investigation of esophagogastric anastomotic wound healing has been hampered by the lack of a practical rodent model. Researchers have turned to large-animal experiments, or used various upper gastrointestinal pseudo-anastomotic techniques in rodents. None of these approaches has proved to be satisfactory. We report our technique of side-to-side esophagogastric anastomosis in the rat. Using this technique we have overcome the problems encountered in our earlier studies of esophagogastric anastomotic wound healing in the rat.

Anastomosis, Surgical↗
PubMedDate not supplied

Media coverage of women's health issues: is there a bias in the reporting of an association between hormone replacement therapy and breast cancer?

Media coverage of scientific research plays a major role in shaping public opinion and influencing medical practice. When an association is controversial, such as with hormone replacement therapy (HRT) and breast cancer, it is important that a balanced picture of the scientific literature be reported. The objective of this study was to assess whether scientific publications that do and do not support an HRT/breast cancer association were cited in the media in proportions similar to those with which they appear in the scientific literature. Scientific publications reporting on the HRT/breast cancer association published from January 1, 1995, to June 30, 2000, were identified through a systematic Medline search. Media reports from newspapers, magazines, television, and radio that reported on HRT and breast cancer were retrieved from an online database. Investigators independently recorded characteristics of the scientific publications and media reports. A total of 32 scientific publications were identified: 20 (62.5%) concluded there was an increased risk of breast cancer associated with HRT (positive publications), and 12 (37.5%) concluded there was no evidence for an association (null publications). Nearly half (47%) of the scientific publications were not cited by the media. There were 203 media citations of scientific publications: 82% were of positive publications and 18% were of null publications, representing a significant excess of citations of positive publications (p < 0.01). Media coverage of this controversial issue is based on a limited sample of the scientific publications. Moreover, the excess of media citations for positive scientific publications suggests a bias against null scientific publications.

Bias↗
PubMedDate not supplied

Control of human vascular smooth muscle cell proliferation by sera derived from 'experimentally stressed' individuals.

Recently we reported that individuals with high scores in standardized hostility evaluation tests, when placed in a environment, may have an association with increases in a blood-borne mitogenic substance(s) for arterial smooth muscle cells. To further investigate the molecular basis for such an association, PDS [plasma derived serum with platelet derived growth factor (PDGF) removed] from individuals showing the greatest differential pre/post-stress mitogenic activity, were tested for ability to modulate changes in the steady state of the c-myc mRNA in cultured VSMC (vascular smooth muscle cells) by Northern blot analysis. Post-stress PDS resulted in a significant increase in c-myc mRNA, when compared with pre-stress PDS of the same individual. These results give further experimental support for the notion that stress (even in the form of transient, episodic psychological challenges) may affect the cardiovascular system via rapid elicited rises in serum mitogenic activity for VSMC.

Cell Division↗