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PubMed Journals Articles About "Airway Conditioning Acute Lung Injury" RSS

07:02 EST 14th December 2018 | BioPortfolio

Airway Conditioning Acute Lung Injury PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Airway Conditioning Acute Lung Injury articles that have been published worldwide.

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Showing "Airway Conditioning Acute Lung Injury" PubMed Articles 1–25 of 15,000+

Apelin-13 Administration Protects Against LPS-Induced Acute Lung Injury by Inhibiting NF-κB Pathway and NLRP3 Inflammasome Activation.

Acute lung injury (ALI) is induced by a variety of external and internal factors and leads to acute progressive respiratory failure. Previous studies have shown that apelin-13 can decrease the acute lung injury induced by LPS, but the specific mechanism is unclear. Therefore, a mouse lung injury model and a cell model were designed to explore the mechanism of how apelin-13 alleviates the acute lung injury caused by LPS.


LL-37 and its analog FF/CAP18 attenuate neutrophil migration in sepsis-induced acute lung injury.

Sepsis can result in acute lung injury. LL-37 is a small cationic host defense peptide involved in anti-inflammatory. In the current study, it was hypothesized that antimicrobial peptide LL-37 could play a protective role in attenuating the progression of sepsis-induced acute lung injury.

Calpain inhibition ameliorates scald burn-induced acute lung injury in rats.

The molecular pattern of severe burn-induced acute lung injury, characterized by cell structure damage and leukocyte infiltration, remains unknown. This study aimed to determine whether calpain, a protease involved in both processes, mediates severe burn-induced acute lung injury.


CRTH2 antagonist, CT‑133, effectively alleviates cigarette smoke-induced acute lung injury.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), characterized by overwhelming lung inflammation, are associated with high mortality. Cigarette smoke (CS) is one of the major causes of ALI/ARDS. Since high expression of prostaglandin (PG) D has been observed in CS-induced lung injury. Currently, no effective pharmacological therapies are available to treat ALI, and supportive therapies remain the mainstay of treatment. Therefore, we investigated the protective effect of CT‑133, a ne...

Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice.

Environmental air pollutants including ozone cause severe lung injury and aggravate respiratory diseases such as asthma and COPD. Here we compared the effect of ozone on respiratory epithelium injury, inflammation, hyperreactivity and airway remodeling in mice upon acute (1ppm, 1 h) and chronic exposure (1.5ppm, 2 h, twice weekly for 6 weeks). Acute ozone exposure caused respiratory epithelial disruption with protein leak and neutrophil recruitment in the broncho-alveolar space, leading to lung inflamma...

The Emerging Role of Neutrophils in Repair after Acute Lung Injury.

Neutrophils are key players in acute lung injury. Once recruited from the circulation, these cells release cytotoxic molecules that lead to tissue disruption, so their blockade has been advocated to prevent lung damage. However, lung injury also occurs during neutropenia, and usually involves a very poor outcome. There is emerging evidence that neutrophils not only contribute to that early damage, but also orchestrate later repair. Neutrophils promote epithelial proliferation and are a source of proteases, ...

Ulinastatin protects rats from sepsis-induced acute lung injury by suppressing the JAK-STAT3 pathway.

Sepsis is usually accompanied by pulmonary inflammations, leading to acute lung injury. During this process, endogenous factors that play a regulatory role could be exploited to therapeutically alleviate such lethal tissue injury. Here, we showed that ulinastatin (UTI) administration could reduce lung tissue necrosis and swelling during sepsis in rats. UTI treatment also decreased the levels of inflammatory mediators both in the lung and in the serum. Mechanistically, we showed that the phosphorylation leve...

G-CSF mediates lung injury in mice with adenine-induced acute kidney injury.

Acute lung injury (ALI) is a serious complication among patients with acute kidney injury (AKI) that is a systemic inflammatory disease with high morbidity and mortality. The pathophysiology of AKI-associated ALI is poorly understood. G-CSF regulates the production and function of neutrophils that mediate lung injury via elastase and other mediators. Here, we used a mouse model of adenine-induced AKI to determine the roles of G-CSF and neutrophil elastase in AKI-associated ALI. We confirmed that ALI was ass...

Telocytes promote VEGF expression and alleviate ventilator-induced lung injury in mice.

Mechanical ventilation (MV) is an important procedure for the treatment of patients with acute lung injury or acute respiratory distress syndrome in a clinical setting; however, MV can lead to severe complications, including ventilator-induced lung injury (VILI). Telocytes (TCs) can promote tissue repair following injury in the heart, kidneys, and other organs. The aim of this study was to investigate the role of TCs in VILI in mice and the associated mechanisms. By using in vivo studies in mice and in vitr...

Cordycepin alleviates lipopolysaccharide-induced acute lung injury via Nrf2/HO-1 pathway.

The present study is to investigate the protective effect of cordycepin on inflammatory reactions in rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS), as well as the underlying mechanism.

Frontline Science: Pathological conditioning of human neutrophils recruited to the airway milieu in cystic fibrosis.

Recruitment of neutrophils to the airways, and their pathological conditioning therein, drive tissue damage and coincide with the loss of lung function in patients with cystic fibrosis (CF). So far, these key processes have not been adequately recapitulated in models, hampering drug development. Here, we hypothesized that the migration of naïve blood neutrophils into CF airway fluid in vitro would induce similar functional adaptation to that observed in vivo, and provide a model to identify new therapies.

Artificial neural network algorithm model as powerful tool to predict acute lung injury following to severe acute pancreatitis.

The aim of this study is to predict the risk of severe acute pancreatitis (SAP) associated with acute lung injury (ALI) by artificial neural networks (ANNs) model.

Characterization of the seven-day course of pulmonary response following unilateral lung acid injury in rats.

Aspiration of gastric acid is an important cause of acute lung injury. The time course of the pulmonary response to such an insult beyond the initial 48 hours is incompletely characterized. The purpose of this study was to comprehensively describe the pulmonary effects of focal lung acid injury over a seven day period in both directly injured and not directly injured lung tissue.

Syndecan-2-positive, Bone Marrow-derived Human Mesenchymal Stromal Cells Attenuate Bacterial-induced Acute Lung Injury and Enhance Resolution of Ventilator-induced Lung Injury in Rats.

WHAT THIS ARTICLE TELLS US THAT IS NEW: BACKGROUND:: Human mesenchymal stromal cells demonstrate promise for acute respiratory distress syndrome, but current studies use highly heterogenous cell populations. We hypothesized that a syndecan 2 (CD362)-expressing human mesenchymal stromal cell subpopulation would attenuate Escherichia coli-induced lung injury and enhance resolution after ventilator-induced lung injury.

Preventive effects of ketone ester BD-AcAc on central nervous system oxygen toxicity and concomitant acute lung injury.

Recent studies indicated that ketone ester R,S-1,3-butanediol acetoacetate diester (BD-AcAc) may be effective in preventing central nervous system oxygen toxicity (CNS-OT) and concomitant acute lung injury, a serious medical problem to be faced when breathing hyperbaric oxygen (HBO). This study aimed to further investigate the protective effects of BD-AcAc against CNS-OT and concomitant acute lung injury (ALI) in mice.

Protective effects of VGX-1027 in PM-induced airway inflammation and bronchial hyperresponsiveness.

Fine particulate matter (PM) can penetrate into alveolar spaces and induce airway inflammation. Recent evidence suggests that the activation of Toll-like receptor 4 (TLR4) signaling may participate in PM-induced acute lung injury. We investigated the effect of VGX-1027, a TLR4 blocker, on PM-induced airway inflammation and bronchial hyperresponsiveness (BHR) in a murine model in vivo and on inflammatory mechanisms in vitro in human airway epithelial cells. Mice were injected intraperitoneally with vehicle (...

Vitamin D to Prevent Lung Injury Following Esophagectomy-A Randomized, Placebo-Controlled Trial.

Observational studies suggest an association between vitamin D deficiency and adverse outcomes of critical illness and identify it as a potential risk factor for the development of lung injury. To determine whether preoperative administration of oral high-dose cholecalciferol ameliorates early acute lung injury postoperatively in adults undergoing elective esophagectomy.

Hydrogen sulfide ameliorated lipopolysaccharide-induced acute lung injury by inhibiting autophagy through PI3K/Akt/mTOR pathway in mice.

Recent studies reported that hydrogen sulfide (HS) is an effective agent for the prevention and treatment of acute lung injury (ALI). But the underlying mechanisms have not been understood clearly. In this study, we explored the possible mechanism from the perspective of autophagy regulation.

3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation.

The increase in inflammatory cytokines and chemokines is a common denominator in the pathogenesis of acute lung injury (ALI) which are involved in the influx of inflammatory cells and lung damage. The aim of the present study was to evaluate the protective effect of 3,4,5-trihydroxycinnamic acid (THC) in lipopolysaccharide (LPS)-induced ALI. THC efficiently decreased the mRNA expression of interleukin-8 (IL-8) in LPS-stimulated A549 airway epithelial cells. THC induced heme oxygenase-1 (HO-1) expression in ...

MicroRNA-494 inhibition alleviates acute lung injury through Nrf2 signaling pathway via NQO1 in sepsis-associated acute respiratory distress syndrome.

Although therapeutic strategies for acute respiratory distress syndrome (ARDS) have achieved improvements, its mortality remains high. It has been reported that microRNAs (miRs) serve as therapeutic strategies for ARDS, while specific mechanisms of miR-494 remain poorly understood. Thus, the present study aimed to assess the effects of miR-494 on acute lung injury (ALI) in rat models of sepsis-associated ARDS and its regulatory mechanism.

Continuous Negative Abdominal Pressure Reduces Ventilator-induced Lung Injury in a Porcine Model.

In supine patients with acute respiratory distress syndrome, the lung typically partitions into regions of dorsal atelectasis and ventral aeration ("baby lung"). Positive airway pressure is often used to recruit atelectasis, but often overinflates ventral (already aerated) regions. A novel approach to selective recruitment of dorsal atelectasis is by "continuous negative abdominal pressure."

Impact of ketamine intervention for acute lung injury on RAGE and TLR9.

The purpose of this study was to explore the benefits of ketamine intervention for acute lung injury (ALI) and its effects on the receptor for advanced glycation end-product (RAGE) and toll-like receptor 9 (TLR9).

Hydrogen-Rich Saline Attenuates Acute Lung Injury Induced by Limb Ischemia/Reperfusion via Down-Regulating Chemerin and NLRP3 In Rats.

Limb ischemia/reperfusion (LI/R) injury is associated with high morbidity and mortality. The hypothesis of this study is that hydrogen-rich solution could attenuateacute lung injury and improve mortality via chemerin and NLRP3 after LI/R in rats. A rat model of LI/R was performed by clamping the bilateral femoral arteries for 3 h followed by reperfusion. HRS was administered intraperitoneally (10 mL/kg or 2.5 mL/kg) when the atraumatic micro clips were released. The rats were euthanized at 2 h after...

Nrf2 Regulates the Hepatoprotective Effects of Remote Ischemic Conditioning in Hemorrhagic Shock.

Remote ischemic conditioning (RIC) protects against organ ischemia/reperfusion injury in experimental and clinical settings. We have demonstrated that RIC prevents liver and lung inflammation/injury following hemorrhagic shock/resuscitation (S/R). In the current study, we used a murine model of S/R to investigate the role of Nrf2 in mediating hepatoprotection.

Design, synthesis, and structure-activity relationships of 2-benzylidene-1-indanone derivatives as anti-inflammatory agents for treatment of acute lung injury.

The purpose of this study was to design and synthesize novel 2-benzylidene-1-indanone derivatives for treatment of acute lung injury.


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