H4K12 lactylation-regulated NLRP3 is involved in cigarette smoke-accelerated Alzheimer-like pathology through mTOR-regulated autophagy and activation of microglia.

Cigarette smoke (CS), an indoor environmental pollution, is an environmental risk factor for diverse neurological disorders. However, the neurotoxicological effects and mechanisms of CS on Alzheimer's disease (AD) progression remain unclear. We found that CS accelerated the progression of AD, including increasing β-amyloid (Aβ) plaque deposition and exacerbating cognitive decline.

A new pathogen pattern of acute respiratory tract infections in primary care after COVID-19 pandemic: a multi-center study in southern China.

Background: After the coronavirus disease 2019 (COVID-19) pandemic, no studies on bacterial and atypical pathogens were conducted in primary care. We aimed to describe the etiological composition of acute respiratory tract infections (ARTIs) presenting to primary care with limited resources after the pandemic.

Methods: 1958 adult patients with ARTIs from 17 primary care clinics were recruited prospectively from January 2024 to March 2024.

Construction of an adverse outcome pathway framework for arsenic-induced lung cancer using a network-based approach.

Environmental pollutants are considered as a cause of tumorigenesis, but approaches to assess their risk of causing tumors remain insufficient. As an alternative approach, the adverse outcome pathway (AOP) framework is used to assess the risk of tumors caused by environmental pollutants. Arsenic is a pollutant associated with lung cancer, but early assessment of lung cancer risk is lacking.

circADAMTS6 via stabilizing CAMK2A is involved in smoking-induced emphysema through driving M2 macrophage polarization.

Cigarette smoke (CS), an indoor environmental pollutant, is a prominent risk factor for emphysema, which is a pathological feature of chronic obstructive pulmonary disease (COPD). Emerging function of circRNAs in immune responses and disease progression shed new light to explore the pathogenesis of emphysema. In this research, we demonstrated, by single-cell RNA sequencing (scRNAseq), that the ratio of M2 macrophages were increased in lung tissues of humans and mice with smoking-related emphysema.

miR-21-Mediated Endothelial Senescence and Dysfunction Are Involved in Cigarette Smoke-Induced Pulmonary Hypertension through Activation of PI3K/AKT/mTOR Signaling.

Smoking is a pathogenic factor for pulmonary hypertension (PH). Our previous study showed that serum miR-21 levels are elevated in smokers. miR-21 is considered as engaged in the PH process; however, its mechanisms remain unclear.

Urea cycle promotion via ammonia-upregulated CPS1 is involved in arsenite-induced pulmonary fibrosis through enhancing collagen synthesis.

Arsenic exposure is connected with lung toxicity and is related to lung fibrotic changes. Idiopathic pulmonary fibrosis (IPF) is characterized by extracellular matrix (ECM) deposition. Various genetic mechanisms and environmental factors induce or exacerbate pulmonary fibrosis.

Stenotrophomonas maltophilia contributes to smoking-related emphysema through IRF1-triggered PANoptosis of alveolar epithelial cells.

Cigarette smoke (CS), the main source of indoor air pollution and the primary risk factor for respiratory diseases, contains chemicals that can perturb microbiota through antibiotic effects. Although smoking induces a disturbance of microbiota in the lower respiratory tract, whether and how it contributes to initiation or promotion of emphysema are not well clarified. Here, we demonstrated an aberrant microbiome in lung tissue of patients with smoking-related COPD.

NSUN2 promotes lung adenocarcinoma progression through stabilizing PIK3R2 mRNA in an mC-dependent manner.

It is well known that 5-methylcytosine (mC) is involved in variety of crucial biological processes in cancers. However, its biological roles in lung adenocarcinoma (LAUD) remain to be determined. The LUAD samples were used to assess the clinical value of NOP2/Sun RNA Methyltransferase 2 (NSUN2).

Novel calcaneal plate versus traditional philos plate for treating split fractures of humeral greater tuberosity.

Purpose: To compare the effect of two internal fixation methods of calcaneal plate fixation and Philos plate fixation in treating split fractures of humeral greater tuberosity.

Patients And Methods: A total of 37 patients with split fractures of humeral greater tuberosity were retrospectively analyzed from September 2016 to April 2021. Enrolled patients were divided into Group A (calcaneal anatomical locking plates), and Group B [Proximal Humeral Internal Locking System (PHILOS)].

miR-153-3p via PIK3R1 Is Involved in Cigarette Smoke-Induced Neurotoxicity in the Brain.

Cigarettes contain various chemicals that cause damage to nerve cells. Exposure to cigarette smoke (CS) causes insulin resistance (IR) in nerve cells. However, the mechanisms for a disorder in the cigarette-induced insulin signaling pathway and in neurotoxicity remain unclear.

Construction of an adverse outcome pathway framework based on integrated data to evaluate arsenic-induced non-alcoholic fatty liver disease.

Arsenic is a recognized environmental pollutant naturally occurring in aquifers through geological processes. Toxicological studies have revealed that liver is the main target organ harmed by arsenic exposure. However, systematic studies of non-alcoholic fatty liver disease (NAFLD) are not comprehensive, and information regarding threats and risk assessment remains insufficient.

The lncRNA H19/miR-29a-3p/SNIP1/c-myc regulatory axis is involved in pulmonary fibrosis induced by Nd2O3.

Some rare earth elements are occupational and environmental toxicants and can cause organ and systemic damage; therefore, they have attracted global attention. Neodymium oxide (Nd2O3) is a rare earth element that is refined and significantly utilized in China. The long noncoding RNA (lncRNA) H19 is encoded by the H19/IGF2 imprinted gene cluster located on human chromosome 11p15.

Retraction Notice to: METTL3-mediated mA modification of ZBTB4 mRNA is involved in the smoking-induced EMT in cancer of the lung.

[This retracts the article DOI: 10.1016/j.omtn.

Smoking-Induced M2-TAMs, via circEML4 in EVs, Promote the Progression of NSCLC through ALKBH5-Regulated m6A Modification of SOCS2 in NSCLC Cells.

Lung cancer is a commonly diagnosed disease worldwide, with non-small cell lung cancers (NSCLCs) accounting for ≈ 85% of cases. Cigarette smoke is an environmental exposure promoting progression of NSCLC, but its role is poorly understood. This study reports that smoking-induced accumulation of M2-type tumor-associated macrophages (M2-TAMs) surrounding NSCLC tissues promotes malignancy.

Cigarette smoking, by accelerating the cell cycle, promotes the progression of non-small cell lung cancer through an HIF-1α-METTL3-mA/CDK2AP2 axis.

Cigarette smoking killed about 8 million people every year and promoted non-small cell lung cancer (NSCLC). We investigated the molecular mechanism of smoking-promoted NSCLC progression. Relative to non-smokers, NSCLC patients who were smokers had a higher tumor malignancy.

[Double-column Die-punch fractures of distal radius treated with butterfly plate fixation via Henry approach].

Objective: To explore clinical effect of open reduction and internal fixation with Henry's approach butterfly plate in treating double-column Die-punch fractures of distal radius.

Methods: From January 2018 to June 2021, 26 patients with double-column Die-column distal radius were treated with open reduction and internal fixation through Henry's surgical approach and using distal radius volar column plate(butterfly plate), including 14 males and 12 females, aged from 20 to 75 years old with an average age of (44.2±3.

N6-Methyladenosine-modified circSAV1 triggers ferroptosis in COPD through recruiting YTHDF1 to facilitate the translation of IREB2.

Epithelial cell damage-initiated chronic obstructive pulmonary disease (COPD) is implicated in regulated cell death (RCD) including ferroptosis triggered by complex gene-environment interactions. Our data showed that iron overload and ferroptosis are associated with COPD progression in COPD patients and in experimental COPD. Furthermore, we found that, in lung tissues of COPD patients, circSAV1 was associated with COPD progression by circRNA-seq screening.

LncRNA H19 via miR-29a-3p is involved in lung inflammation and pulmonary fibrosis induced by neodymium oxide.

The occupational and environmental health safety of rare earths has attracted considerable attention. In China, the rare earth neodymium oxide (NdO) is extensively refined and utilized. However, the mechanisms of NdO-induced lung injury are elusive.

As3MT-mediated SAM consumption, which inhibits the methylation of histones and LINE1, is involved in arsenic-induced male reproductive damage.

Studies have demonstrated that arsenic (As) induces male reproductive injury, however, the mechanism remains unknown. The high levels of arsenic (3) methyltransferase (As3MT) promote As-induced male reproductive toxicity. For As-exposed mice, the germ cells in seminiferous tubules and sperm quality were reduced.

Treatment and surveillance for non-muscle-invasive bladder cancer: a clinical practice guideline (2021 edition).

Non-muscle invasive bladder cancer (NMIBC) is a major type of bladder cancer with a high incidence worldwide, resulting in a great disease burden. Treatment and surveillance are the most important part of NIMBC management. In 2018, we issued "Treatment and surveillance for non-muscle-invasive bladder cancer in China: an evidence-based clinical practice guideline".

The Efficacy and Safety of Transurethral 2 μm Laser Bladder Lesion Mucosal En Bloc Resection in the Treatment of Cystitis Glandularis.

Objective: To study the safety and feasibility of transurethral bladder lesion mucosal en bloc resection with 2 μm laser for cystitis glandularis.

Methods: From July 2018 to July 2019, 58 patients with cystitis glandularis received surgical treatment were selected. All patients in this study were randomly divided into experimental group (transurethral 2 μm laser bladder lesion mucosal en bloc resection) and control group (traditional transurethral resection of bladder lesion mucosal).

CircRNA_0026344 via miR-21 is involved in cigarette smoke-induced autophagy and apoptosis of alveolar epithelial cells in emphysema.

Cigarette smoke (CS), a main source of indoor air pollution, is a primary risk factor for emphysema, and aberrant cellular autophagy is related to the pathogenesis of emphysema. Circular RNAs (circRNAs) affect the expression of mRNAs via acting as microRNA (miRNA) sponges, but their role in emphysema progression is not established. In the present investigation, CS, acting on alveolar epithelial cells, caused higher levels of miR-21, p-ERK, and cleaved-caspase 3 and led to lower levels of circRNA_0026344 and PTEN, which induced autophagy and apoptosis.

The aberrant cross-talk of epithelium-macrophages via METTL3-regulated extracellular vesicle miR-93 in smoking-induced emphysema.

Cigarette smoke (CS), a complex chemical indoor air pollutant, induces degradation of elastin, resulting in emphysema. Aberrant cross-talk between macrophages and bronchial epithelial cells is essential for the degradation of elastin that contributes to emphysema, in which extracellular vesicles (EVs) play a critical role. The formation of N6-methyladenosine (m6A) is a modification in miRNA processing, but its role in the development of emphysema remains unclear.

METTL3-mediated mA modification of ZBTB4 mRNA is involved in the smoking-induced EMT in cancer of the lung.

N6-methyladenosine (mA) is an epigenetic modification associated with various tumors, but its role in tumorigenesis remains unexplored. Here, as confirmed by methylated RNA immunoprecipitation sequencing (meRIP-seq) and RNA sequencing (RNA-seq) analyses, exposure of human bronchial epithelial (HBE) cells to cigarette smoke extract (CSE) caused an mA modification in the 3' UTR of ZBTB4, a transcriptional repressor. For these cells, CSE also elevated methyltransferase-like 3 (METTL3) levels, which increased the mA modification of ZBTB4.

miR-21-regulated M2 polarization of macrophage is involved in arsenicosis-induced hepatic fibrosis through the activation of hepatic stellate cells.

Arsenicosis induced by chronic exposure to arsenic is recognized as one of the main damaging effects on public health. Exposure to arsenic can cause hepatic fibrosis, but the molecular mechanisms by which this occurs are complex and elusive. It is not known if miRNAs are involved in arsenic-induced liver fibrosis.