Showing papers by "Jian Wang published in 2006"

Hypoxia Inducible Factor 1 Mediates Hypoxia-Induced TRPC Expression and Elevated Intracellular Ca2+ in Pulmonary Arterial Smooth Muscle Cells

Abstract: Chronic hypoxia (CH) causes pulmonary vasoconstriction because of increased pulmonary arterial smooth muscle cell (PASMC) contraction and proliferation. We previously demonstrated that intracellular Ca 2+ concentration ([Ca 2+ ] i ) was elevated in PASMCs from chronically hypoxic rats because of Ca 2+ influx through pathways other than L-type Ca 2+ channels and that development of hypoxic pulmonary hypertension required full expression of the transcription factor hypoxia inducible factor 1 (HIF-1). In this study, we examined the effect of CH on the activity and expression of store-operated Ca 2+ channels (SOCCs) and the regulation of these channels by HIF-1. Capacitative Ca 2+ entry (CCE) was enhanced in PASMCs from intrapulmonary arteries of rats exposed to CH (10% O 2 ; 21 days), and exposure to Ca 2+ -free extracellular solution or SOCC antagonists (SKF96365 or NiCl 2 ) decreased resting [Ca 2+ ] i in these cells. Expression of TRPC1 and TRPC6, but not TRPC4, mRNA and protein was increased in PASMCs from rats and wild-type mice exposed to CH, in PASMCs from normoxic animals cultured under hypoxic conditions (4% O 2 ; 60 hours), and in PASMCs in which HIF-1 was overexpressed under nonhypoxic conditions. Hypoxia-induced increases in basal [Ca 2+ ] i and TRPC expression were absent in mice partially deficient for HIF-1. These results suggest that increased TRPC expression, leading to enhanced CCE through SOCCs, may contribute to hypoxic pulmonary hypertension by facilitating Ca 2+ influx and increasing basal [Ca 2+ ] i in PASMCs and that this response is mediated by HIF-1.

HIF-1 regulates hypoxic induction of NHE1 expression and alkalinization of intracellular pH in pulmonary arterial myocytes.

Abstract: Vascular remodeling resulting from altered pulmonary arterial smooth muscle cell (PASMC) growth is a contributing factor to the pathogenesis of hypoxic pulmonary hypertension. PASMC growth requires...

Correction: Streptococcal Toxic Shock Syndrome Caused by Streptococcus suis Serotype 2.

Abstract: In PLoS Medicine, volume 3, issue 5: DOI: 10.1371/journal.pmed.0030151 As part of the revision of this manuscript, additional data on the clinical description of the cases were added, as were four new authors who had been involved in this part of the work. Those same four researchers had also authored a related manuscript, which should have been mentioned in the PLoS Medicine article. The related manuscript is now published: Yu H, Jing H, Chen Z, Zheng H, Zhu X, et al. (2006) Human Streptococcus suis outbreak, Sichuan, China. Emerg Infect Dis 12: 914–920. Available at http://www.cdc.gov/ncidod/EID/vol12no06/05-1194.htm.

Ca2+ Channels and Chronic Hypoxia

Abstract: Many chronic lung diseases are associated with prolonged exposure to alveolar hypoxia, resulting in the development of pulmonary hypertension. While the exact mechanisms underlying the pathogenesis of hypoxic pulmonary hypertension remain poorly understood, a key role for changes in Ca2+ homeostasis has emerged. Intracellular Ca2+ concentration controls a variety of pulmonary vascular cell functions, including contraction, gene expression, growth, barrier function and synthesis of vasoactive substances. Several studies indicate that prolonged exposure to hypoxia causes alterations in the expression and activity of several Ca2+ handling pathways in pulmonary arterial smooth muscle cells. In contrast, the effect of chronic hypoxia on Ca2+ homeostasis in pulmonary arterial endothelial cells is relatively unexplored. In this review, we discuss data from our laboratory and others describing the effects of prolonged hypoxia on pulmonary vascular smooth muscle and endothelial cell Ca2+ homeostasis and the various Ca2+ channels and handling pathways involved in these responses. We will also highlight future directions of investigation that might improve our understanding of the response of pulmonary vascular cells to chronic hypoxia.

A Novel Blue‐Emitting Phosphor LiSrPO4:Eu2+ for White LEDs.

Abstract: A novel blue-emitting phosphor, LiSrPO 4 :Eu 2+ , was prepared by the solid-state reaction and X-ray powder diffraction (XRD) analysis confirmed the formation of LiSrPO 4 :Eu 2+ . Photoluminescence (PL) results showed that the phosphor can be efficiently excited by UV-visible light from 250 to 440 nm, and exhibited bright blue emission. The effects of the doped-Eu 2+ concentration in LiSrPO 4 :Eu 2+ on the PL were investigated in detail. The results showed that the relative PL intensity increases with Eu 2+ -concentration increasing until a maximum intensity is reached, and then it decreases due to concentration quenching and a red-shift appears, which are explained satisfactorily with the luminescent theory. Upon excited with 396 nm light, the present synthesized phosphor has higher emission intensity than that from the commercial blue phosphor, BaMgAl 10 O 17 :Eu 2+ . Bright blue light-emitting diodes were fabricated by the combination of the synthesized LiSrPO 4 :Eu 2+ with ∼397 nm emitting InGaN-based chips.

Phosphorylation site mutated RB exerts contrasting effects on apoptotic response to different stimuli

Abstract: The retinoblastoma tumor-suppressor protein (RB) is an important regulator of cell cycle and apoptosis. RB is phosphorylated by cyclin-dependent protein kinase during cell cycle progression. A phosphorylation site mutated (PSM)-RB has previously been shown to cause G1 arrest and to interfere with S phase progression. In this study, we examined the effect of inducible PSM-RB expression on the apoptotic response to three different death stimuli: doxorubicin (DOXO), staurosporine (STS) and tumor necrosis factor (TNF) in Rat-16 cells. Induced expression of PSM-RB attenuated caspase activation by DOXO as a result of cell cycle arrest. STS has been shown to cause RB-dependent G1 arrest or apoptosis; however, expression of PSM-RB did not prevent caspase activation by STS. Surprisingly, induced expression of PSM-RB stimulated the apoptotic response to TNF in Rat-16 cells, which mostly undergo necrosis in the absence of PSM-RB. These results show that PSM-RB exerts disparate effects on apoptotic response to different stimuli, and that cell cycle arrest does not always associate with resistance to apoptosis.

Relative Efficiency, Scale Effect, and Scope Effect of Public Hospitals: Evidence from Australia

Abstract: Using the 1997-1998 New South Wales public-hospitals comparison data, we investigate the hospital-level inefficiency by applying a stochastic-frontier multiproduct cost function. We use a flexible translog cost function to reduce the measurement errors of the outputs of the hospital. The main findings are: First, inefficiency accounts for 9.3% of total hospital costs in large hospitals and 11.3% in small hospitals, when including complexity indicators. Second, diseconomies of scale exist in very large hospitals, whereas scale economies appear in very small hospitals. Third, scope effects are found in both large and small hospitals. Fourth, small hospitals are more labor-intensive than large hospitals are.