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Non-small cell lung cancer (NSCLC) is a malignant cancer worldwide. Long non-coding RNAs (lncRNAs) have emerged as key players in the development and progression of NSCLC, and may be potential biomarkers of NSCLC. Here, we investigated the clinical significance of lncRNA oxidative stress responsive serine rich 1 antisense RNA 1 (OSER1-AS1) in peripheral blood of patients with NSCLC. OSER1-AS1 in peripheral blood of patients with lung squamous cell carcinoma (LUSC), lung adenocarcinoma (LUAD), and healthy subjects was detected, and the clinical diagnostic efficacy was analyzed. The correlation between OSER1-AS1 expression and clinicopathological features in patients with LUSC and LUAD was analyzed. The downstream mechanism of OSER1-AS1 was explored. The area under the ROC curve of lncRNA OSER1-AS1 and miR-1298-5p/CHSY3 in LUSC and LUAD was compared using the MedCalc analysis. OSER1-AS1 was low in peripheral blood of patients with LUSC and LUAD. The area under the ROC curve for predicting LUSC was 0.800. The area under the ROC curve for predicting LUAD was 0.728. In LUSC and LUAD, OSER1-AS1 deficiency was associated with tumor node metastasis stage, lymph node metastasis, distal metastasis, and poor prognosis. miR-1298-5p was highly expressed, while chondroitin sulfate synthase 3 (CHSY3) was lowly expressed in patients with LUSC and LUAD. miR-1298-5p had target relations with OSER1-AS1 and CHSY3. lncRNA OSER1-AS1 had a higher diagnostic value in patients with NSCLC than miR-1298-5p and CHSY3. Overall, low expression of OSER1-AS1 in peripheral blood of NSCLC patients has high clinical significance, which provides a certain reference value for NSCLC early diagnosis.

Suppression of excessive microglial overactivation can prevent the progression of multiple sclerosis (MS). Histone deacetylases 3 inhibitor (HDAC3i) has been demonstrated to exert anti-inflammatory effects by suppressing microglia (M1-liked) activation. Here, we demonstrate that the RGFP966 (a selective inhibitor of HDAC3) protects white matter after cuprizone-induced demyelination, as shown by reductions in neurological behavioral deficits and increases in myelin basic protein. Moreover, in this study, we found that RGFP966 caused a significant reduction in the levels of inflammatory cytokines, including IL-1β, TNF-α, as well as iNOS, and inhibited microglial (M1-liked) activation in the experimental cuprizone model and LPS-stimulated BV2 cells. Meanwhile, RGFP966 alleviated apoptosis of LPS-induced BV2 cells in vitro. Furthermore, RGFP966 suppressed the expression of P2X7R, NLRP3, ASC, IL-18, IL-1β, and caspase-1, inhibited the ratio of phosphorylated-STAT3/STAT3 and phosphorylated NF-κB p65/NF-κB p65, as well as increased acetylated NF-κB p65 in vitro and in vivo. Furthermore, we confirmed that brilliant blue G (antagonists of P2X7R) suppressed the expression of microglial NLRP3, IL-18, IL-1β, caspase-1, NF-κB p65 (including phosphorylated NF-κB p65), and STAT3 (including phosphorylated STAT3) in vitro. These findings demonstrated that RFFP966 alleviated the inflammatory response and exerted a neuroprotective effect possibly by modulating P2X7R/STAT3/NF-κB65/NLRP3 signaling pathways. Thus, HDAD3 might be considered a promising intervention target for neurodegenerative diseases, such as MS.

Phosphatidylserine (PS) improves learning and memory capacity. In this study, PS formulation was optimized by a response surface methodology. Moreover, we found that PS not only functions as a biologically active component in food preparations but also improves the emulsion's physical stability. Our results showed that the PS emulsions are characterized by a smaller particle size, higher ζ-potential (negative), higher viscosity, and lower surface tension and centrifugal stability constants than the emulsion without PS. Furthermore, we explored the neuroprotective effects of PS emulsion and its underlying mechanisms. Treatment with 2% (w/w) PS emulsion for three months enhanced spatial learning and memory in 5- and 12-week old mice in the Morris water maze test. Western-blotting analysis displayed that the 2% (w/w) PS emulsion treated group upregulated BDNF, TrkB, PSD95, mTOR, MBP, and ErbB4 expression in the hippocampus of 5- and 12-week old mice. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed elevated Nrg-1 and ErbB4 mRNA expression in the 2% (w/w) PS emulsion treated groups, and high Nrg-1 and ErbB4 expression levels were associated with better myelination. In conclusion, we reported PS emulsions with high stability and high bioavailability. Meanwhile, 2% (w/w) PS emulsion enhances learning, memory, and myelination in mice by activating the BDNF/TrkB and Nrg-1/ErbB4 signaling.

Background and AimLow cardiac output syndrome (LCOS) is a serious postoperative complication, affecting the prognosis of patients underwent heart valve replacement (HVR). We aim to create a nomogram to predict LCOS after HVR in cardiac valvular disease patients.MethodsWe performed a retrospective review of 500 cardiac valvular disease patients underwent HVR from 2016 to 2020 in our department. Univariate analysis evaluated the associations between clinical/echocardiographic parameters and LCOS. Independent t-test or Mann–Whitney U‐test: for continuous variables. Fisher's exact test or χ2 test: for categorical variables. Variables with a P

Chemometric modeling concerns both accuracy and computational expense for the prediction of quality-indicating attributes of food materials. Modeling approaches were explored with the hyperspectral images with pH and Brix values of greengages. A two-phase architecture was applied for modeling. Firstly, waveband selection was performed using two approaches, i.e., succession projection algorithm (SPA) and its combination with genetic algorithm (SPA+GA). Secondly, multispectral models based on the two feature sets of wavebands were built via a total of six different modeling methods, i.e., partial least squares regression (PLSR) and extreme learning machine (ELM) in their respective stand-alone versions, their applications combined with genetic algorithm (GA), and their ensemble enhancements with modified Adaboost.RT (MAdaboost.RT). Analysis of accuracy and computational expense showed that supervised feature selection with SPA+GA was superior to unsupervised SPA for better modeling accuracy. MAdaboost.RT-ELM showed high accuracy at low computational expense. ELM models were the better base models than the PLSR ones, for being more randomized and diverse. It indicates that MAdaboost.RT-ELM on SPA is the best choice for a quick test on a newly available dataset, while switching the dimensionality reduction from SPA to SPA+GA may yield more accurate models with added, but well worthy, computational expense.

Background Cerebral embolism after lobectomy is a life-threatening complication during the early postoperative period. However, it is unclear if cerebral embolism can develop after segmentectomy. Case presentation We experienced a case of a 37-year-old man who demonstrated early symptom of acute ischemic stroke in early postoperative period after right upper posterior segmentectomy and performed intra-arterial mechanical thrombectomy (IAMT) successfully. Conclusions Long and irregular pulmonary vein stump (PVS) and endothelial injury caused by surgical procedure may lead to cerebral embolism after segmentectomy. We believe that doing preoperative pulmonary vascular assessment and using appropriate surgical procedure may reduce the rate of cerebral embolism.

Digital volume correlation (DVC) is a powerful and widely used technique for measuring the internal 3D deformation field of a wide range of materials. One of the most popular DVC algorithms is the reliability-guided DVC (RG-DVC) which is good at dealing with large continuous deformation. However, RG-DVC requires a manually specified seed from which computation starts, and suffers from the efficiency due to a huge amount of computation and data dependency. This paper proposes a GPU accelerated parallel reliability-guided DVC algorithm (CuSIFT-RGDVC) on CUDA, which leverages 3D scale-invariant feature transform (3D SIFT) to assist seed selection to realize fully automation and improves performance utilizing GPU computing. In CuSIFT-RGDVC, reliability-guided displacement tracking (RGDT) is rewritten using sorted array-based batch processing mechanism which is a globally sequential locally parallel model, and multi-granularity parallelism is adopted to maximize GPU utilization. The empirical result shows that the proposed CuSIFT-RGDVC provides up to 29.1x speedup compared with our multi-threaded implementation and achieves the same level of computation speed as the state-of-the-art path-independent DVC without sacrificing accuracy.

A novel path independent digital volume correlation (DVC) method is proposed, in which the internal deformation field is determined with the aid of the features extracted from the volume images. The deformation vector at each point of interest is first estimated by tracking the motion of the nearby keypoints obtained through 3D scale-invariant feature transform (SIFT), and then fed as the initial guess into the 3D inverse compositional Gauss-Newton algorithm to achieve high accuracy result. Benefiting from the robustness of SIFT to various deformation and distortion of image, the proposed DVC method demonstrates outstanding performance to automatically process the volume images containing large and complex deformation, which keep challenging to current DVC methods for decades. The proposed DVC method is further powered by the parallel computing on GPU. An ultrafast computation speed (about 10,000 POI/s) can be reached on a personal computer when dealing with the volume images of normal sizes. The 3D SIFT aided DVC method, which achieves unprecedented balance between accuracy, adaptability, and efficiency, shows great potential in the quantitative analysis of internal deformation.

Current iterative digital image correlation (DIC) algorithms can efficiently converge at the deformation vector with high accuracy when they are fed with reliable initial guess. Thus, the adaptability of DIC method is dominated to a large extent by the estimation of initial guess. In recent years, image feature-based technique, especially the scale-invariant feature transform (SIFT), was introduced to DIC for the estimation of initial guess in the case of large and complex deformation, due to its robustness in handling the images with translation, rotation, scaling, and localized distortion. However, feature extraction and matching in SIFT are very time consuming, which limits the applications of the SIFT-aided DIC. In this study, we developed a SIFT-aided path-independent DIC method and accelerated it by introducing the parallel computing on graphics processing unit (GPU) or multi-core CPU. In our method, SIFT features are used to estimate the initial guess for the inverse compositional Gauss-Newton (IC-GN) algorithm at each point of interest (POI). The experimental study shows that the developed method can deal with large and inhomogeneous deformation with high accuracy. Parallel computing (especially on GPU) accelerates significantly the proposed DIC method. The achieved computation speed satisfies the need for real-time processing with high resolution for the images of normal sizes.

Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Here, we studied the hemodynamic changes in tachycardia or volume-overload HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, respectively) on carotid, femoral, and renal arteries function and molecular expression. The ejection fraction was reduced by 50% or 30% in tachycardia or volume-overload model in four weeks, respectively. The LV end diastolic volume was increased from 65 ± 22 to 115 ± 78 ml in tachycardia and 67 ± 19 to 148 ± 68 ml in volume-overload model. Flow reversal was observed in diastolic phase in carotid artery of both models and femoral artery in volume-overload model. The endothelial function was also significantly impaired in carotid and renal arteries of tachycardia and volume-overload animals. The endothelial dysfunction was observed in femoral artery of volume-overload animals but not tachycardia animals. The adrenergic receptor-dependent contractility decreased in carotid and femoral arteries of tachycardia animals. The protein expressions of NADPH oxidase subunits increased in the three arteries and both animal models while expression of MnSOD decreased in carotid artery of tachycardia and volume-overload model. In conclusion, different HF models lead to variable arterial hemodynamic changes but similar vascular and molecular expression changes that reflect the role of both local hemodynamics as well as systemic changes in HF.

An increase in pulse pressure (PP) is highly associated with hypertension. The goal of this study was to determine the effect of increased aortic stiffness on PP and endothelial dysfunction as precursors to hypertension. A rat model of suddenly increased aortic stiffness by use of a nonconstrictive restraint (glue coating) on aortic surface was created to investigate the change of PP and mean arterial pressure (MAP). Group I ( n = 16) underwent aorta restraint for 4 wk. Group II ( n = 12) underwent aortic restraint for 4 wk, followed by restraint removal to evaluate extent of reversibility for additional 4 wk. The aortic and peripheral endothelial function was assessed by ACh-stimulated endothelium-dependent vasodilation. The level of nitrate/nitrite (NOx), endothelin-1 (ET-1), and prostacyclin (PGI2) were measured in the serum and artery tissue. We found that aortic stiffening causes a significant increase in PP and MAP ( P < 0.05). The endothelial function was markedly blunted ( P < 0.05) in both aorta and small peripheral artery. After removal of the restraint, the impaired endothelium function persisted in the aorta likely due to sustained deterioration of aortic wall, but was partially restored in peripheral artery. The endothelial dysfunction was correlated with a decrease in NOx and PGI2 ( P < 0.05) and an increase in ET-1 ( P < 0.05). Our results show that aortic stiffening results in widening of PP, which affected endothelium function through changes in synthesis of NOx, ET-1, and PGI2. These findings suggest that increased aortic stiffness may be a cause of increased PP and a precursor to hypertension.

Slow moving blood flow and changes in flow direction, e.g., negative wall shear stress, can cause increased superoxide (O2·−) production in vascular endothelial cells. The mechanism by which shear stress increases O2·−production, however, is not well established. We tested the hypothesis that actin depolymerization, which occurs during flow reversal, mediates O2·−production in vascular endothelial cells via NADPH oxidase, and more specifically, the subunit p47phox. Using a swine model, we created complete blood flow reversal in one carotid artery, while the contralateral vessel maintained forward blood flow as control. We measured actin depolymerization, NADPH oxidase activity, and reactive oxygen species (ROS) production in the presence of various inhibitors. Flow reversal was found to induce actin depolymerization and a 3.9 ± 1.0-fold increase in ROS production as compared with forward flow. NADPH oxidase activity was 1.4 ± 0.2 times higher in vessel segments subjected to reversed blood flow when measured by a direct enzyme assay. The NADPH oxidase subunits gp91phox(Nox2) and p47phoxcontent in the vessels remained unchanged after 4 h of flow reversal. In contrast, p47phoxphosphorylation was increased in vessels with reversed flow. The response caused by reversed flow was reduced by in vivo treatment with jasplakinolide, an actin stabilizer (only a 1.7 ± 0.3-fold increase). Apocynin (an antioxidant) prevented reversed flow-induced ROS production when the animals were treated in vivo. Cytochalasin D mimicked actin depolymerization in vitro and caused a 5.2 ± 3.0-fold increase in ROS production. These findings suggest that actin filaments play an important role in negative shear stress-induced ROS production by potentiating NADPH oxidase activity, and more specifically, the p47phoxsubunit in vascular endothelium.