Schultzrindom3255

The overexpression of ACE2 significantly inhibited PASMCs proliferation and migration. Moreover, the overexpressed ACE2 could significantly attenuate pulmonary hypertension, pulmonary vascular remodeling, and right ventricular hypertrophy in HPH rat model. CONCLUSIONS ACE2 is related to the formation of pulmonary vascular remodeling and pulmonary hypertension. Furthermore, it may prevent hypoxia-induced pulmonary hypertension by inhibiting the proliferation of PASMCs.The non-invasive management of clinically significant hemoptysis by bronchoscopy remains a therapeutic challenge. Various agents have been used endobronchially in order to control hemoptysis, such as cold saline, tranexamic acid, and epinephrine. This review summarizes all available data in that view, especially in resource limited settings, where more advanced means of controlling hemoptysis are not available.OBJECTIVE The aim of this study was to explore the relationship between serum MALAT1 level and clinical features of elderly patients with severe pneumonia and its impact on patients' survival. PATIENTS AND METHODS A total of 150 elderly patients with severe pneumonia were enrolled in this study. According to patients' prognosis, enrolled subjects were divided into two groups, including death group (n=63) and survival group (n=87). The clinical data and indicators of subjects were collected, and χ2 and t-tests were used for statistical analysis. MALAT1 expression in the serum of all subjects was examined through the qPCR assay. Meanwhile, the predictive value of MALAT1 for patient death was assessed by the receiver operating characteristic curve (ROC). RESULTS PT, APTT, DD, APACHE II scores, and MODS scores in death group were remarkably higher, while HB, HCT, TT, and PaO2/FiO2 were conversely lower than those in survival group (p less then 0.05). QRT-PCR results revealed significantly increased MALAT1 expression in death group when compared with survival group, especially in those patients with a history of smoking and COPD (p less then 0.05). In addition, ROC analysis confirmed the predictive value of MALAT1 for the prognosis of elderly patients with severe pneumonia. PX-12 concentration CONCLUSIONS MALAT1 is highly expressed in the serum of elderly patients with severe pneumonia. Furthermore, it may serve as a marker for the prediction of survival of these patients.OBJECTIVE To explore the expression and significance of miR-223 in mice with pulmonary fibrosis. MATERIALS AND METHODS The rats were separated into a control group (n=15), a sham operation group (n=15), and a model group (n=45) (which was then divided into a 3-day group, a 7-day group, and a 14-day group, with 15 rats in each group). The rat model of pulmonary fibrosis was established. The rats in the model group were injected with bleomycin solution, while those in the control group and sham operation group were given the same operation and injected with the same amount of normal saline. After observing the pulmonary function indexes of the rats on the 3rd, 7th and 14th days after modeling, the rats were sacrificed by cervical dislocation, the pulmonary inflammation and fibrosis of the rats were observed, and the HYP (hydroxyproline) content and miR-223 expression level were determined. Pearson correlation analysis was employed to analyze the correlation between miR-223 and HYP. RESULTS The pulmonary inflammHYP content (p less then 0.05). CONCLUSIONS MiR-572 targeted CDH1 to promote cell metastasis in WT by suppressing EMT.OBJECTIVE This study aims to investigate whether PM2.5 exposure is involved in the induction of alveolar epithelial cell apoptosis and the progression of emphysema in mice, and to further explore its specific molecular mechanism. MATERIALS AND METHODS A certain number of PM2.5 exposed mice and normal control mice were selected, and a lung resection operation was performed to collect the pulmonary tissue samples, which were then analyzed by hematoxylin and eosin (H&E) staining assay. Subsequently, the total protein in the pulmonary tissues of mice in PM2.5 exposure group and control group was extracted, and the p53 protein level was detected by Western blot. Meanwhile, in A549 cells, after treatment of different doses of PM2.5, the protein levels of p53, caspase3, and clv-caspase3 were examined by Western blot while the mRNA levels of p53, Siva-1, and clv-caspase3 were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), respectively. In addition, flow cytometry was carried out to measure the increased the expression of the clv-caspase3 protein, which was reversed by the knockdown of p53; however, simultaneous overexpression of Siva-1 could further increase the clv-caspase3 protein level. Additionally, flow cytometry also revealed that PM2.5 exposure induced apoptosis of alveolar epithelial cells, while the knockdown of p53 reduced that, which could be promoted by the overexpression of Siva-1. CONCLUSIONS PM2.5 exposure can promote the transcription of Siva-1 to induce apoptosis of alveolar epithelial cells and accelerate the progression of emphysema in mice by enhancing p53 protein expression.OBJECTIVE Acute lung disease is characterized by inflammation. This research aimed to investigate effect of trichostatin A (TSA) on microRNA-146a (miR-146a) and tumor necrosis factor α (TNF-α) in lipopolysaccharide (LPS)-induced alveolar macrophage injury model. MATERIALS AND METHODS Rat alveolar macrophage, NR8383, was cultured and induced using LPS to establish acute lung injury model in vitro level. Cell Counting Kit-8 (CCK-8) assay was used to determine cell viability of NR8383 cells. TSA was administrated to LPS-induced NR8383 cells. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay was utilized to evaluate TNF-α and miR-146a mRNA expression in LPS and/or TSA treated NR8383 cells. Enzyme-link immunosorbent assay (ELISA) was used to examine TNF-α levels. RESULTS This study selected 1 ng/ml and 10 ng/ml TSA as the optimal concentrations for treating NR8383 cells. LPS-induced acute lung injury model was successfully established. TSA administration significantly enhanced accounts of LPS-stimulated NR8383 cells. LPS induction significantly increased miR-146a mRNA expression in NR8383 cells compared to NR8383 cells (p less then 0.05). TSA administration significantly reduced the levels of TNF-α in LPS-induced NR8383 cells compared to those in LPS-induced NR8383 cells (p less then 0.05). TSA administration significantly enhanced miR-146a expression in LPS-induced NR8383 cells compared to that in LPS-induced NR8383 cells (p less then 0.05). CONCLUSIONS TSA administration exerted anti-inflammation functions in LPS-induced acute lung injury model in vitro, which might be triggered by inhibiting TNF-α molecule and upregulating miR-146a expression. The present data hint that TSA could be considered as a potential therapeutic agent for treating acute lung injury.OBJECTIVE Information on the long-term safety of electronic cigarettes (e-cig) is still limited. We report the results after six years of follow-up of the first observational study assessing e-cig long-term effectiveness and safety. PATIENTS AND METHODS Participants were adults who smoked ≥1 tobacco cigarette/day (tobacco smokers); or used any type of e-cig inhaling ≥50 puffs weekly (e-cig users); or used both (dual users). Participants were contacted directly or by phone and/or internet interviews. Hospital discharge abstract data and carbon monoxide level tests were also used. RESULTS Data were available for 228 e-cig users (all ex-smokers), 469 tobacco smokers, 215 dual users. A possibly smoking-related disease (PSRD) was recorded in 90 subjects (9.9%); 11 deceased (1.2%). No differences were observed across groups in PSRD rates, with minor changes in self-reported health. Among e-cig users, 64.0% remained tobacco abstinent. Dual users and tobacco smokers did not significantly differ in the rate of cessation of tobacco (38.6% vs. 33.9%, respectively) and all products (23.7% vs. 26.4%). A comparable decrease in daily cigarettes was also observed. 39.5% of the sample switched at least once (tobacco smokers 15.1%; dual users 83.3%). CONCLUSIONS After six years, no evidence of harm reduction was found among e-cig or dual users. The complete switch to e-cig might support tobacco quitters remain abstinent, but the use of e-cig in addition to tobacco did not improve smoking cessation or reduction.OBJECTIVE To explore the protective effect of remifentanil against myocardial ischemia-reperfusion injury (MIRI) in rats and its mechanism. MATERIALS AND METHODS The rat models of IRI were established and randomly divided into 1) sham-operation group (S group), 2) IRI rat model group (M group), 3) low-dose remifentanil group (R-L group), 4) moderate-dose remifentanil group (R-M group), and 5) high-dose remifentanil group (R-H group). The rats in R-L group, R-M group, and R-H group were administrated with remifentanil at 0.4 μg/kg/min, 2 μg/kg/min, and 10 μg/kg/min, respectively. The activity of creatine kinase-MB (CK-MB), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in myocardial cells was detected using the automatic biochemical analyzer, and the apoptosis rate of myocardial cells was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the messenger ribonucleic acid (mRNA) and protein levels of related cytokines in myocardial cells were determined through quantitative Polymerase Chain Reaction (qPCR) and Western blotting, and the content of interleukin-1β (IL-1Symbol ) and IL-18 in peripheral blood was detected via enzyme-linked immunosorbent assay (ELISA). RESULTS Remifentanil at different concentrations could protect myocardium from IRI, and remifentanil at 2 μg/kg/min and 10 μg/kg/min could significantly down-regulate the myocardial enzyme indexes in IRI myocardial cells (p less then 0.01). Besides, remifentanil reduced the mRNA expressions of IL-18, INF-γ, TNF-β, and IL-1β (p less then 0.01), significantly decreased the protein expression of IL-18, and raised the protein expression of IL-18BP, thereby improving myocardial pathological damage. CONCLUSIONS The protective mechanism of remifentanil on the myocardium of MIRI rats may be related to the inhibition on the IL-18 signaling pathway.OBJECTIVE To explore the specific mechanism of sevoflurane in alleviating cerebral ischemia-reperfusion injury (CIRI) in rats through the c-Jun N-terminal kinase (JNK) signaling pathway. MATERIALS AND METHODS A total of 60 male specific pathogen-free Sprague-Dawley rats were randomly divided into sham group (n=20), model group (n=20), and sevoflurane group (n=20). In the sevoflurane group, sevoflurane (2.5%) was inhaled for 60 min at 24 h before the blockage of cerebral blood supply. The CIRI model was established using the suture method in the model group and sevoflurane group, while the right common carotid artery and external carotid artery were separated and ligated only, without suture placement, in the sham group. At 24 h after reperfusion, the neurological deficit score in each group was calculated, the water content in brain tissues in each group was detected based on dry-wet weight ratio, the infarction volume of brain tissues in each group was detected via 2,3,5-triphenyltetrazolium chloride (TTC) staining, and the apoptosis rate of brain cells in each group was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.