Acute respiratory distress syndrome (ARDS) is one of the diseases with a significant mortality rate due to respiratory failure. Yet, malignant microenvironment (MM) composed mainly of inflammatory cytokines (IC) and reactive oxygen species (ROS) limit the therapeutic effect. Herein we construct the nanoparticles (NPs) BSA-MnO2 @Tan-IIA/PSLs (BMTPLs) to disrupt the vicious cycle between IC and ROS by suppressing IC production and scavenging ROS, which effectively remodels the MM of ARDS. The BMTPLs composed of the water-dispersible BSA-MnO2 (BM) and phosphatidylserine (PS)-consisting lipid shell containing lipophilic tanshinone IIA (Tan-IIA). After phagocytosed by activated macrophages (M1) in an efferocytosis-like manner originating from the PS effect, the released Tan-IIA inhibit NF-kappa B pathway and further suppresses the secretion of IC. Concurrently, BM scavenging ROS alleviates the oxidative stress microenvironment, which deeply enhances the anti-inflammation effect of Tan-IIA. Moreover, the low-level ROS and down-regulation IC promote the transformation from pro-inflammatory M1 to anti-inflammatory M2 contributing to restoring tissue homeostasis. The results in vitro and in vivo indicate that the MM of ARDS can be effectively remodeled by BMTPLs, which holds great potential for ARDS treatment. (c) 2026 Published by Elsevier B.V. on behalf of Chinese Chemical Society and Institute of Materia Medica, Chinese Academy of Medical Sciences.

Background: Patients with coexisting lung cancer and COPD are highly susceptible to unplanned readmissions. This study aimed to develop and internally validate a robust predictive nomogram based on the "inflammation-nutrition-tumor" framework to quantify this risk. Methods: A retrospective cohort of 207 clinical episodes from male patients with lung cancer and COPD was analyzed. Participants were categorized into Planned Readmission (PR, n = 165) and Unplanned Readmission (UR, n = 42) groups. Independent risk factors were identified via univariate and multivariable analyses using Generalized Estimating Equations (GEE). A nomogram was subsequently constructed, and its performance was rigorously evaluated using the Area Under the Curve (AUC), calibration plots, and Decision Curve Analysis (DCA). Results: Multivariable GEE analysis demonstrated that the Systemic Immune-Inflammation Index (SII) was a highly significant independent risk factor (OR for a 500-unit increase = 1.490, 95% CI: 1.234-1.798, p < 0.001). Advanced cancer stage (III-IV) was also a significant predictor (OR = 3.590, 95% CI: 1.301-9.909, p = 0.014), while prealbumin (OR = 0.950, 95% CI: 0.896-1.007, p = 0.087) was identified as a key nutritional predictor. The integrated four-variable nomogram (age, cancer stage, SII, prealbumin) demonstrated good discriminative ability with an AUC of 0.809 (95% CI: 0.733-0.885). The calibration plot indicated excellent agreement, and DCA confirmed a substantial clinical net benefit. Conclusions: This SII-based nomogram provides a reliable and practical tool for individualized risk stratification, facilitating targeted clinical interventions to mitigate unplanned readmission rates in this vulnerable population.

BackgroundUltrasonographic diagnosis of thyroid diseases has traditionally relied on changes in thyroid echogenicity, which may appear relatively late in the disease course. This study aims to explore an early diagnosis for thyroid diseases before clinical symptoms occur by investigating the surrounding lymph nodes.MethodsThis study used a combined case-control and prospective design. Initially, a retrospective review was performed on patients who underwent thyroid ultrasound examination and autoantibody testing at our hospital between February 2024 and July 2025. Patients were divided into four groups based on serological results. Ultrasonographic parameters were recorded for each group. Intergroup data comparison was performed using chi-square test and correlation analysis was conducted. Ultimately, the diagnostic efficacy of lymph node manifestations in each group was analyzed among 100 randomly selected patients with abnormal thyroid echogenicity, and a receiver operating characteristic (ROC) curve was plotted.ResultsThe prospective analysis revealed that the area under the ROC curve (AUC) for diagnosing Hashimoto’s antibody positivity using ultrasound detection of prelaryngeal, left paratracheal, and right paratracheal lymph nodes were 0.904, 0.845, and 0.829, respectively. When combining all three lymph node sites, the AUC reached 0.887, indicating high diagnostic accuracy, particularly for prelaryngeal lymph node assessment.ConclusionsUltrasonographic imaging of lymph nodes surrounding the thyroid gland is significantly associated with the presence of Hashimoto’s thyroiditis-specific autoantibodies. These findings suggest that perithyroidal lymph node features may serve as valuable imaging markers for predicting autoimmune thyroid disorders, particularly Hashimoto’s thyroiditis.

Background: Environmental pollutants, such as perfluoroalkyl substances (PFASs), have been implicated in various human diseases. Despite growing evidence from observational studies linking PFASs to type 2 diabetes (T2D), results have been inconsistent. This study aims to investigate the relationships between PFASs exposure and the onset of T2D and its complications, and to elucidate the underlying molecular mechanisms. Methods: Mendelian randomization (MR) analysis was conducted to evaluate the relationships between PFASs exposure and the onset of T2D and its complications. PFASs data were sourced from the GWAS Catalog, while T2D and its complications data were retrieved from the FinnGen database. Network toxicology was utilized to investigate the potential molecular mechanisms underlying the significant associations between compounds and diseases. Molecular docking and molecular dynamics simulations were employed to verify the binding stability between the compounds and their core target genes. Results: PFOS exhibited a statistically significant positive association with the risk of diabetic retinopathy (DR) (P < 0.05, OR > 1). 200 intersection targets were obtained, among which EGFR, ESR1, and MMP9 were identified as core targets. Molecular docking and molecular dynamics simulations indicated that PFOS had strong binding affinity with these core targets. Additionally, PFOS might influence DR by mainly modulating the FoxO signaling pathway. Conclusions: PFOS is significantly associated with DR. EGFR, ESR1, and MMP9 have been identified as core targets associated with DR. These findings may elucidate the mechanisms by which environmental pollutants contribute to the development of DR.

BACKGROUND:While perfluoroalkyl substances (PFASs) exposure has been associated with autoimmune diseases (ADs), the robustness of these associations remains uncertain due to potential confounding and reverse causation in observational studies. This study aims to explore the potential relationship and underlying mechanisms between PFASs exposure and ADs risk. METHODS:We utilized Mendelian randomization (MR) and generalized summary-data-based MR (GSMR) to investigate potential associations between exposure to two major PFASs (perfluorooctanoic acid [PFOA] and perfluorooctanesulfonic acid [PFOS]) and the risk of ten ADs, using genetic data exclusively from European-ancestry populations. For significant associations, we subsequently conducted network toxicology analysis, applied machine learning algorithms to systematically screen and prioritize key genes, and assessed immune infiltration analysis to elucidate mechanisms. We then validated these findings through molecular docking and molecular dynamics simulations. RESULTS:MR and GSMR analyses demonstrated a significant association between PFOS exposure and an increased risk of multiple sclerosis (MS). Among 107 intersecting candidate genes, four genes (CASP3, STAT3, ESR1, and GSK3B) were identified as key target genes through machine learning. Molecular docking and molecular dynamics simulations further confirmed stable binding interactions between PFOS and these proteins. Additionally, immune infiltration analysis suggested these genes may contribute to immune microenvironment dysregulation in MS. Pathway analysis indicated that PFOS potentially influences MS pathogenesis through PPAR signaling and efferocytosis. CONCLUSIONS:Our integrated analysis reveals evidence supporting an association between PFOS and MS and uncovers underlying molecular mechanisms. These findings establish a foundation for further investigation into the role of environmental pollutants in autoimmune disorders.

BackgroundIn acute respiratory distress syndrome (ARDS), neutrophils, as the primary effector immune cells, undergo profound transcriptional and phenotypic reprogramming in response to complex inflammatory stimuli, modulating signal transduction and immune responses. Liquid-liquid phase separation (LLPS) plays a pivotal role in transcriptional dynamics and signal transduction, critically influencing gene expression stability. However, the mechanistic and clinical implications of LLPS in ARDS progression remain elusive.Materials and methodsThis study systematically characterized neutrophil LLPS in ARDS through integrated single-cell transcriptomes (GSE157789), proteomes (GSE32707/GSE76293), and clinical cohorts date. LLPS-associated genes (LCGs) were screened from the PhaSepDB 2.1 database and subsequently integrated with single-cell sequencing data from Gene Expression Omnibus (GEO) to quantify neutrophil LLPS scores and divide patient stratification into high and low LLPS groups for differential expression analysis of critical LCGs and associated pathways. Phase-separated droplets were then isolated from peripheral blood neutrophils of ARDS patients and N-formylmethionyl-leucyl-phenylalanine (fMLP) -stimulated neutrophils, followed by proteomic identification of droplet-associated proteins and candidate gene selection through GEO data analysis. The prognostic value of LLPS scores and candidate genes was subsequently validated in clinical cohorts, while the relationship between phase separation of candidate genes and cellular function was experimentally confirmed through immunofluorescence, Western blotting, and complementary functional assays.ResultsNeutrophils in ARDS exhibit elevated LLPS scores (p<0.05), with differentially expressed LCGs enriched in RhoA/ROCK-mediated cell polarization and migration pathways. Multi-omics integration identified MYL12A as a core phase-separation regulator, whose protein levels in phase-separated droplets positively correlated with oxygenation index (r=0.9536, p=0.0119) but inversely with SOFA scores (r=-0.8896, p=0.0433). Patients with high LLPS scores demonstrated significantly improved overall survival (p=0.046), suggesting a protective role of LLPS in ARDS pathogenesis. Mechanistically, the chemoattractant fMLP triggers reversible MYL12A phase separation via phosphorylation at Ser19, thereby potentiating neutrophil migratory capacity.ConclusionsThis study demonstrates that LLPS dynamically regulates neutrophil migration through MYL12A phosphorylation-dependent phase separation, exerting immunoprotective effect in ARDS. The LLPS status of MYL12A and its activity score may serve as ARDS prognostic biomarkers and offer a novel strategy for developing LLPS-targeted immunomodulatory therapies.

Lung cancer is among the leading causes of cancer-related deaths worldwide, with treatment strategies primarily including surgery, chemotherapy, radiotherapy, and immunotherapy. Although immunotherapies targeting T cells and natural killer (NK) cells are widely used, therapies targeting neutrophils remain underdeveloped. Neutrophils are regarded as a specialized cell population that, once matured, lack the capacity for proliferation and are rapidly depleted in circulation, limiting their role to immune defense. However, recent discoveries have revealed that neutrophils represent a highly heterogeneous immune cell population, across diverse microenvironments. They are referred to as tumor-associated neutrophils when recruited to the tumor microenvironment. Initially, tumor-associated neutrophils were believed to primarily promote tumor growth and metastasis. Contrarily, emerging evidence indicates that tumor-associated neutrophils exhibit anti-tumor functions under specific conditions, acting as inhibitors during the initial growth or metastatic phases of lung cancer. This functional heterogeneity positions neutrophils as a promising focus for novel approaches to lung cancer immunotherapy. This review aims to explore the role of tumor-associated neutrophils in lung cancer progression and to investigate responses in the context of tumor control, thereby deepening the understanding of neutrophil function in lung cancer.

Introduction: Nicotinamide Mononucleotide (NMN) has gained attention as a precursor to Nicotinamide Adenine Dinucleotide (NAD+) in recent years, commonly utilized in anti-aging therapies. The anti-aging effects of NMN on muscle and liver functions in middleaged and elderly people are still unclear. Objective: Based on available randomized controlled trials, we conducted a meta-analysis to evaluate the impact of NMN on muscle and liver functions in middle-aged and elderly individuals. Methods: We conducted searches on three electronic databases (PubMed, Embase, Web of Science) for randomized controlled trials involving NMN interventions in middle-aged and elderly populations. Through the Cochrane Handbook, we assessed the specific methodological quality. All statistical analyses were obtained by Stata15, and statistical significance was set as P<0.05. Results: There were 412 participants from 9 studies in this meta-analysis. Based on changes in gait speed (SMD: 0.34 m/s, 95%CI [0.03, 0.66] p = 0.033), NMN had significant effects on muscle mass. Moreover, NMN had a better effect on ALT (SMD: -0.29 IU/L, 95%CI [-0.55, -0.03] p = 0.028). Subgroup analysis indicated that administering a small dose of NMN exerted the most prominent impact on Homeostasis Model Assessment-Insulin Resistance (HOMA-IR). Conclusion: NMN has positive efficacy in enhancing muscle function, reducing insulin resistance and lowering aminotransferase levels in middle-aged and elderly individuals. NMN is an encouraging and considerable drug for anti-aging treatment.

Lung adenocarcinoma (LUAD) is the most prevalent histological subtype of lung cancer, characterized by high mortality rates. KAT2A has been implicated in oncogenic processes and tumor progression. This study systematically investigated the role of KAT2A in LUAD through comprehensive analyses. Expression profiles and prognostic significance of KAT2A were evaluated using TCGA database and multiple GEO datasets. Functional enrichment analyses including GO and KEGG pathway analyses were conducted to elucidate biological mechanisms associated with KAT2A-regulated differentially expressed genes. Correlations between KAT2A expression levels and immune cell infiltration were analyzed using R software and publicly available databases. Experimental validation was performed through CCK-8 assays, colony formation assays, flow cytometry, and xenograft tumor models. Our findings demonstrated significantly elevated KAT2A expression in LUAD tissues and cells. Expression levels correlated with multiple clinicopathological parameters including TNM stage, pathological stage, sex, and tumor localization. High KAT2A expression was associated with reduced overall survival and exhibited prognostic relevance across diverse clinical subgroups. Multivariate analysis confirmed independent prognostic value of KAT2A expression in the established nomogram model. Functional annotation revealed enrichment of KAT2A-associated genes in critical biological processes and signaling pathways. Moreover, KAT2A expression exhibited correlations with mutational profiles and immune cell infiltration patterns in LUAD. Both in vitro and in vivo experiments demonstrated that KAT2A knockdown significantly suppressed tumor cell proliferation and immune evasion mechanisms, induced apoptosis, and inhibited tumor growth. These findings suggest that KAT2A may serve as a potential prognostic biomarker for LUAD, with therapeutic implications through its regulatory role in immune evasion pathways.

Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are often accompanied by systemic inflammatory responses and can lead to coagulation disorders and thrombotic complications, thereby increasing hospitalization rates and mortality. Platelets play a critical role not only in hemostasis and thrombosis, but also in immunity and inflammation. The aim of the present study was to explore the associations among thrombocytopenia, infection severity and deep vein thrombosis (DVT) formation in patients with AE-COPD, and to develop a predictive model based on platelet-related parameters. The clinical data from 338 patients with AE-COPD who were hospitalized in the Department of Respiratory and Critical Care Medicine of The Affiliated Jiangning Hospital of Nanjing Medical University (Nanjing, China) between January 2021 and December 2023 were retrospectively evaluated. Demographic characteristics, medical history, comorbidities, laboratory test results, lower limb venous ultrasound findings, chest computed tomography scans and mechanical ventilation treatment data were collected. Statistical analyses were performed using SPSS version 26.0, GraphPad Prism version 9.0 and R version 4.1.3. Among the 338 patients with AE-COPD, 72.4% were male and the mean age was 75.60±7.42 years. The thrombocytopenia group (<150x109 platelets/l) had a significantly lower white blood cell count, neutrophil count, monocyte count, platelet-to-lymphocyte ratio (PLR) and plateletcrit compared with the normal platelet group (≥150 to <300x109 platelets/l). Among the 338 patients with AE-COPD, 5 patients in the thrombocytopenia group had DVT, while 29 patients in the normal platelet group had DVT. The incidence of DVT during hospitalization was significantly lower in the thrombocytopenia group than that in the normal platelet group (4.7 vs. 12.5%). In a specific subgroup analysis of patients who were male, >70 years old, and presented with both cardiovascular diseases and concurrent pulmonary infection, the DVT risk was found to be lower in the thrombocytopenia group. Multivariate logistic regression analysis revealed that PLR and D-dimer were independent risk factors for DVT formation during hospitalization in patients with AE-COPD. In conclusion, thrombocytopenia was associated with more severe lung infections in patients with AE-COPD. A model incorporating PLR and D-dimer showed diagnostic efficacy for predicting DVT in hospitalized patients with AE-COPD.

Acute respiratory distress syndrome (ARDS) is a critical condition marked by severe alveolar damage and oxygenation impairment, leading to high mortality rates despite treatment with mechanical ventilation and fluid management. Halotherapy, a non-invasive treatment initially used for chronic respiratory diseases like COPD and asthma, has yet to be fully explored for its efficacy in ARDS. This interventional study involved 97 patients with ARDS, who were divided into a halotherapy treatment group and a standard treatment group. The study collected data through electronic medical records, laboratory tests, and direct patient assessments to evaluate biomarkers, lung function, and clinical outcomes before and after treatment. Compared to standard treatment group, halotherapy significantly reduced levels of NLRP3, IL-1β, Caspase-1, and MMP3. Lung function enhancements included increases in FVC and FEV1. Additionally, the incidence of major adverse cardiac events and renal dysfunction decreased significantly in the halotherapy group, highlighting halotherapy's potential to improve clinical outcomes in ARDS treatment. Halotherapy, with its anti-inflammatory and antibacterial properties, provides an effective treatment option for ARDS patients. Its non-invasive nature and good tolerability make it a promising adjunctive therapy for managing ARDS and potentially other respiratory diseases.

Background: Panax japonicus (P. japonicus) belongs to the Panax genus of Araliaceae and is used as medicine mainly with the bamboo whiplike rhizome, which has the functions of dispelling blood stasis and hemostasis, attenuating swelling and pain, eradicating phlegm and relieving cough, tonifying, and strength. Purpose: This review intends to summarize the chemical constituents and pharmacological activities of P. japonicus to provide a scientific and systematic basis for better utilization of its rational applications. Methods: The literature was searched using PubMed, Baidu Scholar and Science Hub search engines. Results: The chemistry components isolated from P. japonicus are mainly saponins, besides also including polysaccharides, amino acids, volatile oils, inorganic elements, etc. P. japonicus exhibits extensive pharmacological activities including anti-inflammatory, antioxidant, lipid lowering activities, and therefore show extensive protective effects on the central nervous system, cardio-cerebrovascular system, digestive system. Conclusion: This article included a thorough summary of the botany, phytochemistry, and pharmacology of P. japonicus and provided evidence for its further research and clinical applications.

Liquid-liquid phase separation (LLPS) is integral to various biological processes, facilitating signal transduction by creating a condensed, membrane-less environment that plays crucial roles in diverse physiological and pathological processes. Recent evidence has underscored the significance of LLPS in human health and disease. However, its implications in respiratory diseases remain poorly understood. This review explores current insights into the mechanisms and biological roles of LLPS, focusing particularly on its relevance to respiratory diseases, aiming to deepen our understanding and propose a new paradigm for studying phase separation in this context.

The efficacy of cancer therapies is significantly compromised by the immunosuppressive tumor milieu. Herein, we introduce a previously unidentified therapeutic strategy that harnesses the synergistic potential of chitosan-coated bacterial vesicles and a targeted chemotherapeutic agent to activate dendritic cells, thereby reshaping the immunosuppressive milieu for enhanced cancer therapy. Our study focuses on the protein-mediated modification of bacterium-derived minicells with chitosan molecules, facilitating the precise delivery of Doxorubicin to tumor sites guided by folate-mediated homing cues. These engineered minicells demonstrate remarkable specificity in targeting lung carcinomas, triggering immunogenic cell death and releasing tumor antigens and damage-associated molecular patterns, including calreticulin and high mobility group box 1. Additionally, the chitosan coating, coupled with bacterial DNA from the minicells, initiates the generation of reactive oxygen species and mitochondrial DNA release. These orchestrated events culminate in dendritic cell maturation via activation of the stimulator of interferon genes signaling pathway, resulting in the recruitment of CD4+ and CD8+ cytotoxic T cells and the secretion of interferon-β, interferon-γ, and interleukin-12. Consequently, this integrated approach disrupts the immunosuppressive tumor microenvironment, impeding tumor progression. By leveraging bacterial vesicles as potent dendritic cell activators, our strategy presents a promising paradigm for synergistic cancer treatment, seamlessly integrating chemotherapy and immunotherapy.

Introduction: There have been disputes in the association between angiotensin receptor blockers (ARB) and the incidence of lung cancer. Our meta-analysis reevaluated this problem from the perspectives of race, age, drug type, comparison objects and smoking. Method: We used the following databases to carry out our literature search: Pubmed, Medline, Cochrane Library, and Ovid (From 1 January 2020 to 28 November 2021). The correlation between ARBs and the incidence rate of lung cancer was calculated by risk ratios (RRs). Confidence intervals were selected with 95% confidence intervals. Results: A total of 10 randomized controlled trials (RCTs), 18 retrospective studies and 3 case-control studies were found to satisfy the inclusion criteria. The use of ARB drugs reduced the incidence of lung cancer. The pooled results of 10 retrospective studies revealed a decreased lung cancer incidence in patients treated with ARBs, especially in patients using Valsartan. A significantly lower lung cancer incidence was found in the ARB drugs than in calcium channel blockers (CCBs) and angiotensin-converting enzyme inhibitors (ACEIs). Lung cancer occurrence was lower in Asian-based studies, especially in Mongolian-dominated and Caucasian-dominated patient populations. No significant decrease in lung cancer occurrence was found in RCTs or in patients receiving telmisartan, losartan, candesartan, irbesartan, or other placebo or in American and European-dominated patient populations. Conclusion: Compared with ACEIs and CCBs, ARBs significantly reduce the risk of lung cancer, especially in Asian and Mongolian populations. Valsartan has the best effect in reducing the risk of lung cancer in ARB drugs.

Hydrochlorothiazide (HCTZ) is a commonly used diuretic antihypertensive drug that can cause electrolyte disorders, hyperglycemia and hyperuricemia as well as rare life-threatening adverse drug reactions. These include non-cardiogenic pulmonary edema, interstitial pneumonia, angioedema and aplastic anemia. The present report describes a case of a 59-year-old man who developed a hypersensitivity reaction to HCTZ. Specifically, the patient presented with symptoms of cough, chest tightness and shortness of breath, with pneumonic consolidation on chest CT and elevated levels of white blood cell count, neutrophil percentage, C-reactive protein and procalcitonin. A presumptive diagnosis of severe pneumonia was made initially. However, during the gradual recovery of the patient through treatment, he mistakenly ingested HCTZ containing losartan potassium intended for another patient, which resulted in symptoms similar to those observed upon admission. Upon further inquiry into the medical history, it was revealed that the patient had also taken irbesartan/HCTZ 4 h prior to hospitalization. There was no evidence of a pathogenic infection. Therefore, HCTZ-induced anaphylactic reaction was considered to be the most likely etiology for his severe shock. Treatments including epinephrine, methylprednisolone and respiratory support were administered. After 7 days, the patient was transferred from the Respiratory Intensive Care Unit [The Affiliated Jiangning Hospital of Nanjing Medical University (Nanjing, China)] to a general ward. During the follow-up, 12 months after advising the patient to discontinue HCTZ, there had been no recurrence of the aforementioned symptoms. At the time of publication, the patient is currently alive.

Perfluorooctane sulfonate (PFOS), an emerging environmental pollutant, is reported to cause neurotoxicity in animals and humans, but its underlying mechanisms are still unclear. We used in vivo models to investigate the effects of PFOS on cognition-related behaviors and related mechanisms. After 45 days of intragastric administration of PFOS (2 mg/kg or 8 mg/kg) in 7-week-old C57BL/6 mice, muscle strength, cognitive function and anxiety-like behavior were evaluated by a series of behavioral tests. The underling mechanisms of PFOS on impaired behaviors were evaluated by HE/Nissl staining, electron microscopy observation and western blot analysis. The results indicated that PFOS-exposed mice exhibited significant cognitive impairment, anxiety, neuronal degeneration and the abnormities of synaptic ultrastructure in the cortex and hippocampus. Western blot analysis indicated that PFOS exposure increased microtubule-associated protein light chain 3 (LC3) and decreased p62 protein levels, which may be associated with activation of autophagy leading to neuron damage. In summary, our results suggest that chronic exposure to PFOS adversely affects cognitive-related behavior in mice. These findings provide new mechanistic insights into PFOS-induced neurotoxicity.

The controversy over the efficacy of postoperative radiotherapy (PORT) has existed for a long time. The present study reassessed the overall survival (OS) and disease-free survival (DFS) data to investigate whether PORT can improve survival in resectable non-small cell lung cancer (NSCLC) patients. The following databases were used to perform literature search: PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and Embase (from January 1, 1986 to July 5, 2021). The results of overall survival (OS) and disease-free survival (DFS) were calculated as hazard ratio (HR). Confidence intervals are chosen with 95% confidence intervals. A total of 12 RCTs and 19 retrospective cohort studies were found to meet the inclusion criteria. A significant DFS improvement was detected in the PORT group (4111 patients from 15 studies), although statistical difference was not detected for OS between the non-PORT and PORT groups (31 studies, 49,342 total patients). PORT prolonged OS in patients undergoing PORT plus postoperative chemotherapy (POCT) and in pN2 patients. Patients with a median radiation dose of 50.4 Gy and a median radiation dose of 54 Gy had a better OS after PORT. However, if the total radiotherapy dose went up to 60 Gy, PORT increased the risk of death in NSCLC patients. Significant difference in OS was not found in the results of studies with regard to treatment methods, pathologic stages, study type, radiation beam quality, and radiation dose. Patients undergoing postoperative chemoradiotherapy and pN2 patients can benefit from PORT. Patients exposed to median radiation doses of 50.4 and 54 Gy demonstrated relatively good efficacy. For patients with non-small-cell lung cancer, PORT has not been proven to extend OS, but its effect on DFS remains strong.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants (POPs) and are associated with thyroid diseases. Our previous study reported that 2,3',4,4',5-Pentachlorobiphenyl (PCB118) could induce thyroid dysfunction and the rat thyroid tissues exhibit abnormal mitochondrial ultrastructure. However, the more specific effects of PCB118 on mitochondria and the relationship between mitochondria and thyroid dysfunction remain unclear. In this study, Wistar rats were injected with PCB118 intraperitoneally at 0, 10, 100, and 1000 μg/kg/d for 13 weeks and FRTL-5 rat thyroid cells were treated with PCB118 (0, 0.25, 2.5, and 25 nM) for 24 hr, which did not influence the general conditions of rats and FRTL-5 cells viability. The detection of serum levels of thyroid hormones (THs) and the expression of sodium/iodide symporter (NIS) protein demonstrated that thyroid function was impaired after PCB118 exposure. Transmission electron microscopy showed mitochondrial damage in the thyroids of PCB118-treated rats. Biological processes analysis revealed that differentially expressed mRNAs in thyroid tissues induced by PCB118 were enriched in reactive oxygen species (ROS) metabolic process, hydrogen peroxide metabolic process, and hydrogen peroxide catabolic process. Moreover, mRNA expression of mitochondrial respiratory chain genes NDUFB3, UQCRC2, COX17, ATP5I and ATP5E decreased in PCB118-treated groups. In vivo and in vitro data showed that ROS production increased significantly after PCB118 exposure, accompanied by increased levels of phospho-c-Jun N-terminal kinase (P-JNK). Taken together, these results suggest that PCB118 could damage mitochondria by increasing oxidative stress and PCB118-induced thyroid dysfunction may be related to ROS-dependent activation of the JNK pathway.

Background: Parkinson's disease (PD) is the second most common neurodegenerative disease in the world, with clinical manifestations of resting tremor, akinesia (or bradykinesia), rigidity, and postural instability. However, the molecular pathogenesis of PD is still unclear, and its effective treatments are limited. Substantial evidence demonstrates that long non-coding RNAs (lncRNAs) have important functions in various human diseases, such as cancer, cardiovascular disease, and neurodegenerative diseases. Therefore, the main purpose of this study is to review the role of lncRNAs in the pathogenesis of PD. Methods: The role of lncRNAs in the pathogenesis of PD is summarized by reviewing Pubmed. Results: Thirty different lncRNAs are aberrantly expressed in PD and promote or inhibit PD by mediating ubiquitin-proteasome system, autophagy-lysosomal pathway, dopamine (DA) neuronal apoptosis, mitochondrial function, oxidative stress, and neuroinflammation. Conclusion: In this direction, lncRNA may contribute to the treatment of PD as a diagnostic and therapeutic target for PD.