A novel animal model of primary blast lung injury and its pathological changes in mice.

Background: Primary blast lung injury (PBLI) is a major cause of death in military conflict and terrorist attacks on civilian populations. However, the mechanisms of PBLI are not well understood, and a standardized animal model is urgently needed. This study aimed to establish an animal model of PBLI for laboratory study.

[Effects of ZFP580 on ventricular remodeling after myocardial ischemia/reperfusion in rats].

Objective: To investigate the relationship between zinc finger protein(ZFP580)and ventricular remodeling after myocardial is-chemia/reperfusion(I/R) injury in rats.

Methods: Seventy-two rats were divided into sham group and I/R groups which would be tested in se-ries time of 0.5 h, 1 h, 2 h, 4 h, 1 d,7 d,14 d,28 d after reperfusion to observe the expression of ZFP580 in rat myocardium.

The role of ZFP580, a novel zinc finger protein, in TGF-mediated cytoprotection against chemical hypoxia‑induced apoptosis in H9c2 cardiac myocytes.

Zing finger protein 580 (ZFP580) is a novel Cys2-His2 zinc-finger transcription factor that has an anti-apoptotic role in myocardial cells. It is involved in the endothelial transforming growth factor‑β1 (TGF‑β1) signal transduction pathway as a mothers against decapentaplegic homolog (Smad)2 binding partner. The aim of the present study was to determine the involvement of ZFP580 in TGF‑β1‑mediated cytoprotection against chemical hypoxia‑induced apoptosis, using H9c2 cardiac myocytes.

SILAC-based proteomic analysis reveals that salidroside antagonizes cobalt chloride-induced hypoxic effects by restoring the tricarboxylic acid cycle in cardiomyocytes.

Hypoxic status alters the energy metabolism and induces cell injury in cardiomyocytes, and it further triggers the occurrence and development of cardiovascular diseases. Our previous studies have shown that salidroside (SAL) exhibits anti-hypoxic activity. However, the mechanisms remain obscure.

[The effects of intermittent hypobaric hypoxia on myocardial ischemia/reperfusion injury and ZFP580 expression].

Objective: To elucidate whether ZFP580 is involved in the cardioprotective effects of intermittent hypobaric hypoxia (IHH) against myocardial ischemia/reperfusion (I/R) injury.

Methods: Thirty two male Wistar rats were randomly divided into 2 groups (n = 16): normoxia control group and IHH preconditioning group. Rats in IHH group were exposed in a hypobaric chamber (equivalent to an altitude of 5 000 m) for a 6 h period each day for 42 d.

ZFP580, a novel zinc-finger transcription factor, is involved in cardioprotection of intermittent high-altitude hypoxia against myocardial ischemia-reperfusion injury.

Background: ZFP580 is a novel C2H2 type zinc-finger transcription factor recently identified by our laboratory. We previously showed that ZFP580 may be involved in cell survival and growth. The aim of this study was to elucidate whether ZFP580 is involved in the cardioprotective effects of intermittent high-altitude (IHA) hypoxia against myocardial ischemia-reperfusion (I/R) injury.

Interleukin-8 secretion by ovarian cancer cells increases anchorage-independent growth, proliferation, angiogenic potential, adhesion and invasion.

It has been shown that IL-8 is elevated in ovarian cyst fluid, ascites, serum, and tumor tissue from ovarian cancer (OVCA) patients, and increased IL-8 expression correlates with poor prognosis and survival. However, the exact role that IL-8 plays in this malignancy or whether IL-8 can regulate malignant behavior has not been established. Here we demonstrate that overexpression of IL-8 in non-IL-8-expressing A2780 cells (by transfecting with plasmid encoding for sense IL-8) increases anchorage-independent growth, proliferation, angiogenic potential, adhesion and invasion while depletion of endogenous IL-8 expression in IL-8-overexpressing SKOV-3 cells (by transfecting with plasmid encoding for antisense IL-8) decreases the above effects.

Arsenic biotransformation and volatilization in transgenic rice.

• Biotransformation of arsenic includes oxidation, reduction, methylation, and conversion to more complex organic arsenicals. Members of the class of arsenite (As(III)) S-adenosylmethyltransferase enzymes catalyze As(III) methylation to a variety of mono-, di-, and trimethylated species, some of which are less toxic than As(III) itself. However, no methyltransferase gene has been identified in plants.

[Administration of hydrogen sulfide intraperitoneally reverses the hyporesponsiveness of rat pulmonary artery induced by lipopolysaccharide and its relationship with carbon monoxide].

Objective: To explore the effect of hydrogen sulfide (H(2)S) on abnormal pulmonary artery reactivity induced by lipopolysaccharide (LPS) and its relationship with carbon monoxide (CO).

Methods: Forty eight rats were divided into four groups randomly according to table of random number: control group (normal saline, NS), LPS group, a donor of H(2)S sodium hydrosulfide (NaHS)+LPS group, and NaHS+NS group (n=12 in each group). Rats were given LPS by intratracheal instillation (0.

[Effect of hydrogen sulfide on rat pulmonary artery reactivity and injury induced by lipopolysaccharide].

Objective: To explore the effects of hydrogen sulfide (H2S) on abnormal pulmonary artery reactivity and injury induced by lipopolysaccharide (LPS).

Methods: Seventy-two rats were divided into four groups randomly according to table of random number: control group, LPS group, sodium hydrosulfide (NaHS) as a donor of H2S+LPS group and NaHS+normal saline (NS) group (n=18 in each group). Rats were challenged with 0.

[Role of endogenous hydrogen sulfide in pulmonary hypertension induced by lipopolysaccharide].

The purpose of the present study was to explore the role of endogenous hydrogen sulfide (H2S) in pulmonary arterial hypertension induced by endotoxin. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group (0.5 mL/kg body weight of normal saline, i.