First-Line Treatment Options for PD-L1-Negative Non-Small Cell Lung Cancer: A Bayesian Network Meta-Analysis.

Background: First-line treatment strategies for programmed death-ligand 1 (PD-L1) negative non-small cell lung cancer (NSCLC) patients include chemotherapy and combination with anti-angiogenesis drugs and/or immune checkpoint inhibitor. We conducted a Bayesian network meta-analysis to evaluate the efficacy of these therapeutic options.

Methods: We included phase III randomized controlled trials comparing two or more treatments in the first-line setting for NSCLC, including data in PD-L1-negative patients.

Resveratrol downregulates TNF-α-induced monocyte chemoattractant protein-1 in primary rat pulmonary artery endothelial cells by P38 mitogen-activated protein kinase signaling.

To evaluate the effects of resveratrol to monocyte chemoattractant protein-1 (MCP-1) and the role of p38 mitogen-activated protein kinase (MAPK) in this process in vitro. Animal acute pulmonary thromboembolism (PTE) model: rat model was established by infusion of an autologous blood clot into the pulmonary artery through a polyethylene catheter. One hundred and thirty-two rats were randomly and equally divided into ten groups: rats-control (untreated), rats-1% DMSO, rats-TNF-α, rats-TNF-α + resveratrol, rats-TNF-α +C1142, rats-TNF-α+SB203580, rats-TNF-α+resveratrol + SB203580, rats-resveratrol only, rats-C1142 only, and rats-SB203580 only.

Seawater inhalation induces acute lung injury via ROS generation and the endoplasmic reticulum stress pathway.

Seawater (SW) inhalation can induce acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In the present study, SW induced apoptosis of rat alveolar epithelial cells and histopathological alterations to lung tissue. Furthermore, SW administration increased generation of reactive oxygen species (ROS), whereas pretreatment with the ROS scavenger, N‑acetyl‑L‑cysteine (NAC), significantly decreased ROS generation, apoptosis and histopathological alterations.

MiR-23a-5p modulates mycobacterial survival and autophagy during mycobacterium tuberculosis infection through TLR2/MyD88/NF-κB pathway by targeting TLR2.

Autophagy plays a pivotal role in activating the antimicrobial host defense against Mycobacterium tuberculosis (M.tb.).

Suppressive effects of intrathecal paeoniflorin on bee venom-induced pain-related behaviors and spinal neuronal activation.

Recently, paeoniflorin (PF) administered systemically was found to have analgesic effects against inflammatory pain and hypersensitivity in a naloxone-reversible manner. In the present study, we adopted intrathecal administration to evaluate whether PF has direct antinociceptive actions at the spinal level. Pain-related behaviors and spinal c-Fos expression were induced by subcutaneous injection of bee venom (BV) into one hind paw of a rat.

Sodium tanshinone iia sulfonate attenuates seawater aspiration-induced acute pulmonary edema by up-regulating Na(+),K(+)-ATPase activity.

Relieving pulmonary edema is the key of a successful treatment to seawater drowning. Sodium tanshinone IIA sulfonate (STS) has been observed to reduce lung edema from lipopolysaccharide (LPS)-induced lung injury. In this study the authors investigated whether STS attenuates seawater aspiration-induced acute pulmonary edema, and examined the effects of sodium-potassium adensosine triphosphatase (Na(+),K(+)-ATPase) on it.

Tanshinone IIA attenuates seawater aspiration-induced lung injury by inhibiting macrophage migration inhibitory factor.

Inflammation takes responsibility for the seawater aspiration-induced lung injury. Tanshinone IIA (TIIA) can protect lipopolysaccharide-induced lung injury in mice through the inhibition of inflammation, but it is not reported whether TIIA have a protective effect on lung injury induced by seawater aspiration. Macrophage migration inhibitory factor (MIF) plays an important role in acute lung injury.

Tanshinone IIA suppresses lung injury and apoptosis, and modulates protein kinase B and extracellular signal-regulated protein kinase pathways in rats challenged with seawater exposure.

1. Tanshinone IIA (TIIA) is one of the main active components of the Chinese herb, Danshen. In the present study, we investigated the role of apoptosis in seawater exposure-induced acute lung injury (ALI), and explored the effects of TIIA on lung injury, apoptosis, and protein kinase B (Akt) and extracellular signal-regulated protein kinase (ERK) pathways in seawater-challenged rats.

[Joint application of 7 interventional pulmonology methods in early diagnosis of lung cancer].

Objective: To evaluate the combination of 7 interventional pulmonology methods in early diagnosis of lung cancer.

Methods: A total of 467 patients with thoracic and pulmonary lesions (include hilum pulmonis lymphadenectasis, mediastinal lymphadenectasis, pulmonary scobination, lump, lamellar infiltration, small amount of pleural fluid and pleural scobination) had negative results via exfoliative cytology, bacteriology and routine bronchoscopy. All these patients had ultrathin bronchoscopy with biopsy and brushing.

[Efficacy and safety of argon plasma coagulation in the treatment of obstructive tracheobronchial stenosis].

Objective: To evaluate the efficacy and safety of argon plasma coagulation (APC) in the treatment of large airway obstruction.

Methods: Totally 389 patients with treacheobronchial stenosis were treated with APC (ARCO3000 type) by bronchoscopy. The stenoses were caused by carcinomas (203 cases, 52.

[Effect of IL-4 on ABCG2 expression in human lung adenocarcinoma cell lines].

Aim: To investigate the effect of IL-4 on the expression of ABCG2 in lung adencarcinoma cell lines.

Methods: The ABCG2 mRNA and protein expression was determined by semi-quantitative RT-PCR and Western blot respectively.

Results: The ABCG2 mRNA and protein was detectable in lung adencarcinoma cell lines A549 and SPC-A-1.

[Exploration of serum endothelin-1 as a marker of early radiation lung injury].

Aim: To explore the possibility of endothelin-1(ET-1) as a serological marker of early diagnosis and progression of radiation induced lung injury.

Methods: One hundred and ninety female rats were randomly divided into control group (group C) and experimental groups, namely, radiation group (group R), fluvastatin treatment group (group Flu), retinoic acid treatment group (group Ra) and dexemethasone treatment group (group Dex). The chests of rats in experimental groups were exposed to radiation by linear accelerator after anesthesia.