Expression and pathological significance of CC chemokine receptor 7 and its ligands in the airway of asthmatic rats exposed to cigarette smoke.

Background: Cigarette smoking aggravates the symptoms of asthma, leading to the rapid decline of lung function. Dendritic cells (DCs) and lymphocytes are considered initiating and promoting factors for the airway inflammation reactions of asthma. In addition, activation of CC chemokine receptor 7 (CCR7) by chemokine (C-C motif) ligand (CCL) 19 and 21 promotes DCs and T cells migration to lymphoid tissues during inflammation.

[Cool/Hot target effect of the water fog infrared stealth].

Artificial spray fog will come into being cool target because of the strong evaporation and convection but weak radiation heat flux, when it is used for defence of infrared imaging guided missile. Also, when it is the contrary condition, the water fog will come into being hot target. In order to open out the phenomenon particularly, a math model which can account for the cool/hot effect produced by water fog shielding the thermal radiation is established by coupling the calculation of radiation transfer equation and energy conversation equation, based on the Mie theory.

Deficiency of ubiquitin A20 promotes antigen transport across airway epithelial cells via a transcellular pathway.

The epithelial barrier dysfunction is associated with the pathogenesis of a number of diseases. Ubiquitin E3 ligase A20 (A20) plays a critical role in maintaining the homeostasis in the body. This study aimed to investigate the role of A20 in the degradation of endocytic antigens in airway epithelial cells.

Expression and significance of myeloid differentiation factor 88 in marrow dendritic cells in asthmatic rats with cigarette smoke exposure.

Background: Smoking causes frequent asthma attacks, leading to a rapid decline in lung function in patients with asthma, and it can also reduce the therapeutic effect of glucocorticoids in patients with asthma. Therefore, the present study aimed to investigate the effect of cigarette smoke on the expression of myeloid differentiation factor 88 (MyD88) in marrow dendritic cells (DCs) in asthmatic rats, and to explore the molecular mechanism of cigarette smoke exposure on asthma by DCs.

Methods: Forty Wistar rats were randomly divided into the following groups: control, smoke exposure, asthma, and asthma combined with smoke exposure.

Cigarette smoke extract stimulates rat pulmonary artery smooth muscle cell proliferation via PKC-PDGFB signaling.

Accumulating evidence suggests a direct role for cigarette smoke in pulmonary vascular remodeling, which contributes to the development of pulmonary hypertension. However, the molecular mechanisms underlying this process remain poorly understood. Platelet-derived growth factor (PDGF) is a potential mitogen and chemoattractant implicated in several biological processes, including cell survival, proliferation, and migration.

Implication of PDGF signaling in cigarette smoke-induced pulmonary arterial hypertension in rat.

Pulmonary artery hypertension (PAH) is a severe disease characterized with progressive increase of pulmonary vascular resistance that finally causes right ventricular failure and premature death. Cigarette smoke (CS) is a major factor of Chronic Obstructive Pulmonary Disease (COPD) that can lead to PAH. However, the mechanism of CS-induced PAH is poorly understood.

[Monte-Carlo algorithm for phase function of medium scattering in radiative heat transfer].

Phase function of the compley distributed systems is the significant parameter in the field of radiative heat transfer in medium. The Monte-Carlo method has the advantages of both numerical algorithm and experiment measurement. Multiple scattering phase function of the complex distributed systems based on the Monte-Carlo method overcomes the former deficiency and expresses the influence of the multiple scattering, also, it can calculate phase functions of any controlled volume.

[Interaction of protein kinase C-extracellular signal-regulated kinase 1/2 signal pathway in the process of plasminogen activator inhibitor-1 expression induced by nicotine in human umbilical vein endothelial cells].

Objective: To explore the role of protein kinase C (PKC)- extracellular signal-regulated kinase (ERK)1/2 signal pathway in the process of plasminogen activator inhibitor-1 (PAI-1) protein and mRNA expression in cultured human umbilical vein endothelial cells (HUVECs) induced by nicotine.

Methods: HUVECs were cultured to examine the effect of nicotine on the expression of secreting PAI-1 in HUVECs on different experimental conditions. The expression of PAI-1 protein was measured by ELISA.

Effect of glucocorticoid on MIP-1α and NF-κB expressing in the lung of rats undergoing mechanical ventilation with a high tidal volume.

Background: Ventilator induced lung injury (VILI) is a serious complication in the treatment of mechanical ventilating patients, and it is also the main cause that results in exacerbation or death of patients. In this study, we produced VILI models by using glucocorticoid in rats with high tidal volume mechanical ventilation, and observed the content of macrophage inflammatory protein-1α (MIP-1α) in plasma and bronchoalveolar lavage fluid (BALF) and the expression of MIP-1α mRNA and nuclear factor-kappa B (NF-κB) p65 mRNA in the lung so as to explore the role of glucocorticoid in mechanical ventilation.

Methods: Thirty-two healthy Wistar rats were randomly divided into a control group, a ventilator induced lung injury (VILI) group, a dexamethasone (DEX) group and a budesonide (BUD) group.

[Study on the correctional method for the attenuation calculation of infrared radiation in the water fogs].

Water fogs system can mightily attenuate the infrared spectrum, so more and more attention has been paid to this problem in military. Based on the Mie theory, the collective characteristic of the particles forward scattering was analyzed. The near forward scattering ratio was defined, also the particle size and scattering DBC case were confirmed when the Lambert-Beer law was applied.

[Effect of cigarette smoke exposure on the percentage of CD(4)(+)CD(25)(+) regulatory T cells and the expression of transcription factor Foxp3 in asthmatic rats].

Objective: To investigate the effect of cigarette smoke exposure on the ratio of CD(4)(+)CD(25)(+) regulatory T cells (Treg) and expression of transcription factor Foxp3 in asthmatic rats.

Methods: Forty male Wistar rats were randomly divided into 4 groups (n = 10 for each group): a normal saline group, an aerosolized ovalbumin (OVA) exposure group, a cigarette smoke exposure group and a combined OVA and cigarette smoke exposure group. The rats were exposed to air or cigarette smoke and to normal saline or OVA aerosol for 8 weeks respectively.

[The effect of cigarette smoke on the expression of transforming growth factor-beta1 mRNA and collagen type III in airways of asthmatic rats].

Objective: To study the effect of cigarette smoke on the expression of transforming growth factor-beta l (TGF-beta1), and collagen type III in lung tissues, and therefore to investigate the mechanism of airway remodeling.

Methods: Thirty male Wistar rats were randomly divided into a control group, an asthmatic group and a cigarette smoke treated group, with 10 rats in each group. The expression level of TGF-beta1 mRNA was measured by reverse transcription polymerase chain reaction (RT-PCR) and collagen type III by immunohistochemistry.

[Role of neutrophil activation in ventilator induced lung injury].

Objective: To probe further the role of neutrophil activation in the lung injury induced by mechanical ventilation.

Methods: Thirty-two normal Wistar rats were randomly divided into four groups: control group, low tidal volume group, conventional tidal volume group, and high tidal volume group. The counts of white blood cell (WBC) and neutrophil in bronchoalveolar lavage fluid (BALF) were carried out.

Effects of angiotensin II receptor antagonist on expression of collagen III, collagen V, and transforming growth factor beta1 in the airway walls of sensitized rats.

Background: Repeated attacks of bronchial asthma lead to different degrees of airway remodeling, the mechanism of which is not yet clear. Some evidences indicate that it is related to the excessive expression of some growth promotion factors. Angiotensin II is a polypeptide that may be involved in airway remodeling.