Biomedical subjects

Hong Jiang

Publications and source records attributed to Hong Jiang.

183 records · Page 11Linked to original sources

PubMedDate not supplied

Circadian variation in ischemic threshold in patients with stable angina: relation to plasma endothelin-1.

To investigate circadian variation in ischemic threshold in chronic coronary heart disease (CHD) and its relation to plasma endothelin-1 (ET-1), 21 patients with stable angina underwent treadmill exercise tests twice within a day, performed at 8-9 AM for the first test and at 3-4 PM for the second one. Ischemic threshold was defined as the heart rate at the onset of 1 mm ST segment depression during exercise tests. Blood samples were taken at 5 minutes before each exercise test, and plasma ET-1 was measured for determining the possible relation to ischemic threshold in patients with CHD. The results showed that the heart rate-ischemic threshold in individual patients varied by 10 +/- 1% (range, 2-15%) in the morning and 9 +/- 1% (range, 2-14%) in the afternoon, while there was a mean (11.2%) reduction in the ischemic threshold between 2 time points, with the ischemic threshold being significantly lower in the morning compared with that in the afternoon (115 +/- 22 bpm vs 128 +/- 31 bpm p<0.04). ET-1 values were 6.20 +/- 2.44 ng/L in the morning hours and 4.02 +/- 1.61 ng/L in the afternoon hours, with a statistical significant difference (p<0.01). In conclusion, the present study indicated that circadian variation of plasma levels of ET-1 was likely to be one of the most likely mechanisms involved in reduction in the ischemic threshold in the morning hours.

Adult↗

PubMedDate not supplied

Increased C-reactive protein level after renal stent implantation in patients with atherosclerotic renal stenosis.

Elevated C-reactive protein (CRP) level has been demonstrated in patients with coronary artery disease after coronary stent implantation, but no data are available in patients with atherosclerotic renal artery stenosis concerning whether such changes of CRP also exist after renal artery stent implantation. The authors hypothesize that elevated CRP level may also be present in patients with atherosclerotic renal artery stenosis after stent implantation owing to mechanical disruption of atherosclerotic plaque. In total, 24 patients were enrolled in this study. Of these, 14 patients with atherosclerotic renal artery stenosis received renal angioplasty plus stent implantation (group A, mean age 51 +/- 8 years), and 14 age- and gender-matched patients underwent renal angiography for diagnostic purpose as a control group (group B, mean age 50 +/- 8 years). Peripheral blood samples were taken before the procedure and at 6 and 24 hours after the procedure in both groups. Plasma CRP concentration was measured by using immunoturbidimetry. The results showed that there was no difference in clinical characteristics or in baseline CRP levels between the 2 groups. However, median CRP level was found to increase significantly at 6 hours from 0.13 to 0.17 mg/dL (p < 0.05), and peaked at 24 hours (0.21 mg/dL) after renal artery stent implantation (p < 0.001). Mean CRP rose from 0.30 +/- 0.09 to 0.37 +/- 0.15 mg/dL at 6 hours (p < 0.05) and peaked at 24 hours (0.43 +/- 0.18 mg/dL) after renal artery stent implantation (p < 0.01), while no such changes were observed after renal angiography in group B (p > 0.05, respectively, at different time points). The results of the present study indicate, from evidence of increased plasma CRP concentrations, that renal artery stent implantation could trigger an inflammatory response due to mechanical disruption of atherosclerotic plaque of the renal artery, which is a pattern very similar to that of coronary stent implantation.

Adult↗

PubMedDate not supplied

Cisplatin-induced ubiquitination of RNA polymerase II large subunit and suppression of induction by 7-hydroxystaurosporine (UCN-01).

Exposure of cells to DNA-damaging agents induces hyperphosphorylation of the C-terminal domain (CTD) of mammalian RNA polymerase II (RNAP II) large subunit (LS); the hyperphosphorylated RNAP II is then ubiquitinated. The purpose of this study was to verify that cisplatin-induced RNAP II ubiquitination is transcription dependent in living cells and to determine whether 7-hydroxystaurosporine (UCN-01) inhibits the ubiquitination induced by cisplatin. Cisplatin at clinically achievable concentrations (2.5-10 micro M) induced the ubiquitination of RNAP II in exponentially growing A2780 human ovarian tumor cells; the effect was drug-dose and exposure-time dependent. Such induction, however, was not observed in colcemid-selected mitotic cells. When detergent extraction was applied, the ubiquitinated RNAP II was recovered in the detergent-insoluble fraction, indicating that the protein was tightly bound to DNA. In an in vitro transcription reaction that consists of nuclear extracts and an immobilized DNA template containing a site-specific cisplatin lesion, the elongating RNAP II that was stalled at a cisplatin lesion site on the template was targeted by ubiquitins. Together, our results indicate that the ubiquitination is associated with transcription-coupled repair. We previously showed that the Ser/The kinase-inhibitor UCN-01 inhibits nucleotide excision repair. Here, we further determined the effect of UCN-01 on the phosphorylation and ubiquitination of RNAP II LS in a whole-cell system. Immunoblotting results showed that UCN-01 suppressed the cisplatin-induced ubiquitination and the cisplatin-induced shift from the hypophosphorylated IIa to the hyperphosphorylated IIo, without affecting the basal levels of the IIo and IIa forms of the RNAP II CTD, suggesting that UCN-01 acts by suppressing cisplatin-mediated induction of the one or more kinases that is responsible for the conversion of the IIo that is important for ubiquitination.

Antineoplastic Agents↗