A retrospective comparison of induction chemoimmunotherapy versus chemotherapy followed by concurrent chemoradiotherapy and consolidation immunotherapy in stage III non-small cell lung cancer.

Background: Patients with locally advanced non-small cell lung cancer (LA-NSCLC) usually bear high tumor burden and are not tolerated well to concurrent chemoradiation therapy (CRT) followed by consolidation immunotherapy. We investigated the feasibility of chemoimmunotherapy as induction therapy before CRT for LA-NSCLC.

Methods: We retrospectively analyzed data from 91 patients with unresectable stage III NSCLC treated with either induction chemoimmunotherapy or chemotherapy before CRT.

CCL11/CCR3-dependent eosinophilia alleviates malignant pleural effusions and improves prognosis.

Malignant pleural effusion (MPE) is a common occurrence in advanced cancer and is often linked with a poor prognosis. Eosinophils were reported to involve in the development of MPE. However, the role of eosinophils in MPE remains unclear.

The CURB65 score predicted 180-day mortality of non-small cell lung carcinoma patients with immune checkpoint inhibitor-associated pneumonitis: A pilot retrospective analysis.

Introduction: The immune checkpoint inhibitor-associated pneumonitis (CIP) is a particularly worrisome and potentially lethal form of immune-related adverse events. An objective and evidence-based assessment tool for evaluating the severity of CIP is in urgent need. CURB65 (consciousness, urea nitrogen, respiratory rate, blood pressure, and age) is a potential candidate to meet the need.

Oxymatrine inhibits the pyroptosis in rat insulinoma cells by affecting nuclear factor kappa B and nuclear factor (erythroid-derived 2)-like 2 protein/heme oxygenase-1 pathways.

As the mechanism underlying glucose metabolism regulation by oxymatrine is unclear, this study investigated the effects of oxymatrine on pyroptosis in INS-1 cells. Flow cytometry was employed to examine cell pyroptosis and reactive oxygen species (ROS) production. Cell pyroptosis was also investigated via transmission electron microscopy and lactate dehydrogenase (LDH) release.

Downregulated long intergenic non-coding RNA 00,174 represses malignant biological behaviors of lung cancer cells by regulating microRNA-584-3p/ribosomal protein S24 axis.

The detailed regulatory mechanism of LINC00174 in lung cancer (LC) development remains largely unknown. This research was designed to probe into the impacts of LINC00174 in LC cells through modulating the microRNA (miR)-584-3p/ribosomal protein S24 (RPS24) axis. LINC00174, miR-584-3p, and RPS24 expression levels in LC cells and tissues were examined.

Circular RNA circ_0061140 accelerates hypoxia-induced glycolysis, migration, and invasion in lung adenocarcinoma through the microRNA-653/hexokinase 2 (HK2) axis.

Circular RNA (circRNA) is considered to be an essential regulator of multiple human malignancies. However, the role and molecular mechanism of circ_0061140 in lung adenocarcinoma ((LUAD) remain elusive. The levels of circ_0061140, microRNA (miR)-653 and hexokinase 2 (HK2) were examined by RT-qPCR.

Gap between risk factors and prevention strategies? A nationwide survey of fall prevention among medical and surgical patients.

Aims: This study aimed to determine the extent to which nurses report assessing evidence-based falls risk factors and implementing targeted prevention for medical and surgical patients in China.

Design: This study was a national online survey.

Methods: The respondents were registered nurses working in medical and surgical units in 662 Chinese hospitals.

Case Report: Tumor Microenvironment Characteristics in a Patient With HER2 Mutant Lung Squamous Cell Carcinoma Harboring High PD-L1 Expression Who Presented Hyperprogressive Disease.

Background: High PD-L1 expression in non-small cell lung cancer (NSCLC) is evident to predict elevated immunotherapy efficacy, to which NSCLC with onco-driver gene mutations is probed with poor responsiveness. Thus, it is of great interest to investigate how effective immune monotherapy is in the presence of concurrent high PD-L1 expression and driving gene mutation.

Patients And Methods: We present a case of squamous lung cancer with high PD-L1 expression and HER2 exon 20 insertion (20Ins) who presented hyperprogressive disease (HPD) after being treated with PD-1 inhibitor.

-Mutated Squamous Cell Lung Cancer and Its Association With Outcomes.

Background: The therapeutic efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in advanced -mutant lung squamous cell carcinoma (SCC) patients remains uncertain. Furthermore, the factors underlying the responsiveness have not been fully investigated. We therefore investigated the link between genomic profiles and EGFR-TKI efficacy.

The Application of Combined Immune Checkpoint Inhibitor Modalities in Previously Treated Non-Small Cell Lung Cancer Patients and the Associations Thereof With the Lung Immune Prognostic Index.

Background: Immune checkpoint inhibitor (ICI) monotherapy remains the standard of care for patients with previously treated non-small cell lung cancer. However, few reports have compared the clinical benefits of second-line ICIs alone with those of ICIs combined with other therapies, including anti-angiogenesis therapy or chemotherapy.

Methods: Patients with previously treated advanced non-small cell lung cancer who received ICIs were retrospectively reviewed.

Voltage-gated potassium channels are involved in oxymatrine-regulated islet function in rat islet β cells and INS-1 cells.

Objectives: Oxymatrine can regulate glucose metabolism. But the underlying mechanisms remain unclear. We investigated the relationship of oxymatrine and voltage-gated potassium (Kv) channel in rat islet β cells and INS-1 cells.

Induction of ferroptosis-like cell death of eosinophils exerts synergistic effects with glucocorticoids in allergic airway inflammation.

Introduction: Eosinophils are critical in allergic disorders, and promoting eosinophil death effectively attenuates allergic airway inflammation. Ferroptosis is a recently described novel form of cell death; however, little is known about ferroptosis in eosinophils and related diseases. This study aimed to investigate the effects of ferroptosis-inducing agents (FINs) on eosinophil death and allergic airway inflammation, and to explore their potential synergistic effect with glucocorticoids (GCs).

Homeostatic and early-recruited CD101 eosinophils suppress endotoxin-induced acute lung injury.

Introduction: Acute lung injury (ALI) is a fatal but undertreated condition with severe neutrophilic inflammation, although little is known about the functions of eosinophils in the pathogenesis of ALI. Our objectives were to investigate the roles and molecular mechanisms of eosinophils in ALI.

Methods: Pulmonary eosinophils were identified by flow cytometry.

Variation on the Microstructure and Mechanical Properties of Ti-Al-N Films Induced by RF-ICP Ion Source Enhanced Reactive Nitrogen Plasma Atmosphere.

Acquiring the optimum growth conditions of Ti-Al-N films, the effects of gas atmosphere, especially the reactive plasma on the material microstructures, and mechanical properties are still a fundamental and important issue. In this study, Ti-Al-N films are reactively deposited by radio frequency inductively coupled plasma ion source (RF-ICPIS) enhanced sputtering system. Different nitrogen gas flow rates in letting into the ion source are adopted to obtain nitrogen plasma densities and alter deposition atmosphere.

Author Correction: Eosinophil differentiation in the bone marrow is promoted by protein tyrosine phosphatase SHP2.

Since the publication of the article, the authors became aware that Figs. 1c, 5k and 6m contained errors in representative image and PAS score in control groups. The corrected Figs.

mTOR complexes differentially orchestrates eosinophil development in allergy.

Eosinophil infiltration is considered a hallmark in allergic airway inflammation, and the blockade of eosinophil differentiation may be an effective approach for treating eosinophil-related disorders. Mammalian target of rapamycin (mTOR) is a vital modulator in cell growth control and related diseases, and we have recently demonstrated that rapamycin can suppress eosinophil differentiation in allergic airway inflammation. Considering its critical role in haematopoiesis, we further investigated the role of mTOR in eosinophil differentiation in the context of asthmatic pathogenesis.

Bcl-2 inhibitors reduce steroid-insensitive airway inflammation.

Background: Asthmatic inflammation is dominated by accumulation of either eosinophils, neutrophils, or both in the airways. Disposal of these inflammatory cells is the key to disease control. Eosinophilic airway inflammation is responsive to corticosteroid treatment, whereas neutrophilic inflammation is resistant and increases the burden of global health care.

Role of macrophage colony-stimulating factor (M-CSF) in human granulosa cells.

Macrophage colony-stimulating factor (M-CSF) has been proved to have a positive role in the follicular development. We investigated its effect on human granulosa cells and found that M-CSF could stimulate the production of E. The production of FSH receptors was enhanced by M-CSF in vitro in a dose-dependent manner with or without the addition of tamoxifen (p <0.

Ozone-induced IL-17A and neutrophilic airway inflammation is orchestrated by the caspase-1-IL-1 cascade.

Ozone is a common environmental air pollutant leading to respiratory illness. The mechanisms regulating ozone-induced airway inflammation remain poorly understood. We hypothesize that ozone-triggered inflammasome activation and interleukin (IL)-1 production regulate neutrophilic airway inflammation through IL-17A.

Rapamycin inhibition of eosinophil differentiation attenuates allergic airway inflammation in mice.

Background And Objective: The mammalian target of rapamycin (mTOR) signalling pathway regulates immune responses, and promotes cell growth and differentiation. Inhibition of mTOR with rapamycin modulates allergic asthma, while the underlying molecular mechanisms remain elusive. Here, we demonstrate that rapamycin, effectively inhibits eosinophil differentiation, contributing to its overall protective role in allergic airway inflammation.

Tc17 cells are associated with cigarette smoke-induced lung inflammation and emphysema.

Background And Objective: Some types of T lymphocytes, especially cytotoxic T-cells (Tc1) and T-helper (Th17) cells, play a pivotal role in cigarette smoke-induced lung diseases. However, whether Tc17 cells are involved remains largely unknown. We investigated Tc17 involvement using a cigarette smoke-exposure model.

Nuclear erythroid 2 p45-related factor-2 Nrf2 ameliorates cigarette smoking-induced mucus overproduction in airway epithelium and mouse lungs.

Background And Objective: Nuclear erythroid 2 p45-related factor-2 (Nrf2) is known to play important roles in airway disorders, whereas little has been investigated about its direct role in airway mucus hypersecretion. The aim of this study is to determine whether this factor could protect pulmonary epithelium and mouse airway from cigarette-induced mucus overproduction.

Methods: Using genetic approaches, the role of Nrf2 on cigarette smoking extracts (CSE) induced MUC5AC expression was investigated in lung A549 cells.

Exogenous interleukin-17A inhibits eosinophil differentiation and alleviates allergic airway inflammation.

IL-17 is known to play important roles in immune and inflammatory disease, such as in asthma, but its functions in allergic airway inflammation are still controversial, and the molecular mechanisms mediating these functions remain unclear. Increased production of eosinophils in bone marrow and their emergence in the airway have been linked to the onset and progression of allergic asthma. In this study, we investigated the effects of exogenous IL-17 on allergic airway inflammation and explored the underlying molecular mechanisms through eosinophil generation.

Balance of apoptotic cell death and survival in allergic diseases.

Allergic diseases result from over-reaction of the immune system in response to exogenous allergens, where inflammatory cells have constantly extended longevity and contribute to an on-going immune response in allergic tissues. Here, we review disequilibrium in the death and survival of epithelial cells and inflammatory cells in the pathological processes of asthma, atopic dermatitis, and other allergic diseases.

Prevention of allergic airway hyperresponsiveness and remodeling in mice by Astragaliradix antiasthmatic decoction.

Background: Astragali radix Antiasthmatic Decoction (AAD), a traditional Chinese medication, is found effective in treating allergic diseases and chronic cough. The purpose of this study is to determine whether this medication could suppress allergen-induced airway hyperresponsiveness (AHR) and remodeling in mice, and its possible mechanisms.

Methods: A mouse model of chronic asthma was used to investigate the effects of AAD on the airway lesions.