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Cigarette smoking (CS) exposure-induced airway inflammatory responses drive the occurrence and development of emphysema and chronic obstructive pulmonary disease (COPD). However, its precise mechanisms have not been fully elucidated. In this study, we explore the role of Rab26 in CS exposure modulating the inflammatory response of airway epithelium and the novel mechanism of CS exposure regulation Rab26. These data showed that CS exposure and H 2 O 2 (a type of ROS) suppressed the expression of Rab26 and increased the expression of DNMT3b in vivo and in vitro. GEO data analysis found the level of Rab26 was decreased in the lung tissue of COPD patients. CSE-induced ROS promoted DNA methylation of the Rab26 promoter and inhibited its promoter activity by elevating the DNMT3b level. Antioxidants N-Acetyl- l -cysteine (NAC), 5-Aza-2′-deoxycytidine (5-AZA) (DNA methylation inhibitor) and DNMT3B siRNA alleviated CSE's inhibitory effect on Rab26 expression in vitro. Importantly, NAC alleviated the improved expression of Rab26 and reduced DNMT3B expression, in the airway of smoking exposure as well as attenuated the inflammatory response in vivo. Overexpression of Rab26 attenuated CSE-induced production of inflammatory mediators through part inactivation of p38 and JNK MAPK. On the contrary, silencing Rab26 enhanced p38 and JNK activation and aggravated inflammatory response. These findings suggest that ROS-mediated Rab26 promoter hypermethylation is a critical step in cigarette smoking-induced airway epithelial inflammatory response. Restoring Rab26 in the airway epithelium might be a potential strategy for treating airway inflammation and COPD. [Display omitted] • CSE-induced ROS promoted DNA methylation of Rab26 promoter in airway epithelium. • Rab26 suppressed the CSE-induced inflammatory response of airway epithelium by partly inactivating the MAPK signaling pathway. • Downregulation of Rab26 promoted CSE-induced inflammatory response through enhanced activation of p38 and JNK MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Metastatic variants are characterized with an acquired focal chromosomal amplification that corresponds to a much larger amplification in human metastatic melanomas and the analyses has identified Nedd9, an adaptor protein related to p130CAS, as the only gene within the minimal common region that displayed amplification-associated overexpression. The comparative oncogenomics has helped in the identification and has facilitated the validation of a highly relevant cancer gene governing metastatic potential in human melanoma.

An RNAi-based genetic screen for genes that suppress transformation of human mammary epithelial cells is reported. The results implicate REST gene as a human tumor suppressor and provide a novel approach to identifying candidate genes that suppress the development of human cancer.

• A method using RevCol network as the Backbone of YOLOv8 is developed. • A new lightweight LEMA Block fused with EMA mechanism is designed to optimize the C2f module of Neck in YOLOv8. • A Squeeze-and-Excitation (SE) attention is introduced into the Neck of YOLOv8. • Ultimately, an improved YOLOv8-based lightweight defect detection model for PV panel is proposed. The detection of defect types of photovoltaic (PV) panel is a crucial task in PV system. Existing detection models face challenges in effectively balancing the trade-off between detection accuracy and resource consumption. To address this issue, this paper proposes a new defect detection method for PV panel based on the improved YOLOv8 model, which realizes both the high detection accuracy and the lightweight. Firstly, Reversible Column Networks (RevCol) is used as the Backbone of YOLOv8, which makes sure to preserve the feature information in the process of network transmission and also reduces the number of parameters and Giga floating-point operations per second (GFLOPs). Subsequently, a new lightweight Bottleneck fused with Efficient Multi-Scale Attention (EMA) is designed to optimize the CSPDarknet53 to 2-Stage FPN (C2f) module of Neck in YOLOv8 to enhance the robustness and further decrease network parameters. Finally, Squeeze-and-Excitation (SE) Attention is integrated into the Head of YOLOv8 to prioritize the important channel features and thus enhance the detection performance. The experimental results on the PVEL-AD dataset demonstrate that parameters and GFLOPs of the proposed model are declined by 38.46% and 34.39% respectively, and mAP0.5:0.95 is increased by 2.6% compared with the baseline model. The lightweight improved YOLOv8 model facilitates the deployment of deep learning model on edge devices and provides a novel approach for the online detection of PV panel defects. [ABSTRACT FROM AUTHOR]

Background: Pulmonary vein isolation (PVI) for paroxysmal atrial fibrillation (AF) is associated with a non-negligible long-term recurrence rate.Objectives: The purpose of this study was to investigate whether PVI combined with 6 short ablation lines on the PVI circumferences (PVI+6L group) yields higher success rates than PVI alone (PVI group).Methods: In this multicenter, single-blind, randomized trial, a total of 390 patients with paroxysmal AF were randomly assigned to the PVI group (n = 193) or the PVI+6L group (n = 197). The primary endpoint was freedom from AF/atrial tachycardia recurrence between 91 and 365 days. Secondary endpoints included AF burden, procedural parameters, and complications.Results: Freedom from atrial tachyarrhythmia was achieved in 160 of 197 patients (81.2%) in the PVI+6L group and 142 of 193 patients (73.6%) in the PVI group (hazard ratio 0.61; 95% confidence interval 0.39-0.97; P = .040). Mean AF burden tended to be lower in the PVI+6L group compared to the PVI group (1.95% vs 0.53%, P = .097). Procedural and ablation times were slightly longer in the PVI+6L group than in the PVI group (130 ± 25 minutes vs 121 ± 28 minutes; P = .002; and 46 ± 14 minutes vs 41 ± 16 minutes, P = .001, respectively). X-ray exposure was similar (60 ± 54 seconds vs 61 ± 60 seconds; P = .964). Complications occurred in 3 patients (1.6%) in the PVI group and 3 patients (1.5%) in the PVI+6L group.Conclusion: In patients with paroxysmal AF undergoing catheter ablation, adding 6 short ablation lines on the PVI circumferences could reduce the AF recurrence rate. [ABSTRACT FROM AUTHOR]

This study focuses on the variation in activity-controlling factors during CO catalytic ignition over a CuO–CeO 2 catalyst. The activity for CO combustion follows the decreasing order of CuO–CeO 2 > CuO > CeO 2. Except for inactive CeO 2 , increasing temperature induces CO ignition to achieve self-sustained combustion over CuO and CuO–CeO 2. However, CuO provides enough copper sites to adsorb CO, and abundant active lattice oxygen, thus obtaining a higher hot zone temperature (208.3°C) than that of CuO–CeO 2 (197.3 °C). Catalytic ignition triggers a kinetic transition from the low-rate steady-state regime to a high-rate steady-state regime. During the induction process, Raman, X-ray photoelectron spectroscopy (XPS), CO temperature-programmed desorption (CO-TPD) and infrared (IR) spectroscopy results suggested that CO is preferentially adsorbed on oxygen vacancies (Cu+-[O v ]-Ce3+) to yield Cu+-[C O]-Ce3+ complexes. Because of the self-poisoning of CO, the adsorbed CO and traces of adsorbed oxygen react at a relative rate, which is entirely governed by the kinetics on the CO-covered surface and the heat transport until the pre-ignition regime. Nonetheless, the Cu+-[C O]-Ce3+ complex is a major contributor to CO ignition. The step-response runs and kinetic models testified that after ignition, a kinetic phase transition occurs from a CO-covered surface to an active lattice oxygen-covered surface. During CO self-sustained combustion, the rapid gas diffusivity and mass transfer is beneficial for handling the low coverage of CO. The active lattice oxygen of CuO takes part in CO oxidation. [ABSTRACT FROM AUTHOR]

• Both early repolarization (ER) and atrial fibrillation (AF) are highly prevalent in Wolff-Parkinson-White syndrome (WPW). • Inferior-lead ER after ablation is associated with AF recurrence in WPW patients. • Additional pulmonary vein isolation might be considered in WPW patients with AF and ER. Both atrial fibrillation (AF) and early repolarization (ER) are highly prevalent in patients with Wolff–Parkinson–White (WPW) syndrome. We retrospectively identified 123 WPW patients with manifest accessory pathway (mAP) and 105 patients with concealed accessory pathways (cAP) who underwent successful ablation of the APs. AF history prior to the ablation was investigated. The presence of ER was evaluated from the 12-lead electrocardiograms performed both before and immediately after the ablation. Patients were further followed up for AF occurrence after the AP ablation. Compared with cAP patients, WPW patients presented with higher incidence of previous AF, as well as ER after the AP ablation. Compared with those without AF history, WPW patients with comorbid AF were more prone to presenting ER, especially in the inferior leads, after the mAP ablation. Regression analysis suggested that the post-ablation ER in the inferior leads was strongly associated with AF in WPW patients [OR = 5.85; 95% confidence interval (CI): 2.29–14.96], even after adjusting for age and left atrial diameter (OR = 5.14; 95% CI: 1.80–14.74). Moreover, post-ablation inferior-lead ER was predictive of AF recurrence after mAP ablation during the follow-up of 22.6 ± 11.1 months. In comparison, ER was correlated with neither AF history nor AF recurrence in patients undergoing cAP ablation. ER in the inferior leads after the mAP ablation is highly correlated with AF history and recurrence in WPW patients. [ABSTRACT FROM AUTHOR]

Abstract The self-sustained combustion of carbon monoxide (CO) has been studied over the CuCe 0.75 Zr 0.25 O δ catalyst by sol–gel method, and compared with the CuCe 0.75 Zr 0.25 O δ (H) and Ce 0.75 Zr 0.25 O δ to investigate sensitivity of different active sites, such as dispersed CuO, Cu–Ce and Ce–Zr solid solution. The CuCe 0.75 Zr 0.25 O δ (H) is obtained via CuCe 0.75 Zr 0.25 O δ sonicated in nitric acid to remove surficial CuO species, and the Ce 0.75 Zr 0.25 O δ is prepared as the reference catalyst. Using the temperature programmed oxidation of CO together with an infrared camera (CO-TPO + FLIR), the catalytic activity for CO self-sustained combustion is determined not only by the ignition temperatures, following the decreasing order CuCe 0.75 Zr 0.25 O δ (81 °C) > CuCe 0.75 Zr 0.25 O δ (H) (131 °C) > Ce 0.75 Zr 0.25 O δ (167 °C) at the flow rate of 200 mL/min, but also by corresponding limits of lean combustion (equivalence ratio Φ) of 0.06–0.09, 0.10–0.13, 0.24–0.37, respectively, under the flow rate of 100–1000 mL/min. The M-K mechanism, in which adsorbed CO reacts with lattice oxygen, is crucial for all the catalysts via temperature programmed surficial reaction and in situ infrared analysis (TPSR + DRIFT). The sensitivity of active sites as follows: well-dispersed CuO > Cu–Ce solid solution > Ce–Zr solid solution. As rate-determining step for CO self-sustained combustion, CO is preferentially adsorbed on surficial dispersed CuO to yield carbonyls, and then the carbonyls interact with lattice oxygen to form CO 2 release. CO is secondly adsorbed on the surficial oxygen of copper and cerium sites in solid solution to yield carbonates. The carbonates formed are more stable and thus CO 2 is produced at the lower rate than carbonyls, indicating that the solid solution is less active than dispersed CuO. Exposed Ce3+ favors to form vacancies on the Cu–Ce solid solution surface, which is beneficial to adsorbing both CO and O 2 , thus presenting the higher activity than Ce–Zr solid solution. [ABSTRACT FROM AUTHOR]

• Catalpol is an iridoid glucoside isolated from Rehmannia glutinosa Libosch. • Catalpol alleviated collagen II-induced arthritis in rats. • Catalpol inhibited LPS-induced inflammatory response in SW982 cells. • Catalpol suppressed LPS-induced MAPK, NF-κB and AP-1 pathways in SW982 cells. Catalpol, an effective component of China's functional food Rehmannia glutinosa Libosch, has a wide range of pharmacological effects. However, it is unclear whether catalpol exhibits protective and therapeutic potential against rheumatoid arthritis. In this study, the effects of catalpol in rats with collagen II-induced arthritis (CIA) and in LPS-stimulated SW982 human synovial cells were investigated. Catalpol significantly reduced paw swelling and thickness in rats with CIA. Histopathology revealed that catalpol alleviated articular cartilage damage, infiltration of inflammatory cells and synovial hyperplasia. Catalpol also inhibited protein and mRNA levels of IL-6, IL-8 and MMP-1, and the expression of COX-2 and mPGEs-1 in LPS-stimulated SW982 cells. Furthermore, the phosphorylation levels of ERK, JNK, p65, IκBα and c-Jun were suppressed by catalpol. Taken together, these findings showed that catalpol had inhibitory effects against arthritis, which may be related to decreased production of pro-inflammatory mediators and suppression of the MAPK, NF-κB and AP-1 pathways. [ABSTRACT FROM AUTHOR]

The present study shows the basis for the anti-inflammatory effects of pitavastatin in interleukin (IL)-1β-induced human synovial cells. The SW982 cells were pretreated with pitavastatin at different concentrations (5 μM and 10 μM), followed by IL-1β (10 ng/mL) stimulation. The results showed that pitavastatin inhibited the expression of inflammatory mediators IL-6 and IL-8. Furthermore, pitavastatin inhibited the phosphorylation of p38, extracellular signal-related kinase (ERK), c-jun N-terminal kinase (JNK) and protein kinase B (Akt). It also suppressed the degradation of I kappa B alpha and blocked p65 translocation into the nucleus. These findings suggest that the mechanism underlying the inhibitory effects of pitavastatin on IL-1β-induced IL-6 and IL-8 release might be mediated by the suppression of mitogen-activated protein kinase (MAPK), Akt, and nuclear factor-κB (NF-κB) signaling pathways. These results may also indicate that pitavastatin may be potentially utilized as an effective therapeutic agent for the treatment of osteoarthritis. [ABSTRACT FROM AUTHOR]

As a result of vitamin A abuse, excessive retinoic acid can induce apoptosis in neural cells. Mild-hypothermia and cold-inducible protein RBM3 protect neural cells from apoptosis. However, whether hypothermia/RBM3 protect neural cells from retinoic acid-induced apoptosis remains unclear. The SH-SY5Y neuroblastoma cell line, a common neural cell model of apoptosis, was employed here. Interestingly, retinoic acid overdose induced apoptosis in SH-SY5Y cells, which was prevented by mild-hypothermia. When RBM3 was silenced, hypothermia-related protection was completely abolished. RBM3 overexpression significantly prevented retinoic acid-induced apoptosis. Screening of signaling pathways revealed that RBM3 overexpression markedly inhibited retinoic acid-induced upregulation of p38 and JNK signaling, and antagonized downregulation of AMPK signaling. Subsequent assays demonstrated that p38 and JNK signaling were pro-apoptotic, while AMPK was anti-apoptotic. Overall, these data showed that mild-hypothermia protects neural cells from retinoic acid-induced apoptosis via induction of RBM3, which subsequently mediates the neuroprotective effects via AMPK, p38 and JNK signaling. [ABSTRACT FROM AUTHOR]