Metagenomic next-generation sequencing for pleural effusions induced by viral pleurisy: A case report.

Background: Viral pleurisy is a viral infected disease with exudative pleural effusions. It is one of the causes for pleural effusions. Because of the difficult etiology diagnosis, clinically pleural effusions tend to be misdiagnosed as tuberculous pleurisy or idiopathic pleural effusion.

PK/PD modeling of Ceftiofur Sodium against Haemophilus parasuis infection in pigs.

Background: Ceftiofur Sodium is widely used in China. Our aim was to determine Ceftiofur Sodium activity and optimize dosing regimens against the pathogen Haemophilus parasuis using an in vitro and ex vivo pharmacokinetics/pharmacodynamics modeling approach. By adopting these strategies, we wanted to extend the effective life of Ceftiofur Sodium in reduce drug-resistance in pigs.

Predictive Value of Combined LIPS and ANG-2 Level in Critically Ill Patients with ARDS Risk Factors.

To investigate the predictive value of the acute physiology and chronic health evaluation 2 (APACHE2) score and lung injury prediction score (LIPS) for acute respiratory distress syndrome (ARDS) when combined with biomarkers for this condition in patients with ARDS risk factors. In total, 158 Han Chinese patients with ARDS risk factors were recruited from the Respiratory and Emergency Intensive Care Units. The LIPS, APACHE2 score, primary diagnosis at admission, and ARDS risk factors were determined within 6 h of admission, and PaO/FiO was determined on the day of admission.

The involvement of aquaporin 1 in the hepatopulmonary syndrome rat serum-induced migration of pulmonary arterial smooth muscle cells via the p38-MAPK pathway.

Hepatopulmonary syndrome (HPS) is characterized by arterial oxygenation defects induced by intrapulmonary vascular dilation (IPVD). Pulmonary vascular remodeling (PVR) is an important pathological feature of IPVD; however, the details regarding the underlying mechanisms of this process remain undefined. Recent studies have determined that the abnormal migration of pulmonary arterial smooth muscle cells (PASMCs) plays a role in the pathogenesis of the PVR associated with HPS.

Requirement of miR-9-dependent regulation of Myocd in PASMCs phenotypic modulation and proliferation induced by hepatopulmonary syndrome rat serum.

Hepatopulmonary syndrome (HPS) is characterized by a triad of severe liver disease, intrapulmonary vascular dilation and hypoxaemia. Pulmonary vascular remodelling (PVR) is a key feature of HPS pathology. Our previous studies have established the role of the pulmonary artery smooth muscle cell (PASMC) phenotypic modulation and proliferation in HPS-associated PVR.

Bone morphogenic protein-2 regulates the myogenic differentiation of PMVECs in CBDL rat serum-induced pulmonary microvascular remodeling.

Hepatopulmonary syndrome (HPS) is characterized by an arterial oxygenation defect induced by intrapulmonary vasodilation (IPVD) that increases morbidity and mortality. In our previous study, it was determined that both the proliferation and the myogenic differentiation of pulmonary microvascular endothelial cells (PMVECs) play a key role in the development of IPVD. However, the molecular mechanism underlying the relationship between IPVD and the myogenic differentiation of PMVECs remains unknown.

MiR-206 controls the phenotypic modulation of pulmonary arterial smooth muscle cells induced by serum from rats with hepatopulmonary syndrome by regulating the target gene, annexin A2.

Background: Hepatopulmonary syndrome (HPS) is a serious complication of advanced liver disease that is characterised by intrapulmonary vascular dilatation (IPVD) and arterial hypoxemia. Pulmonary vascular remodelling (PVR) is an important pathological feature of HPS, but the potential mechanisms underlying PVR remain undefined. Recent findings have established the essential role of changes in Annexin A2 (ANXA2) in controlling the phenotypic modulation of pulmonary artery smooth muscle cells (PASMCs) in PVR associated with HPS.

Directed evolution of an LBP/CD14 inhibitory peptide and its anti-endotoxin activity.

Background: LPS-binding protein (LBP) and its ligand CD14 are located upstream of the signaling pathway for LPS-induced inflammation. Blocking LBP and CD14 binding might prevent LPS-induced inflammation. In previous studies, we obtained a peptide analog (MP12) for the LBP/CD14 binding site and showed that this peptide analog had anti-endotoxin activity.

Over-expression of PKGIα inhibits hypoxia-induced proliferation, Akt activation, and phenotype modulation of human PASMCs: the role of phenotype modulation of PASMCs in pulmonary vascular remodeling.

The proliferation of pulmonary artery smooth muscle cells (PASMCs) plays a role in pulmonary vascular remodeling (PVR). Recently, it was shown that vascular smooth muscular cell phenotype modulation is important for their proliferation in other diseases. However, little is known about the role of human PASMC phenotype modulation in the proliferation induced by hypoxia and its molecular mechanism during PVR.

Relationship between the anti-inflammatory properties of salmeterol/fluticasone and the expression of CD4⁺CD25⁺Foxp3⁺ regulatory T cells in COPD.

Background: Salmeterol and fluticasone combination (SFC) has anti-inflammatory effects and improves clinical symptoms in patients with chronic obstructive pulmonary disease (COPD). However, the anti-inflammatory mechanism of SFC remains unclear. In this study, we investigated the inflammatory responses of COPD, as well as the relationship of the inflammatory factors with the levels of CD4+CD25+Foxp3+ regulatory T cells (Foxp3+Tregs) after SFC therapy.

[Effects of methyl β cyclodextrin on the proliferation and transdifferentiation of type II alveolar epithelial cells].

Objective: To study the destructive effects of the membrane lipid microdomain with methyl β cyclodextrin (MβCD) on the proliferation, transdifferentiation and cell cycle of type II alveolar epithelial cell (AEC II).

Methods: The membrane lipid microdomain of AEC II was destroyed by MβCD (MβCD interference group) in vitro, and then cultured with DMEM as control. Cell number was counted with hemacytometer; the proliferation rate was measured by methyl thiazolyl tetrazolium (MTT); flow cytometry was used to assay the cell cycle.

Over-starvation aggravates intestinal injury and promotes bacterial and endotoxin translocation under high-altitude hypoxic environment.

Aim: To study whether over-starvation aggravates intestinal mucosal injury and promotes bacterial and endotoxin translocation in a high-altitude hypoxic environment.

Methods: Sprague-Dawley rats were exposed to hypobaric hypoxia at a simulated altitude of 7000 m for 72 h. Lanthanum nitrate was used as a tracer to detect intestinal injury.

[Adenovirus-mediated protein-kinase-GIalpha suppresses the hypoxia-induced proliferation and phenotype-switching of pulmonary arterial smooth muscle cell].

Objective: To observe the proliferation and phenotype-switching of pulmonary arterial smooth muscle cell (PASMC) induced by hypoxia and interfered by Ad-PKGIα. And to investigate the potential regulative role of PKGIα gene in the molecule mechanism of hypoxia pulmonary vessel remodeling (HPVR).

Methods: To establish the pure PASMC cultured by tissue-sticking methods.

[The effect of seawater on expression of protease-activated receptor 2 in adenocarcinoma of lung cell line A549 cells].

Objective: To investigate the effect of seawater on expression of protease-activated receptor 2 (PAR-2) in adenocarcinoma of lung cell line A549 cells, and the inflammatory injury on A549 cells induced by seawater.

Methods: A549 cells were randomly divided into four groups: control group, 2 hours group, 4 hours group, 8 hours group, in which cells were treated with seawater for 2, 4 and 8 hours respectively. After seawater treatment, cells were collected for real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis to determine the expression of PAR-2 mRNA and its protein.

Restoration of SOCS3 suppresses human lung adenocarcinoma cell growth by downregulating activation of Erk1/2, Akt apart from STAT3.

SOCS3 is regarded as a major negative regulator of STAT3. Recent evidence indicates that SOCS3 regulates strength and duration of other signaling pathways including ras/ERK1/2/MAPK, PI3-K/Akt in non-malignant cells. The repression or silence of SOCS3 expression in a few tumor types has led to speculation that loss of SOCS3 gene is closely related to deregulation of multiple signal pathways during tumorigenesis.

[Study on expression of liver X receptor-alpha in rat lung tissue in acute lung injury].

Objective: To observe changes in liver X receptor-alpha (LXR alpha) in acute lung injury (ALI) in rats induced by lipopolysaccharide (LPS) to explore mechanism of LXR alpha in pathogenesis of ALI.

Methods: Forty-eight Wistar rats were randomly divided into two groups. ALI model was reproduced by intravenous injection of LPS (5 mg/kg), and control group was injected with normal saline (2.

[Effect of nuclear factor-kappaB on peroxisome proliferator activated receptor gamma expression in Ana-1 cells].

Objective: To determine the effects of nuclear factor-alpha B (NF-alpha B) on peroxisome proliferator activated receptor gamma (PPAR gamma) expression in the murine macrophage cell line Ana-1, based on the investigation of the PPAR gamma expression stimulated by lipopolysaccharide (LPS).

Methods: Ana-1 cells were divided randomly into seven groups: control group, LPS groups (cells were activated by 0.1 mg/L LPS for 1, 2, 4, 8 hours respectively), SN50 group (cells were stimulated by 50 mg/L SN50 for 4 hours) and NF-alpha B high expression plasmid transfected group.

JAK-STAT signaling pathway in pulmonary arterial smooth muscle cells is activated by hypoxia.

Pulmonary arterial smooth muscle cells (PASMC) were divided into a normoxic group (N), 2, 8 and 12 h hypoxic groups (H2, H8 and H12) and an AG490 plus 8 h hypoxic group (AG490). The expression of JAK1, JAK2, JAK3 and TYK2 mRNA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). STAT1 and STAT3 protein expressions were determined by Western blotting.

[Changes of interleukin-6 and Janus kinases in rats with hypoxic pulmonary hypertension].

Objective: To investigate the expressions of interleukin 6 (IL-6) and Janus kinases (JAKs) in rats with hypoxia induced pulmonary hypertension (HPH).

Methods: Sixty male Wistar rats were randomized into 5 groups with 12 animals in each: a one-week hypoxic group (H(1) group), a two-week hypoxic group (H(2) group), a three-week hypoxic group (H(3) group), a four-week hypoxic group (H(4) group), a normal oxygen group (N group). The rat model of HPH was replicated in normal baric hypoxic cabin.

[Enhanced expression of signal transducers and activators of transcription in lung tissue of hypoxic pulmonary hypertension rat models].

Objective: To investigate the expression levels of signal transducers and activators of transcription (STATs) in the lung tissue of hypoxic pulmonary hypertension (HPH) rat models.

Methods: The Wister rat HPH models were divided into 4 groups: 1 week group (H1), 2 week group (H3), 3 week group (H3), and 4 week group (H4) (n = 12 in each group). The levels of STATsmRNA expression of the lung tissue were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot.