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Nuclear factor kappa B (NF-κB), a key nuclear transcription factor, is associated with prognosis in a variety of human cancers. However, the clinical value of NF-κB in non-small cell lung cancer (NSCLC) is still controversial. Therefore, the aim of this meta-analysis was to obtain an accurate evaluation of the relationship between NF-κB expression and survival prognosis of NSCLC patients based on published articles. PubMed, EMBASE and Web of Science databases were systematically searched for potential articles. A total of 1159 patients from 7 eligible studies comparing prognostic significance of NF-κB expression levels in NSCLC were included in our meta-analysis. I2 statistic and P value were performed to evaluate heterogeneity. The results of analysis were presented as hazard ratio (HR) or odds ratios (OR) with 95% confidence interval (95% CI). Subgroup analysis based on ethnicity of NSCLC patients and NF-kB cellular localization within cancer cells were conducted to illustrate the potential discrepancy. Significant heterogeneity was considered at I2>50% and P<0.05, and random-effects model was used. The combined results indicated that higher NF-κB expression was associated with shorter overall survival (OS) of NSCLC patients (HR = 2.78, 95% CI = 1.51-5.12, P = 0.001). Moreover, NF-κB expression was closely associated with tumor stage (HR = 0.32, 95% CI = 0.18-0.57, P<0.0001), lymph node metastasis (HR = 0.56, 95% CI = 0.38-0.83, P = 0.004) and 5-year OS for NSCLC patients (OR = 1.83, 95% CI = 1.02-3.31, P = 0.04). We conclude that NF-κB expression may be a potential unfavorable prognostic marker for NSCLC patients.

Background Infantile pneumonia is a common infectious disease affecting infants and young children, which can lead to severe complications such as heart failure, significantly increasing morbidity and mortality rates among affected populations. Curcumin (CUR), a prominent natural polyphenol found in turmeric and other species of Curcuma, exhibits anti-inflammatory, antioxidant, and anticancer properties. Consequently, CUR has been hoped to be a therapeutic or preventive agent for several main human diseases. This study aims to explore the effects of CUR on lipopolysaccharide (LPS)-treated Wistsar Institute (WI)-38 cells. Methods The cell vitality, proliferation, and apoptosis were assessed by cell counting kit-8 (CCK8) assay, 5-ethynyl-2’-deoxyuridine (EdU), and flow cytometry assays. Inflammation and oxidative stress were examined by measuring interleukins (IL)-6, IL-1β, tumor necrosis factor α (TNF-α), malondialdehyde (MDA), and superoxide dismutase (SOD) levels using the corresponding enzyme-linked immunosorbent assay (ELISA) test kits. The network pharmacology and molecule docking were carried out to predict the critical targets and potential therapeutic mechanisms of CUR in infantile pneumonia. The key target genes were predicted using PPI in the CUR protected-infantile pneumonia effect. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to exhibit the biological function. The results of prediction were confirmed in vitro experiments. Results LPS inhibited the vitality, proliferation, and SOD levels of WI-38 cells and facilitated the cell apoptosis, IL-6, IL-1β, TNF-α, and MDA levels. CUR abolished LPS-induced regulation WI-38 cell biological functions. Besides, the 16 hub genes from potential target genes of CUR and infantile pneumonia were screened. Moreover, six hub genes (enhanced green fluorescent protein (EGFP), v-akt murine thymoma viral oncogene homolog 1 (AKT1), prostaglandin endoperoxide synthase (PTGS2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase 9 (MMP9), and tumor necrosis factor (TNF)) in the CUR-protected-infantile pneumonia effect were identified by PPI analysis. The therapeutic effects of CUR on infantile pneumonia might relate to anti-viral and anti-inflammatory effects predicted by GO and KEGG enrichment analysis. Interestingly, CUR repressed LPS-stimulated facilitation of PTGS2 expression. The molecular docking demonstrated that PTGS2 could directly bind to CUR. The PTGS2 levels were inhibited by CUR treatment and negatively related to the time after WI-38 cells were treated with cycloheximide (CHX). PTGS2 knockdown could promote LPS-induced injury in WI-38 cells. CUR expedited cell vitality and proliferation and suppressed cell apoptosis, inflammation, and oxidative stress in LPS-induced WI-38 cells via down-regulating PTGS2. Conclusion CUR attenuates LPS-induced WI-38 cell injury by downregulating PTGS2. CUR may be the potential drug for alleviating LPS-induced WI-38 cell inflammation damage via regulating PTGS2 expression.

Respiration monitoring is a promising alternative to medical diagnosis of several diseases. However, current techniques of respiration monitoring often require expensive and cumbersome devices which greatly limit their medical applications. Here, we present a fully integrated wearable device consisting of a flexible LCP-copper interdigital electrode, a sensing layer and a wireless electrochemical analysis system. The developed humidity sensor exhibits a high sensitivity, a good repeatability and a rapid response/recover time. The long-term stability is over 30 days at different relative humidity. By integrating the flexible humidity sensor with miniaturized electrochemical analysis system (0.8 cm × 1.8 cm), response current concerning respiration can be wirelessly transmitted to App-assisted smartphone in real time. Furthermore, the fabricated humidity sensor can realize skin moisture monitoring in a touch-less way. The large-scale production of miniaturized flexible sensor (4 mm × 6 mm) has significantly contributed to commercial deployment.

The efficacy of Fluorouracil (FU) in the treatment of colorectal cancer (CRC) is greatly limited by drug resistance. Autophagy has been implicated in chemoresistance, but the role of selective autophagic degradation in regulating chemoresistance remains unknown. In this study, we revealed a critical role of ABHD5 in charging CRC sensitivity to FU via regulating autophagic uracil yield. We demonstrated that ABHD5 localizes to lysosome and interacts with PDIA5 to prevent PDIA5 from interacting with RNASET2 and inactivating RNASET2. ABHD5 deficiency releases PDIA5 to directly interact with RNASET2 and leave RNASET2 in an inactivate state, which impairs RNASET2-mediated autophagic uracil yield and promotes CRC cells to uptake FU as an exogenous uracil, thus increasing their sensitivity to FU. Our findings for the first time reveal a novel role of ABHD5 in regulating lysosome function, highlighting the significance of ABHD5 as a compelling biomarker predicting the sensitivity of CRCs to FU-based chemotherapy. The mechanisms underlying differential chemotherapeutic response to 5-fluorouracil are not fully known. Here, the authors show that ABDH5 regulates sensitivity to 5-fluorouracil in colorectal cancer by regulating lysosome function.

The reduction in near-surface wind speed (NSWS), followed by its recent recovery, could be a feature of decadal variations. However, existing studies mainly analyse the characteristics and causes of NSWS changes on regional scales and over short periods. The decadal variations and underlying causes of global NSWS changes over long timescales remain underexplored. In this study, we investigated the characteristics of NSWS changes in the Northern Hemisphere (NH) on a centennial scale (1900–2010) and identify the potential causes of decadal variations by using an information flow technique. The results indicate that NSWS in the NH experienced a remarkable decadal variation, increasing during 1900–1945 and 1970–1980 and decreasing during 1945–1970 and 1980–2010. Furthermore, regional differences in the distribution features and decadal variations of NSWS were observed. Asia and North America showed the highest data overlap compared to other regions, reaching 59.4%. The longest period of decadal variation in NSWS was found in North America (14 years), followed by Europe (11 years), with Asia showing the smallest period (10 years). When determining the effects of large-scale ocean–atmosphere circulation fields or internal climate models on NSWS changes, prioritising causality between the two variables and the study period is essential, rather than relying solely on simple correlation analysis. According to the information flow technique, the decadal variations in NSWS over North America during 1950–2010 were linked with the Western Hemisphere Warm Pool, whereas the North Atlantic Oscillation influenced those in Europe. The Tropical Northern Atlantic was the driver over Asia. This study offers a scientific foundation for understanding NSWS characteristics on a centennial timescale and the primary causes of decadal variations in NSWS across the NH.

Wind energy development in Central Asia can help alleviate drought and fragile ecosystems. Nevertheless, current studies mainly used the global climate models (GCMs) to project wind speed and energy. The simulated biases in GCMs remain prominent, which induce a large uncertainty in the projected results. To reduce the uncertainties of projected near-surface wind speed (NSW) and better serve the wind energy development in Central Asia, the Weather Research and Forecasting (WRF) model with bias-corrected GCMs was employed. Compared with the outputs of GCMs, dynamical downscaling acquired using the WRF model can better capture the high- and low-value centres of NSWS, especially those of Central Asia's mountains. Meanwhile, the simulated NSWS bias was also reduced. For future changes in wind speed and wind energy, under the Representative Concentration Pathway 4.5 (RCP4.5) scenario, NSWS during 2031–2050 is projected to decrease compared with that in 1986–2005. The magnitude of NSWS reduction during 2031–2050 will reach 0.1 m s−1, and the maximum reduction is projected to occur over the central and western regions (>0.2 m s−1). Furthermore, future wind power density (WPD) can reveal nonstationarity and strong volatility, although a downward trend is expected during 2031–2050. In addition, the higher frequency of wind speeds at the turbine hub height exceeding 3.0 m s−1 can render the plain regions more suitable for wind energy development than the mountains from 2031 to 2050. This study can serve as a guide in gaining insights into future changes in wind energy across Central Asia and provide a scientific basis for decision makers in the formulation of policies for addressing climate change.

Brown/beige adipocytes are therapeutic targets to combat obesity due to their abilities to dissipate energy through adaptive thermogenesis. Most studies investigating induction of brown/beige adipocytes were conducted in cold condition (e.g., 4°C); much is unknown about how the thermogenic program of brown/beige adipocytes is regulated in thermoneutral condition (e.g., 30°C), which is within the thermal comfort zone of human dwellings in daily life. Therefore, this study aims to characterize the thermogenic program of brown/beige adipocytes in mice housed under ambient (22°C) versus thermoneutral condition (30°C). Male mice raised at 22°C or 30°C were fed either chow diet or high‐fat (HF) diet for 20 weeks. Despite less food intake, chow‐fed mice housed at 30°C remained the same body weight compared to mice at 22°C. However, these thermoneutrally housed mice displayed a decrease in the expression of thermogenic program in both brown and white fat depots with larger adipocytes. When pair‐fed with chow diet, thermoneutrally housed mice showed an increase in body weight. Moreover, thermoneutrality increased body weight of mice fed with HF diet. This was associated with decreased expression of the thermogenic program in both brown and white fat depots of the thermoneutrally housed mice. The downregulation of the thermogenic program might have resulted from decreased sympathetic drive in the thermoneutrally housed mice evident by decreased expression of tyrosine hydroxylase expression and norepinephrine turnover in both brown and white fat depots. Our data demonstrate that thermoneutrality may negatively regulate the thermogenic program and sympathetic drive, leading to increased adiposity in mice. Our study demonstrates that thermoneutrality may negatively regulate the thermogenic program and sympathetic drive, leading to increased adiposity in mice.

Asthma is regarded as a chronic inflammation of the airway. Research has highlighted the significance of Vitamin D in asthma. This study explored the mechanism of vitamin D on asthma. The asthma mouse model was established by ovalbumin (OVA) sensitization and treated with vitamin D (50 or 100 ng/ml). The morphological changes of the airway were observed by HE staining. The serum IgE contents and MDA, ROS, and SOD expressions in the bronchoalveolar lavage fluid (BALF) were detected by ELISA. The Th17 and Treg cells were detected using flow cytometry. The RORγt and Foxp 3 expressions were detected by Reverse transcription quantitative polymerase chain reaction (RT‐qPCR). IL‐17, IL‐10, and TGF‐β1 expressions were detected using ELISA. The NF‐κB pathway was blocked using the NF‐κB pathway inhibitor, Andrographolide sulfonate. The NF‐κB pathway‐related indexes were detected by western blotting. After blockade of the NF‐κB pathway, the IL‐17, IL‐10, and TGF‐G1 expressions were detected. OVA‐sensitized asthma induced airway remodeling and elevated IgE content in mice, which was downregulated after vitamin D treatment. MDA and ROS were upregulated and SOD was downregulated in asthmatic mice, while vitamin D inverted the changes. Th17/Treg ratio was imbalanced, RORγt and IL‐17 were upregulated, and Foxp 3, IL‐10, and TGF‐β1 were downregulated after OVA sensitization, while vitamin D treatment inverted these changes and inhibited the NF‐κB‐p65 phosphorylation level. After blockade of the NF‐κB pathway, IL‐17 was downregulated and IL‐10 and TGF‐β1 were upregulated. In conclusion, vitamin D rectified the Th17/Treg balance and alleviated airway inflammation by inhibiting the NF‐κB pathway in asthmatic mice.

Decreased epithelial cadherin (E-cadherin) gene expression, a hallmark of epithelial–mesenchymal transition (EMT), is essential for triggering metastatic advantage of the colon cancer. Genetic mechanisms underlying the regulation of E-cadherin expression in EMT have been extensively investigated; however, much is unknown about the epigenetic mechanism underlying this process. Here, we identified ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX), a histone demethylase involved in demethylating di- or tri-methylated histone 3 lysine 27 (H3K27me2/3), as a positive regulator for the expression of E-cadherin in the colon cancer cell line HCT-116. We showed that inactivation of UTX down-regulated E-cadherin gene expression, while overexpression of UTX did the opposite. Notably, overexpression of UTX inhibited migration and invasion of HCT-116 cells. Moreover, UTX demethylated H3K27me3, a histone transcriptional repressive mark, leading to decreased H3K27me3 at the E-cadherin promoter. Further, UTX interacted with the histone acetyltransferase (HAT) protein CBP and recruited it to the E-cadherin promoter, resulting in increased H3K27 acetylation (H3K27ac), a histone transcriptional active mark. UTX positively regulates E-cadherin expression through coordinated regulation of H3K27 demethylation and acetylation, switching the transcriptional repressive state to the transcriptional active state at the E-cadherin promoter. We conclude that UTX may play a role in regulation of E-cadherin gene expression in HCT-116 cells and that UTX may serve as a therapeutic target against the metastasis in the treatment of colon cancer.

A self-designed oxygen-kerosene ablation system was employed to research the ablation properties of silicone rubber-based insulation material under different oxygen-rich conditions, that is, 0%, 5.00%, 7.71%, 17.01%, and 18.50%. The morphology of posttest specimens was analyzed via a scanning electron microscope (SEM), and the ablation rates were calculated. Experimental results showed that when the particle concentration was a fixed value, the mass and the linear ablation rates increased first and then decreased with the rise of oxygen content; the maximum values were 0.572 g/s and 0.933 mm/s, respectively. Under high oxygen-rich conditions, the formation of silicone rubber restricted the further increase of the ablation rates, filling more gaps of the reaction layer with liquid silicone rubber. Meanwhile, the thickness of the liquid glass layer attached to the surface was increased, which acted as a buffer against the impacts and erosion of particles and retarded the consumption and recession of materials. Excess oxygen spread to the edge of the ablation pit and reacted. Finally, these led to the increase in diameter of the ablation pit and the decrease of two types of ablation rates.