[Effects of exogenous hydrogen sulfide on pulmonary hypertension in rabbits with endotoxic shock].

To investigate the effects of exogenous hydrogen sulfide (HS) on pulmonary vascular reactivity induced by endotoxic shock (ES) in rabbits. In this experiment, the model of endotoxic shock (ES) was induced by injection of lipopolysaccharides (LPS) to New Zealand big eared white rabbit through jugular vein (8 mg/0.8 ml/kg), the intervention was performed by HS donor(sodium hydrosulfide, NaHS) which was injected intraperitoneally (28 μmol/kg) 15 min in advance.

Xylomexicanins K-N: limonoids from the leaves and twigs of .

Six new compounds, xylomexicanins K-N (-), granasteroid () and 5-methoxy-2-pentylbenzofuran-7-ol (), along with nine known compounds were isolated from the leaves and twigs of . Among them, was a biogenetic precursor of 1,8,9-phragmalin limonoid, and represent the first example of degraded A-ring limonoid. The structures of them were elucidated on the basis of one- and two-dimensional NMR spectroscopic data (including H, C-NMR, DEPT, H-H COSY, HSQC, HMBC, and NOESY) and confirmed by high-resolution mass spectrometry.

MicroRNA-214 protects L6 skeletal myoblasts against hydrogen peroxide-induced apoptosis.

MicroRNAs (miRNAs) have been reported as key gene regulators, and they control many fundamental biological processes. Previously, we demonstrated that miR-214 had a protective effect against myocardial apoptosis and myocardial fibrosis. In this study, we sought to investigate the expression of miR-214 in L6 skeletal myoblast (SKM), the regulatory effect of miR-214 on hydrogen peroxide (HO) induced cell apoptosis and the underlying mechanisms of the antiapoptotic effect.

Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats.

Introduction: Recent studies suggested that sulfur dioxide (SO2) can be produced endogenously by pulmonary vessels and attenuate acute lung injury (ALI) with vasorelaxant effects. This study was conducted to determine whether SO2 can inhibit lung inflammation and relax pulmonary arteries via inhibition of the mitogen-activated protein kinase (MAPK) pathway.

Material And Methods: Forty-eight adult male Sprague Dawley rats (250~300 g) were randomly divided into six treatment groups: control (n = 8), control + SO2 (n = 8), control + L-aspartic acid--hydroxamate (HDX) (n = 8), LPS (n = 8), LPS + SO2 (n = 8) and LPS + HDX (n = 8).

[The interventional effects of saturated hydrogen saline on lung injury in rats with cecal ligation and puncture operation].

Objective: To investigate the hypothesis that hydrogen could ameliorate cecal ligation and puncture (CLP)-induced lung injury of rats by inhibiting cystathionine-gamma-lyase/hydrogen sulfide (CSE/HS) system.

Methods: A total number of 24 healthy male SD rats weighting 250～300 g were randomly divided into four groups (n=6 in each group): sham operation group(sham group), hydrogen-rich saline control group(H group), CLP group and hydrogen-rich saline treatment group(CLP+H group). The rats were treated with hydrogen-rich saline or saline 10 min before CLP or sham operation.

Anti-IL-20 monoclonal antibody suppresses hepatocellular carcinoma progression.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In the present study, it was observed that IL-20 mRNA and protein levels were markedly increased in the HCC tissues examined via reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining.

Complete mitochondrial genome sequence and mutations of the liver cancer model inbred C57BL/6 mice strain.

In the present work, we undertook the complete mitochondrial genome sequencing of an important liver cancer model inbred rat strain for the first time. The total length of the mitogenome was 16,308 bp. It harbored 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes and 1 non-coding control region (D-loop region).

[Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats].

To investigate the influence of hydrogen sulfide (H₂S) on p38 MAPK signaling pathway during acute lung injury (ALI) caused by lipopolysaccharide (LPS), the rats were randomly divided into six groups: control group, LPS group, LPS + NaHS group, LPS + PPG (cystathionine-γ-lyase inhibitor) group, NaHS group and PPG group. The rats were sacrificed 6 h after injection and lung tissues were obtained. The structure of lung tissues and the number of polymorphonuclear leucocyte (PMN) was observed under optical microscope; the lung myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were tested; intercellular adhesion molecule-1 (ICAM-1) protein expression changes were detected by immunohistochemical staining; phosphorylated p38 MAPK (p-p38 MAPK) protein expression was detected by Western blotting.

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis.

Aim: We speculated that the enhanced apoptosis of polymorphonuclear neutrophil (PMN) might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide (SO(2)) on PMN apoptosis in vivo and in vitro, which may mediate the protective action of SO(2) on pulmonary diseases.

Methods: Acute lung injury (ALI) was induced by intratracheally instillation of lipopolysaccharide (LPS, 100 μg/100 g, in 200 μL saline) in adult male SD rats.

Berberine ameliorates COX-2 expression in rat small intestinal mucosa partially through PPARγ pathway during acute endotoxemia.

Berberine hydrochloride (BBR), a plant alkaloid, has been used to treat intestinal inflammation or infection for years. Cyclooxygenase-2 (COX-2) is pro-inflammatory mediator and involved in the induction of gut inflammation. The expression of COX-2 in small bowel mucosa was determined and the mechanism by which BBR modulated COX-2 expression was explored in a rat model of endotoxemia induced by lipopolysaccharide (LPS).

[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 exogenous hydrogen sulfide on polymorphonuclear neutrophil accumulation in acute lung injury rat induced by lipopolysaccharides and its mechanism].

Objective: To study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced polymorphonuclear neutrophil (PMN) accumulation and its mechanism.

Methods: The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS). Adult male Spraguce-Dawley (SD) rats were randomly divided into four groups (n = 8 - 12 per group): Control group (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.

Clinical, cytogenetic, and molecular characterization of a girl with some clinical features of Down syndrome resulting from a pure partial trisomy 21q22.11-qter due to a de novo intrachromosomal duplication.

We report a girl with a de novo pure partial trisomy 21 with some clinical features of Down syndrome. The girl patient presented a flat broad face, brachycephaly, and a flat nasal bridge. She also had upwardly slanted palpebral fissures, epicanthal folds, blepharitis, brushfield spots, and strabismus.

[Ameliorative effects of exogenous sulfur dioxide on lipopolysaccharide-induced acute lung injury in rats].

To investigate the influence of sulfur dioxide (SO₂) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO₂ on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO₂ group (IV injection of 0.

[Application of fluorescence in situ hybridization in prenatal diagnosis of complex chromosomal abnormalities].

Objective: To investigate the application of fluorescence in situ hybridization (FISH) technique in prenatal diagnosis of complex chromosomal abnormalities.

Methods: Eleven prenatal diagnosis cases (8 from amniocentesis and 3 from cord blood) with complex chromosomal abnormalities detected by routine G-banding, were further analyzed by FISH.

Results: The FISH technique confirmed the results of balanced chromosome rearrangements detected by G-banding, and clarified the structure of the derivative chromosomes in the 3 amniocentesis samples and the origin of the mark chromosomes in the 2 cord blood samples.

[Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury].

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected.

[Role of endogenous and exogenous hydrogen sulfide in acute lung injury induced by LPS in rats].

Aim: To explore the role of endogenous and exogenous hydrogen sulfide (H2S) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats and the underlying mechanisms.

Methods: 120 Sprague-Dawley rats were randomly divided into four groups: control, LPS (instilled intratracheally to induce ALI), NaHS (H2S donor) + LPS, and propargylglycin (PPG) + LPS. Animals were sacrificed at 4 h or 8 h after agent administration.

A 14-year follow-up of a case detected prenatally of partial trisomy 13q21.32-qter and monosomy 18q22.3-qter as a result of a maternal complex chromosome rearrangement involving chromosomes 6, 13, and 18.

A balanced complex chromosome rearrangement (CCR) involving three chromosomes is rare and may lead to different types of aneuploid germ cells. We report here a 14-year follow-up of a boy with a karyotype defined as 46,XY,der(18)t(6;13;18)(q21;q21.32;q22.

[Role of hydrogen sulfide/cystathionine-gamma-lyase system in acute lung injury induced by lipopolysaccharide in rats].

Objective: To explore the role of hydrogen sulfide/cystathionine-gamma-lyase (H(2)S/CSE) system in lipopolysaccharide (LPS)- induced acute lung injury (ALI) in rats and the underlying mechanisms.

Methods: Sixty-four Sprague-Dawley (SD) rats were randomly divided into four groups: control, LPS (instilled intratracheally to induce ALI), sodium hydrosulfide (NaHS), propargylglycine (PPG). Animals were sacrificed at 4 and 8 hours (n=8) after administration of the above agents.

Protection of carbon monoxide-releasing molecule against lung injury induced by limb ischemia-reperfusion.

Objective: To observe the role and mechanism of CO-releasing molecule (CORM)-2 in lung injury induced by ischemia-reperfusion (IR) of hind limbs in rats.

Methods: A rat model of lung injury induced by IR of hind limbs was established. A total of 40 Sprague Dawley (SD) rats were randomly divided into 5 groups (n equal to 8): sham, sham + CORM-2, IR, IR + CORM-2 and IR + dimethyl sulfoxide (DMSO).

[The role of hydrogen sulfide in acute lung injury during endotoxic shock and its relationship with nitric oxide and carbon monoxide].

Objective: To explore the role of hydrogen sulfide (H2S) in acute lung injury (ALI) during endotoxic shock (ES) and its relationship with nitric oxide (NO) and carbon monoxide (CO).

Methods: Sixty-four adult male SD rats were randomly divided into 4 equal groups: control group injected with normal saline via the caudal vein, lipopolysaccharide (LPS)-treated group injected with LPS to establish ES model, LPS + NaHS group injected with LPS and sodium hydrosulfide (NaHS, an exogenous H2S donor], and LPS + PPG group injected with LPS and polypropylene glycol (PPG, a H2S synthase inhibitor). The mean artery pressure (MAP) was measured via a polyethylene catheter in the right common carotid artery for 6 h.