Biomedical subjects

Qing H Meng

Publications and source records attributed to Qing H Meng.

8 recordsLinked to original sources

PubMed2006

Effects of hydrogen sulfide on homocysteine-induced oxidative stress in vascular smooth muscle cells.

Hydrogen sulfide (H(2)S) is an important gasotransmitter that generated in mammalian cells from l-cysteine metabolism. Little is known about its protective role in oxidative stress. In the present study, we investigated whether H(2)S could affect homocysteine (HCY)-induced cytotoxicity and oxidative stress in vascular smooth muscle cells. Cultured A-10 cells were exposed to HCY treatment in the presence or absence of NaHS (donor of H(2)S). HCY induced cytotoxicity, increased levels of H(2)O(2), ONOO(-), and O2- in a time- and concentration-dependent manner. Low levels of NaHS (30 or 50microM) protected A-10 cells from cytotoxicity, decreased the production of H(2)O(2), ONOO(-), and O2- in the presence of HCY. Furthermore, NaHS enhanced inhibitory effects of NAC, GSH, DPI, SOD, L-NAME, or vitamin C on oxidized DCF or O2- formation induced by HCY. In conclusion, our findings provide the first evidence that low levels of H(2)S decrease reactive oxygen species and improve cell viability and by doing so limit cellular damage induced by HCY.

Acetylcysteine↗

PubMed2006

Inhibitory effects of micronized fenofibrate on carotid atherosclerosis in patients with essential hypertension.

BACKGROUND: The coexistence of hypertension and dyslipidemia synergistically increases the risk of cardiovascular events. We investigated the effect of the lipid-lowering agent micronized fenofibrate on inhibition of carotid atherosclerosis in patients with essential hypertension and mild hyperlipidemia. METHODS: We measured serum lipid profiles and inflammatory markers on chemistry or immune analyzers and common or internal carotid intima-media thickness (IMT) and diameter (D) by ultrasonography. RESULTS: Patients receiving micronized fenofibrate for 24 months in addition to antihypertensive treatment had decreased concentrations of total cholesterol, LDL-cholesterol, triglyceride, apolipoprotein B100, oxidized LDL, high-sensitivity C-reactive protein, P-selectin, and cytokines. These patients had increased concentrations of HDL-cholesterol, apolipoprotein A-I, and nitric oxide. Common carotid artery IMT (CCAIMT) and internal carotid artery IMT (ICAIMT) remained unchanged during the 24-month intervention. Moreover, the mean CCAIMT/D ratio and ICAIMT/D ratio were significantly decreased in the fenofibrate intervention group. In contrast, CCAIMT/D and ICAIMT/D ratios were increased in the control group. The incidence rates of carotid artery plaque formation and stroke in the fenofibrate intervention group were significantly lower than those in the control group. CONCLUSION: The combination of antihypertensive agents with micronized fenofibrate can effectively prevent the progression of carotid atherosclerosis and reduce the incidence of stroke in patients with essential hypertension.

Anti-Inflammatory Agents↗

PubMed2006

Fructose-induced peroxynitrite production is mediated by methylglyoxal in vascular smooth muscle cells.

Methylglyoxal (MG), a highly reactive molecule, has been implicated in the development of insulin resistance. We investigated whether fructose, a precursor of MG, induced ONOO(-) generation and whether this process was mediated via endogenously increased MG formation. Fructose significantly increased MG generation in vascular smooth muscle cells (VSMCs) in a concentration and time dependent manner. The intracellular production of MG was increased by 153+/-23% or 259+/-28% after cells were treated 6 h with fructose (15 mM or 30 mM), compared with production from untreated cells (p<0.01, n=4 for each group). A significant increase in the production of ONOO(-), NO, and O(2)(*-), was found in the cells treated with fructose (15 mM) or MG (10 microM). Fructose- or MG-induced ONOO(-) generation was significantly inhibited by MG scavengers, including reduced glutathione or N-acetyl-l-cysteine, and by O(2)(*-) or NO inhibitors, such as diphenylene iodonium, superoxide dismutase or N-nitro-l-arginine methyl ester. Moreover, an enhanced iNOS expression was also observed in the cells treated directly with MG which was significantly inhibited when co-application with N-acetyl-l-cysteine. Our results demonstrated that fructose is capable of inducing a significant increase in ONOO(-) production, which is mediated by an enhanced formation of endogenous MG in VSMCs.

Acetylcysteine↗

PubMed2006

Impact of the cardiac troponin testing algorithm on excessive and inappropriate troponin test requests.

Cardiac troponin (cTn) is a key biomarker for the assessment of myocardial injury, but overutilization of this test has increased workload and costs. We developed and implemented an algorithm to eliminate excessive utilization. Significant reduction was observed after the implementation of the algorithm in total cTnI requests (29.9%; P = .007), requests from outpatient clinics (70.7%; P = .003), and other wards (42.8%; P = .003). Stat requests, the number of third requests, and more than 3 requests per patient were reduced significantly by 42.8% (P = .004), 35.8% (P = .003), and 49.4% (P = .008), respectively. The test and labor costs each were reduced by 29.9% (P = .007 for each). There was no significant change in cTnI orders from emergency and critical care departments. The cTnI testing algorithm reduced unnecessary orders for cTnI tests with no reduction in meeting patients'critical needs. Reduction in unnecessary and inappropriate requests reduces labor and test costs.

Algorithms↗

PubMed2005

Simultaneous analysis of citalopram and desmethylcitalopram by liquid chromatography with fluorescence detection after solid-phase extraction.

OBJECTIVES: To develop a HPLC method for the determination of citalopram (CIT) and desmethylcitalopram (DCIT). METHODS: Solid-phase extraction followed by fluorescence detection was used to measure CIT and DCIT in deproteinized plasma. RESULTS: The extraction recovery for both analytes was 104 +/- 3%. The calibration was linear over the concentration range of 12-1600 ng/mL for CIT and 6-800 ng/mL for DCIT. The within-run CVs were 2.5% for CIT (400 ng/mL) and 2.9% for DCIT (200 ng/mL) and the between-run CVs were 5.2% for CIT and 2.9% for DCIT, respectively. With low concentrations of CIT (50 ng/mL) and DCIT (25 ng/mL), the within-run CVs were 3.1% and 1.1% and the between-run CVs were 7.4% and 8.8%, respectively. The lower limit of quantification was 12 ng/mL for CIT and 6 ng/mL for DCIT. CONCLUSIONS: This method allows for the simultaneous determination of CIT and DCIT in plasma at therapeutic and toxic drug concentrations.

Chromatography, High Pressure Liquid↗

PubMed2005

The effects of high-dose heparin on inflammatory and coagulation parameters following cardiopulmonary bypass.

Systemic inflammation and the activation of the coagulation system following cardiopulmonary bypass (CPB) may contribute to postoperative complications. In vitro studies have demonstrated that heparin possesses anti-inflammatory properties. To ascertain the relative benefits of high versus low heparin doses, we studied the impact of varying heparin doses on the inflammatory response and coagulation system during and following CPB. Forty patients scheduled for elective coronary artery bypass surgery requiring CPB were randomized to either a low dose (300 U/kg) (Group L) or a high dose of unfractionated heparin (600 U/kg) (Group H). To evaluate the inflammatory response, proinflammatory cytokines [tumor necrosis factor-alpha and interleukin-6 (IL-6)] were measured at four different times: before CPB (T0), 30 min after the institution of CPB (T1), 30 min after cross-clamp release (T2), and 4 h after the end of CPB (T3). Thrombin-antithrombin complex, platelet factor 4 and anti-activated factor X heparin concentrations were also measured. Patients in Group H received greater heparin (44.934 U versus 27.741 U, P<0.001) and protamine (P=0.003) doses. Postoperative blood loss and blood products transfusions were not significantly different in the groups. At T1, mean heparin plasma concentration was higher in Group H (P<0.001). IL-6 was significantly lower in Group H compared with Group L (P=0.01) only at T1. Using a mixed-effects statistical model, tumor necrosis factor-alpha and IL-6 levels were comparable regardless of the heparin dose. Thrombin-antithrombin complex levels were lower in Group H (P=0.04) and platelet factor 4 levels were significantly lower in Group H at T2 (P=0.04). Higher heparin doses were associated with higher heparin concentrations during CPB. A high heparin dose achieved a better preservation of the coagulation system with less thrombin formation and platelet activation. The heparin dose had small influence on proinflammatory cytokines release.

Aged↗

PubMed2005

Interference of ascorbic acid with chemical analytes.

BACKGROUND: Ascorbic acid can interfere with methodologies involving redox reactions, while comprehensive studies on main chemistry analysers have not been reported. We therefore attempted to determine the interference of ascorbic acid with analytes on the Beckman Synchron LX20. METHODS: Various concentrations of ascorbic acid were added to serum, and the serum analytes were measured on the LX20. RESULTS: With a serum ascorbic acid concentration of 12.0 mmol/L, the values for sodium, potassium, calcium and creatinine increased by 43%, 58%, 103% and 26%, respectively (P<0.01). With a serum ascorbic acid concentration of 12.0 mmol/L, the values for chloride, total bilirubin and uric acid decreased by 33%, 62% and 83%, respectively (P<0.01), and were undetectable for total cholesterol, triglyceride, ammonia and lactate. There was no definite influence of ascorbic acid on analytical values for total CO(2), urea, glucose, phosphate, total protein, albumin, amylase, creatine kinase, creatine kinase-MB, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total iron, unbound iron-binding capacity or magnesium. CONCLUSIONS: Ascorbic acid causes a false increase in sodium, potassium, calcium and creatinine results and a false decrease in chloride, total bilirubin, uric acid, total cholesterol, triglyceride, ammonia and lactate results.

Ascorbic Acid↗

PubMed2005

Vitamin C and aberrant electrolyte results.

Vitamin C interferes with assays involving the redox-reaction. However, the interference of Vitamin C with electrolytes has not been reported. In the present case, we describe a 61-year-old lady with severe electrolyte abnormalities after administration of high doses of vitamin C. This patient, who had terminal colon cancer, presented to hospital with anuria. Her electrolytes were extremely abnormal (determined on the Beckman Synchron LX20): serum sodium 200 mmol/L, potassium 7.0 mmol/L, and chloride 50 mmol/L. Repeated measurements showed similar abnormalities. However, these critical abnormalities did not fit her clinical picture, as she was alert with normal vital signs. One of the specimens was also run on both the ABL700 and the Bayer644 analyzers, and the electrolytes appeared normal. Pooled serum from healthy individuals to which various amounts of vitamin C was added then was analyzed on Beckman Synchron LX20 for electrolytes, demonstrating the interference of vitamin C consistent with the initial finding. Thus, we eventually figured out that the aberrant results were due to the vitamin C caused analytical interference.

Ascorbic Acid↗