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Abstract Objective To compare neuronavigation-assisted intracerebral hematoma puncture and drainage with neuroendoscopic hematoma removal for treatment of hypertensive cerebral hemorrhage. Method Ninety-one patients with hypertensive cerebral hemorrhage admitted to our neurosurgery department from June 2022 to May 2023 were selected: 47 patients who underwent endoscopic hematoma removal with the aid of neuronavigation in observation Group A and 44 who underwent intracerebral hematoma puncture and drainage in control Group B. The duration of surgery, intraoperative bleeding, hematoma clearance rate, pre- and postoperative GCS score, National Institutes of Health Stroke Scale (NIHSS) score, mRS score and postoperative complications were compared between the two groups. Results The duration of surgery, intraoperative bleeding and hematoma clearance were significantly lower in Group B than in Group A (p

Abstract Osteoclasts are over-activated as we age, which results in bone loss. Src deficiency in mice leads to severe osteopetrosis due to a functional defect in osteoclasts, indicating that Src function is essential in osteoclasts. G-protein-coupled receptors (GPCRs) are the targets for ∼35% of approved drugs but it is still unclear how GPCRs regulate Src kinase activity. Here, we reveal that GPR54 activation by its natural ligand Kisspeptin-10 (Kp-10) causes Dusp18 to dephosphorylate Src at Tyr 416. Mechanistically, Gpr54 recruits both active Src and the Dusp18 phosphatase at its proline/arginine-rich motif in its C terminus. We show that Kp-10 binding to Gpr54 leads to the up-regulation of Dusp18. Kiss1, Gpr54 and Dusp18 knockout mice all exhibit osteoclast hyperactivation and bone loss, and Kp-10 abrogated bone loss by suppressing osteoclast activity in vivo. Therefore, Kp-10/Gpr54 is a promising therapeutic target to abrogate bone resorption by Dusp18-mediated Src dephosphorylation.

Abstract Putrescine plays a role in superficial scald development during the cold storage of pear fruit. However, the molecular mechanism behind this phenomenon has not been un-fully clarified until recently. In this study, a conjoint analysis of metabolites and gene expression profiles in the putrescine-metabolic pathway of P. bretschneideri Rehd. fruit followed by experimental validation revealed that PbrADC1, forming a homodimer in the chloroplast, was involved in putrescine biosynthesis and thus fruit chilling resistance. Additionally, the substrate-binding residue Cys546 in PbrADC1, whose activity was modified by H2O2, played a crucial role in arginine decarboxylation into agmatine. Through a combined analysis of the distribution of cis-acting elements in the PbrADC1 promoter as well as the expression profiles of related transcription factors (TFs), several TFs were identified as upstream regulators of PbrADC1 gene. Further investigation revealed that the nuclear PbrWRKY62 could directly bind to the W-box elements in the PbrADC1 promoter, activate its expression, enhance putrescine accumulation, and thus increase fruit chilling tolerance. In conclusion, our results suggest that the PbrWRKY62-PbrADC1 module is involved in the development of superficial scald in P. bretschneideri Rehd. fruit via regulating putrescine biosynthesis. Consequently, these findings could serve as valuable genetic resources for breeding scald-resistant pear fruit. Graphical Abstract

Microstructured reactors offer fast chemical engineering transfer and precise microfluidic control, enabling the determination of reactions’ kinetic parameters. This review examines recent advancements in measuring microreaction kinetics. It explores kinetic modeling, reaction mechanisms, and intrinsic kinetic equations pertaining to two types of microreaction: esterification and transesterification reactions involving acids, bases, or biocatalysts. The utilization of a micro packed-bed reactor successfully achieves a harmonious combination of the micro-dispersion state and the reaction kinetic characteristics. Additionally, this review presents micro-process simulation software and explores the advanced integration of microreactors with spectroscopic analyses for reaction monitoring and data acquisition. Furthermore, it elaborates on the control principles of the micro platform. The superiority of online measurement, automation, and the digitalization of the microreaction process for kinetic measurements is highlighted, showcasing the vast prospects of artificial intelligence applications.

Pyroptosis, a unique lytic programmed cell death, inspired tempting implications as potent anti-tumor strategy in pertinent to its potentials in stimulating anti-tumor immunity for eradication of primary tumors and metastasis. Nonetheless, rare therapeutics have been reported to successfully stimulate pyroptosis. In view of the intimate participation of reactive oxygen species (ROS) in stimulating pyroptosis, we attempted to devise a spectrum of well-defined subcellular organelle (including mitochondria, lysosomes and endoplasmic reticulum)-targeting photosensitizers with the aim of precisely localizing ROS (produced from photosensitizers) at the subcellular compartments and explore their potentials in urging pyroptosis and immunogenic cell death (ICD). The subsequent investigations revealed varied degrees of pyroptosis upon photodynamic therapy (PDT) towards cancerous cells, as supported by not only observation of the distinctive morphological and mechanistic characteristics of pyroptosis, but for the first-time explicit validation from comprehensive RNA-Seq analysis. Furthermore, in vivo anti-tumor PDT could exert eradication of the primary tumors, more importantly suppressed the distant tumor and metastatic tumor growth through an abscopal effect, approving the acquirement of specific anti-tumor immunity as a consequence of pyroptosis. Hence, pyroptosis was concluded unprecedently by our proposed organelles-targeting PDT strategy and explicitly delineated with molecular insights into its occurrence and the consequent ICD.

With the introduction of Earth observation satellites, the classification technology through high-definition remote sensing images appeared. After decades of evolution, the land cover classification method in high-definition satellite maps has been gradually improved. Recently, high-definition remote sensing maps have been applied to land cover classification. Nowadays, classification methods using high-definition maps have these following problems. First, the traditional land cover classification methods cannot process the rich details in high-definition maps. Second, there are different acquisition conditions in the maps of different regions, which leads to distortion, deformation, and illumination blur of remote sensing images. Third, the existing methods are unable to provide a good generalization performance. To address these issues, a dual-branch parallel network structure is proposed, called Sgformer, to improve the performance of the transformer in the context of high-definition remote sensing maps. The network enhances perceptual learning with convolution operators that extract local features and a self-attention module that captures global representations. Local information and global representations with semantic divergence are fused through a feature coupling module. At last, a decoder is designed to maximize the preservation of local features and global representations and to better recover high-definition feature maps. The results of semantic segmentation experiments show that the methodology in this study has higher accuracy than the other methodologies.

In the previous years, vision transformer has demonstrated a global information extraction capability in the field of computer vision that convolutional neural network (CNN) lacks. Due to the lack of inductive bias in vision transformer, it requires a large amount of data to support its training. In the field of remote sensing, it costs a lot to obtain a significant number of high-resolution remote sensing images. Most existing change detection networks based on deep learning rely heavily on the CNN, which cannot effectively utilize the long-distance dependence between pixels for difference discrimination. Therefore, this work aims to use a high-performance vision transformer to conduct change detection research with limited data. A bibranch fusion network based on axial cross attention (ACABFNet) is proposed. The network extracts local and global information of images through the CNN branch and transformer branch, respectively, and then, fuses local and global features by the bidirectional fusion approach. In the upsampling stage, similar feature information and difference feature information of the two branches are explicitly generated by feature addition and feature subtraction. Considering that the self-attention mechanism is not efficient enough for global attention over small datasets, we propose the axial cross attention. First, global attention along the height and width dimensions of images is performed respectively, and then cross attention is used to fuse the global feature information along two dimensions. Compared with the original self-attention, the structure is more graphics processing unit friendly and efficient. Experimental results on three datasets reveal that the ACABFNet outperforms existing change detection algorithms.

Cloud detection is one of the important links in high-resolution remote sensing image processing. Cloud detection methods can be mainly divided into the following three categories: threshold methods, clustering methods based on machine learning, and deep learning methods. The traditional threshold method needs cumbersome manual calibration, which has high cost and poor universality. The generalization of clustering-based method is very poor. In addition, existing deep learning methods tend to have many model parameters and high training costs. To solve the abovementioned problems, a light-weighted cloud detection network (LCDNet) based on deep learning method is proposed. The network can complete the task of high-precision segmentation with less parameters and computation. Its light-weighted bottleneck layer can quickly capture the multiscale feature information in the image and segment the cloud with high efficiency. The gated channel excitation module can effectively reduce the feature redundancy in the network, so as to highlight the details of the cloud layer and improve the detection accuracy. The function of light-weighted self attention module is to quickly establish the spatial location information in the feature map, so as to locate the unpredictable targets and reduce the false detection rate. The experimental results show that the model shows an excellent performance on cloud and cloud shadow datasets with 353.76 k parameters and 456.28 Mmac computation. In addition, the training results on GF1_WHU and L8 Biome datasets further show that our model has an excellent generalization performance, which is of great significance for the efficient implementation of cloud detection.

Understanding surface changes requires the ability to identify changes in high resolution remote sensing images. Because current deep learning-based change detection algorithms are not able to accurately discriminate between altered and unmodified areas, which leads to the problem of edge uncertainty and small target missing in the detection process. To identify changes in high resolution remote sensing images, this research proposes an unique Attention-Guided Siamese Network (SAGNet). In this network, bitemporal images’ highly representative deep semantic features are retrieved using a fully convolutional dual-stream architecture, and the extracted deep semantic features are then used to extract semantic variation data from the Global Semantic Aggregation Module (GSAM). In the feature decoding stage, the extracted features are refined layer by layer through the Attention Fusion Module (AFM) for change map reconstruction. In addition, we propose two other auxiliary modules: Cross-scale Fusion Module (CFM) and Bilateral Feature Fusion Module (BFFM), which enable the network to remove background noise while improving the recognition accuracy of changing object boundaries and small-changing targets in the output change map. A public dataset called LEVIR-CD and a challenging dataset called BICD made up of bitemporal images from Google Earth covering various parts of China are used to experimentally test SAGNet. Finally, experimental evidence shows that our approach outperforms current cutting-edge change detection techniques.

In Remote Sensing(RS) data analysis, Remote Sensing Change Detection(CD) is an important technology. The existing Remote Sensing Change Detection(RS-CD) methods do not fully consider the advantages and disadvantages of Convolution and Transformer in feature extraction, which will restrict the overall performance of the network to a certain extent. Therefore, this paper proposes a Dual Branch Feature Guided Aggregation Network composed of convolutional neural network(CNN) and Transformer. In the encoding stage, based on the respective characteristics of Convolution and Transformer, a dual-branch backbone network is constructed to extract the spatial information and semantic information of the image respectively; And through the Feature Guidance Aggregation Module, the two branches can guide each other for feature mining, so as to avoid the occurrence of false detection and missed detection of change areas due to insufficient fusion to the greatest extent. Finally, in the decoding stage, the different levels of features extracted by the two branches are fully used for fusion and decoding. And the experiment shows that compared with the existing methods, the mean intersection over union(MIoU) index on the four public datasets are improved by 1.25%, 1.55%, 1.38% and 1.71%.

Plant regeneration through somatic embryogenesis provides a solution for maintaining and genetically improving crop or fruit varieties with desirable agronomic traits. For the fruit tree pomegranate (Punica granatum L.), despite some successful applications, the existing somatic embryogenesis protocols are limited by low availability of explants and susceptibility to browning. To address these problems, in this study, we developed an effective system for induction of high-vigor pomegranate somatic embryos derived from stem explants. The usage of stem explants breaks through the difficulty in obtaining material, thus making our system suitable for widespread commercial production. To enhance the performance of our system, we identified the optimal explants, subculture cycles and combination of basal media and plant growth regulators for each step. The results showed that inoculating stem explants onto a Murashige and Skoog (MS) medium supplemented with 1.0 mg/L 6-benzylaminopurine (6-BA) and 1.0 mg/L 1-naphthaleneacetic acid (NAA) achieved the best induction rate and growth status of pomegranate calli (induction rate = ~72%), and MS medium containing 0.5 mg/L 6-BA and 1.0 mg/L NAA was the optimal condition for the induction of embryogenic calli and somatic embryos (induction rate = ~74% and 79%, respectively). The optimal subculture period for embryogenic calli was found to be 30–35 days. Strong roots were then induced in the developed somatic embryo seedlings, which survived and grew well after transplantation to the natural environment, indicating the good vitality of the induced pomegranate somatic embryos. Together, our system provides a solution to mass somatic embryo induction and plant regeneration of pomegranate and lays a foundation for future genetic transformation and bioengineering improvement of pomegranate with favorable agronomic traits.

Objective: Tyloxapol is a non-ionic surfactant with diverse pharmacological effects including anti-inflammatory, anti-malignant tumor and antioxidant activities. However, the effect of tyloxapol on osteoclastogenesis has not been elucidated. In this study, we intended to clarify the effect of tyloxapol on RANKL-stimulated osteoclastogenesis and the molecular mechanism both ex vivo and in vivo. Methods: In vitro osteoclastogenesis assay was performed in BMMs and Raw 264.7 cells. The mature osteoclasts were visualized by TRAP staining. The osteoblsats were visualized by alkaline phosphatase (ALP) staining and Von Kossa staining. To assess whether tyloxapol inhibited the function of mature osteoclasts, F-actin belts and pit formation assays were carried out in BMMs. To evaluate the effect of tyloxapol on post-menopausal osteoporosis, the OVX mouse model were utilized. The bone tissue TRAP staining was used to evaluate the osteoclast activity in vivo. The von kossa staining and micro computed tomography were used to evaluate the histomorphometric parameters. The Goldner's staining was used to evaluate the osteoblast activity. The expression of osteoclastogenesis-associated markers were evaluated by Real-time PCR. The NF-κB and NFATc1 transcriptional activities were illustrated utilizing the assay of luciferase reporter. The effect of tyloxapol pretreatment on IκBa degradation and p65 phosphorylation was evaluated using Western bloting assay. The effect of tyloxapol pretreatment on p65 nuclear translocation was evaluated utilizing immunofluorescence. The effect of tyloxapol pretreatment on the phosphorylatio of ERK, p38 and JNK was examined utilizing Western bloting assay. Results: In our research, we found that tyloxapol suppresses RANKL-stimulated osteoclastogenesis in a dose dependent manner and in the initial stage of osteoclastogenesis. Through F-actin belts and pit formation assays, we found that tyloxapol had the ability to inhibit the function of mature osteoclasts in vitro. The results of animal experiments demonstrated that tyloxapol inhibits OVX-induced bone mass loss by inhibiting the activity of osteoclasts but had a limited effect on osteoblastic differentiation and mineralization. Molecularly, we found that tyloxapol suppresses RANKL-stimulated NF-κB activation through suppressing degradation of IκBα, phosphorylation and nuclear translocation of p65. At last, MAPK signaling pathway was also suppressed by tyloxapol in dose and time-dependent manners. Conclusion: Our research illustrated that tyloxapol was able to suppress osteoclastogenesis in vitro and ovariectomized-induced bone loss in vivo by restraining NF-κB and MAPK activation. This is pioneer research could pave the way for the development of tyloxapol as a potential therapeutic treatment for osteoporosis. The translational potential of this article: This study explores that tyloxapol, also known as Triton WR-1339, may be a drug candidate for osteoclastogenic sicknesses like osteoporosis. Our study may also extend the clinical therapeutic spectrum of tyloxapol.

Abstract Background Scar formation, which may be caused by myofibroblast aggregations, is the greatest challenge during skin wound healing in the clinical setting. Studies have indicated that epidermal stem cells (EPSC) improve wound healing and reduce scar formation. Methods We investigated the therapeutic effects of EPSC-derived exosomes (EPSC-Exos) on skin wound healing in a skin-defect rat model. We also examined the roles of EPSC-Exos-specific microRNAs in inhibiting the differentiation of human dermal fibroblasts (HDF) into myofibroblasts. Results We found that EPSC-Exos increased the wound healing rate and reduced scar formation in rats. Also, EPSC-Exos improved the regeneration levels of skin appendages, nerves and vessels, as well as the natural distribution of collagen. Furthermore, we found these functions may be achieved by inhibiting the activity of transforming growth factor-β1 (TGF-β1) and its downstream genes. The results showed that some specific microRNAs, including miR-16, let-7a, miR-425-5p and miR-142-3p, were enriched in EPSC-Exos. EPSC-Exos-specific microRNAs, especially miR-425-5p and miR-142-3p, played vital roles in inhibiting myofibroblast differentiation via reducing the TGF-β1 expression in dermal fibroblasts. Conclusion We found a novel function of EPSC-Exos-specific microRNAs, suggesting that EPSC-Exos might represent a strategy to prevent scar formation during wound healing in the clinical setting.

Link prediction is a hot issue in information filtering. Link prediction algorithms, based on local similarity indices, are widely used in many fields due to their high efficiency and high prediction accuracy. However, most existing link prediction algorithms are available for unweighted networks, and there are relatively few studies for weighted networks. In the previous studies on weighted networks, some scholars pointed out that links with small weights play a more important role in link prediction and emphasized that weak-ties theory has a significant impact on prediction accuracy. On this basis, we studied the edges with different weights, and we discovered that, for edges with large weights, this weak-ties theory actually does not work; Instead, the weak-ties theory works in the prediction of edges with small weights. Our discovery has instructive implications for link predictions in weighted networks.

Remote sensing image change detection is an essential aspect of remote sensing technology application. Existing change detection algorithms based on deep learning do not distinguish between changed and unchanged areas explicitly, resulting in serious loss of edge detail information during detection. Therefore, a new attentional change detection network based on Siamese U-shaped structure (SUACDNet) is proposed in this paper. In the feature encoding stage, three branches are introduced between the Siamese structure to focus on the global information, difference information and similarity information of bitemporal images respectively. In the feature decoding stage, an U-shaped structure is constructed for upsampling and recovery layer by layer. Multi-scale Convolution Residual Module (MCRM) is a new convolution structure designed for multi-scale feature extraction in the network. In addition, this work also proposes three auxiliary modules to optimize the network, namely Spatial Attention Module (SAM), Feature Fusion Module (FFM) and Cross-scale Global Context Semantic Information Aggregation Module (CGCAM), making the network more sensitive to the changed area while filtering out the background noise. Comparative experiments on three datasets show that our method is superior to the existing methods.

Obesity has a strong impact on the pathogenesis of cardiovascular disease, which raises enthusiasm to understand how excess adiposity causes vascular injury. Adipose tissue is an essential regulator of cardiovascular system through its endocrine and paracrine bioactive products. Obesity induces endothelial dysfunction, which often precedes and leads to the development of cardiovascular diseases. Connecting adipose tissue-endothelial cell interplay to endothelial dysfunction may help us to better understand obesity-induced cardiovascular disease. This Mini Review discussed (1) the general interactions and obesity-induced endothelial dysfunction, (2) potential targets, and (3) the outstanding questions for future research.

Abstract Background Polygalacturonase (PG), as an important hydrolase participating in the degradation of pectin, plays an important role in softening process of fruit. However, information on PG gene family in pear genome and the specific member involved in fruit softening is still rudimentary. Results In this study, a total of 61 PG genes, which could be divided into six subclasses, were identified from the pear genome with diverse chromosome locations, gene structures, motifs and cis-acting elements. Most PbrPGs were derived from WGD/segmental duplication blocks, and purifying selection was the main driving force for their expansion. The expression profiles of PbrPGs in pear were tissue/development-stage/cultivar-dependent. During ‘Housui’ pear storage, associated with the reduction of firmness was the accumulation of PG activity. Totally, 28 PbrPGs were expressed during fruit storage, which could be classified into five categories based on different expression patterns; most demonstrated an increased trend. Of these, PbrPG6 were proposed to account for pear softening in combination of the phylogenetic and correlation analysis among firmness, PG activity and PbrPGs. By constructing the silencing vector, a higher firmness was observed in PbrPG6-silenced fruit when compared with that of the control (empty vector). In a further study, we found that the expression of PbrPG6 was regulated by postharvest 1-MCP/ethrel treatment, and several PbrERFs might function in this process. Conclusions We identified 61 PbrPG genes from pear genome; of these, PbrPG6 was involved in fruit softening process; furthermore, the expression of PbrPG6 might be under the control of PbrERF. This study provides a foundation for future work aimed at elucidating the molecular mechanism underlying pear softening.

The internal gear grease pump is a mechanical device used for transfer of high viscosity fluid. The existing clearance between the end faces of the internal or external gear and the floating side plate might cause pump leakage during operation. In order to obtain the optimal end clearance of the internal gear grease pump, the rheological features of the lubricating lithium-based grease for various temperatures are explored via rotating rheometer. Shear force and apparent viscosity are chosen as monitored experimental parameters. The experimental data is fitted to obtain grease rheological features at various temperatures. The end clearance flow field model and the leakage model are established. Fluent software is employed for solving the flow field model and exploring the effect of temperature, end clearance, and speed on grease leakage. Superior grease flow performance is observed with an increase in temperature, which makes it to easier for the grease to leak from the end clearance. With an increase in the end clearance and the working pressure of the pump, an increase in leakage is also observed. Furthermore, it is found that rotational speed also affects the pump leakage. The leakage mechanism is obtained by combining the rheological features of the grease at the end clearance. The mathematical model method is utilized to solve for the optimal value of the end clearance.

Background/Aims: Giant cell tumor of bone (GCTB), one of the most common primary bone tumors, leads to extensive bone destruction. However, the mechanisms underlying GCTB progression remain elusive and prognostic factors and treatment targets are required. In the current study, we explored the function of the chemokine family member CCL20 in GCTB progression. Methods: We explored the expression of CCL20 in stromal cells (GCTSCs) using microarray. Clinical analyses of the role of CCL20 in tumor progression were performed based on the patient cohort of our institution. The role of CCL20 in tumor proliferation was evaluated by MTS assay, migration ability was measured by a Transwell assay, and osteoclastogenesis was induced by CCL20 or GCTSC-conditioned medium. Quantitative PCR and western blot were used to measure the expression levels of mRNAs and proteins related to tumor progression. Results: CCL20 was upregulated in GCTSCs and correlated with tumor progression and prognosis. CCL20 induced GCTSC proliferation and migration in an autocrine manner. In addition, CCL20 recruited mononuclear cells and induced osteoclastogenesis by overactivating the AKT and NF-κB signaling pathways. Antibody blockade of CCL20 abolished the exacerbated osteoclastogenesis. Conclusion: Taken together, our data indicate that GCTSC secretion of CCL20 acts as a key modulator in the pathological progression of GCTB. It can promote GCTSC proliferation and migration in an autocrine manner and can recruit bone marrow monocytes to the tumor microenvironment and enhance osteoclastogenesis in a paracrine manner. These findings strongly indicate the potential prognostic and therapeutic value of CCL20 in GCTB.

Abstract TMC-incorporated carbon nitride (CN) with hexagonal and quadrangle honeycomb-like structure and having periodic lattice defects linked by –CONH– bond was synthesized through combining the high calcination with the chemical condensation of melamine and 1,3,5-benzenetricarbonyl trichloride. The obtained CN has a tri-s-triazine ring and benzene ring skeleton, which makes it have excellent mechanical and thermal stability. The BET specific surface area was enhanced to about 125.6 m2/g, and the mean pore size is about 3.43 nm. This CN exhibited an excellent adsorption-enhanced photocatalytic performance. Graphical abstract

Background/Aims: In our previous study, we demonstrated that elevated expression of miR-328 is a potent determinant of cardiac fibrosis during myocardial infarction (MI). In the present study, histological examination revealed progressive fibrosis in transgenic mice overexpressing cardiomyocyte-specific miR-328. This study investigated whether the transfer of miR-328 from cardiomyocytes (CMs) to cardiac fibroblasts (CFs) in a paracrine manner contributes to myocardial fibrosis. Methods: Myocardial infarction was established by the occlusion of the left coronary artery. Masson’s trichrome staining and collagen assays were used to evaluate the progression of fibrosis. The vesicles and translocation of miR-328 in a co-culture assay system were respectively observed using transmission electron microscopy (TEM) and immunofluorescence staining (IF). Real-time PCR was employed to detect the level of miR-328, Col1α1 and Col3α1. The protein expression of Col1α1, TGF-βRIII, p-smad2/3 (phosphorylated-smad2/3) and TGF-β1 were probed using western blot analysis. Results: Cardiomyocyte-specific miR-328 overexpressing transgenic (TG) mice showed enhanced collagen deposition and provoked cardiac fibrosis by the activation of the TGF-β1 pathway, and this effect was abrogated after knockdown of endogenous miR-328 in mice. Correspondingly, the expression of miR-328 was increased in CFs co-cultured with CMs transfected with miR-328 mimics, likely in a paracrine manner. The cardiomyocyte-mediated augmentation of miR-328 contributes to fibrogenesis in CFs, and this pro-fibrotic effect was reversed after the transfection of miR-328 inhibitor in CFs. Conclusion: A novel molecular mechanism for miR-328 derived from CMs as a paracrine signaling mediator of cardiac fibrogenesis further demonstrates that miR-328 is a potential therapeutic target.

Background/Aims: Cardiac interstitial fibrosis is an abnormality of various cardiovascular diseases, including myocardial infarction, hypertrophy, and atrial fibrillation, and it can ultimately lead to heart failure. However, there is a lack of practical therapeutic approaches to treat fibrosis and reverse the damage to the heart. The purpose of this study was to investigate the effect of long-term aspirin administration on pressure overload–induced cardiac fibrosis in mice and reveal the underlying mechanisms of aspirin treatment. Methods: C57BL/6 mice were subjected to transverse aortic constriction (TAC), and treated with 10 mg·kg-1·day-1 of aspirin for 4 weeks. Masson staining and a collagen content assay were used to detect the effects of aspirin on cardiac fibrosis in vivo and in vitro. Western blot and qRT-PCR were applied to examine the impact of aspirin on extracellular signal-regulated kinases (Erks), p-Akt/β-catenin, SerpinE2, collagen I, and collagen III levels in the mice heart. Results: Aspirin significantly suppressed the expression of α-smooth muscle actin (α-SMA; 1.19±0.19-fold) and collagen I (0.95±0.09-fold) in TAC mice. Aspirin, at doses of 100 and 1000 µM, also significantly suppressed angiotensin II-induced α-SMA and collagen I in cultured CFs. The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49±0.19-fold; p-Erk2, 1.96±0.68-fold) was suppressed by aspirin (p-Erk1, 1.04±0.15-fold; p-Erk2, 0.87±0.06-fold). SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36±0.12-fold for TAC; 1.06±0.07-fold for aspirin+TAC). The p-Akt and β-catenin levels were also significantly inhibited in vivo and in vitro. Conclusions: Our study reveals a novel mechanism by which aspirin alleviates pressure overload-induced cardiac interstitial fibrosis in TAC mice by suppressing the p-Erk1/2 and p-Akt/β-catenin signalling pathways.

Abstract Objective This paper presents the use of the texture matching method to measure the rabbit carotid artery elasticity value of the experimental group and control group respectively. It compares the experimental rabbits, when they are prompted by pathological histology to be at the period of carotid atherosclerosis fatty streaks and fiber plaques, with the control group. Methods We have used ultrasound linear array probe for scanning the rabbit carotid arteries. This allows us to obtain the wall shear stress (WSS) and the elasticity values in the atherosclerotic arteries. Using statistical analysis, we are able to clarify whether the texture matching method can diagnose atherosclerosis at the early stage. We also analyze the rabbit carotid artery elasticity and WSS values to make sure whether there is a correlation between both. Combining the texture matching method with the WSS quantitative analysis in the future can enable better prediction of the occurrence and development of atherosclerosis by using noninvasive medical imaging techniques. Results This study has confirmed that from the 2nd to the 10th week, with the development of atherosclerosis, the arterial WSS reduction has a negative correlation with the increasing of artery wall elasticity, which means that as the arterial WSS decreases the arterial wall becomes less elastic. Correlating shear stress with atherosclerosis can clarify that WSS can be used as one of the effective parameters of early diagnosis of atherosclerosis. Conclusion In summary, we have found that the elasticity value can reflect the degree of atherosclerosis more objectively. Therefore, by using noninvasive imaging, the quantitative analysis of shear stress and combined with texture matching method can assist in the early diagnosis of atherosclerosis.

Abstract Background This paper presents quantitative analysis of blood flow shear stress by measuring the carotid arterial wall shear stress (WSS) and the intima-media thickness (IMT) of experimental rabbits fed with high-fat feedstuff on a weekly basis in order to cause atherosclerosis. Methods This study is based on establishing an atherosclerosis model of high-fat rabbits, and measuring the rabbits’ common carotid arterial WSS of the experimental group and control group on a weekly basis. Detailed analysis was performed by using WSS quantification. Results We have demonstrated small significant difference of rabbit carotid artery WSS between the experimental group and the control group (P

Abstract Background We aim to present an unique case of inflammatory myofibroblastic tumor (IMT) of the brain parenchyma and study the clinical presentation, imagine characteristic, intraoperative findings, and histopathology features of IMT in the brain parenchyma. Case Presentation A 36-year-old female with IMT come to see doctor presented with a 3-month history of progressively worsening weakness in the left upper limb along with alalia. Serial magnetic resonance imaging studies revealed a lesion within the right frontal lobe. The lesions were locally clear boundary with peripheral tissues. A right frontotemporal craniotomy was performed and the specimens were detected by immunohistochemical staining and light microscopy. Through the microscope, the tumor was composed of large number of chronic inflammatory cells and spindle cells. From immunohistochemical stains, it demonstrated CD34 (+), SMA (+), Vimentin (+), and actin (+) were positive meanwhile S-100(-) was negative. Conclusion IMT of the right frontal lobe is a rare lesions. Surgical resection is the best and the most effective treatment.

After the implementation of "double reduction" policy, parental education anxiety becomes a hit subject in the society. Aimed to figure out formation logic and countermeasures of it, this paper adopts literature survey method, through numerous researches, discovers that on the one hand, the policy has comprehensively standardized cram schooling market, optimized the homework design and relieved students' burden, which renders the overall educational ecology sustainable. But on the other hand, affected by multiple factors, such as the weakening function of family education, the imbalance between the supply and demand of educational resources, single selection criterion and unpredictable educational deviation, parents' educational anxiety keeps swelling, bearing several features like the heterogeneity of anxiety, classification of anxious crowds, different stages of anxiety and intergenerational mobility. Therefore, only by synchronous implementation of multiple measures, reconstructing education ecological system, standardizing the policy and continuing to strengthen faculty force, can we relieve parental education anxiety and give a push to the genuine implementation of "double reduction" policy.

Background/Aims: Acute myocardial infarction (AMI) is a devastating cardiovascular disease with a high rate of morbidity and mortality, partly due to enhanced arrhythmogenicity. MicroRNAs (miRNAs) have been shown to participate in the regulation of cardiac ion channels and the associated arrhythmias. The purpose of this study was to test our hypothesis that miR-223-3p contributes to the electrical disorders in AMI via modulating KCND2, the gene encoding voltage-gated channel Kv4.2 that carries transient outward K+ current Ito. Methods: AMI model was established in male Sprague-Dawley (SD) rats by left anterior descending artery (LAD) ligation. Evans blue and TTC staining was used to measure infarct area. Ito was recorded in isolated ventricular cardiomyocytes or cultured neonatal rat ventricular cells (NRVCs) by whole-cell patch-clamp techniques. Western blot analysis was employed to detect the protein level of Kv4.2 and real-time RT-PCR to determine the transcript level of miR-223-3p. Luciferase assay was used to examine the interaction between miR-223-3p and KCND2 in cultured NRVCs. Results: Expression of miR-223-3p was remarkably upregulated in AMI relative to sham control rats. On the contrary, the protein level of Kv4.2 and Ito density were significantly decreased in AMI. Consistently, transfection of miR-223-3p mimic markedly reduced Kv4.2 protein level and Ito current in cultured NRVCs. Co-transfection of AMO-223-3p (an antisense inhibitor of miR-223-3p) reversed the repressive effect of miR-223-3p. Luciferase assay showed that miR-223-3p, but not the negative control, substantially suppressed the luciferase activity, confirming the direct binding of miR-223-3p to the seed site within the KCND2 sequence. Finally, direct intramuscular injection of AMO-223-3p into the ischemic myocardium to knockdown endogenous miR-223-3p decreased the propensity of ischemic arrhythmias. Conclusions: Upregulation of miR-223-3p in AMI repressed the expression of KCND2/Kv4.2 resulting in reduction of Ito density that can cause APD prolongation and promote arrhythmias in AMI, and therefore knockdown of endogenous miR-223-3p might be considered a new approach for antiarrhythmic therapy of ischemic arrhythmias.

Atherosclerosis is a chronic progressive inflammatory process that can eventually lead to cardiovascular disease (CVD). Despite available treatment, the prevalence of atherosclerotic CVD, which has become the leading cause of death worldwide, persists. Identification of new mechanisms of atherogenesis are highly needed in order to develop an effective therapeutic treatment. The blood vessels contain two primary major cell types: endothelial cells (EC) and vascular smooth muscle cells (VSMC). Each of these performs an essential function in sustaining vascular homeostasis. EC-VSMC communication is essential not only to development, but also to the homeostasis of mature blood vessels. Aberrant EC-VSMC interaction could promote atherogenesis. Identification of the mode of EC-VSMC crosstalk that regulates vascular functionality and sustains homeostasis may offer strategic insights for prevention and treatment of atherosclerotic CVD. Here we will review the molecular mechanisms underlying the interplay between EC and VSMC that could contribute to atherosclerosis. We also highlight open questions for future research directions.

β-galactosidases are cell wall hydrolases that play an important role in fruit softening. However, PpBGALs mechanism impacting on ethylene-dependent peach fruit softening was still unclear. In this study, we found that PpBGAL4, -6, -8, -10, -16, and -17 may be required for ethylene-dependent peach softening and PpBGAL10, -16 may make a main contribution to it among 17 PpBGALs. Utilization of virus-induced gene silencing (VIGS) showed that fruits were firmer than those of the control at 4 and 6 days after harvest (DAH) when PpBGAL10 and PpBGAL16 expression was down-regulated. Suppression of PpBGAL10 and PpBGAL16 expression also reduced PpPG21 and PpPME3 transcription, and polygalacturonase (PG) and pectinmethylesterases (PME) activity. Overall, total cell wall material and protopectin slowly declined, water-soluble pectin slowly increased, and cellulose and hemicellulose was altered significantly at 4 DAH, relative to control fruit. In addition, PpACO1 expression and ethylene production were also suppressed at 4 DAH because of inhibiting PpBGAL10 and PpBGAL16 expression. These results suggested that down-regulation of PpBGAL10 and PpBGAL16 expression delays peach fruit softening by decreasing PG and PME activity, which inhibits cell wall degradation and ethylene production.

Mechanical stimuli drives many physiological processes through mechanically activated channels, and the recent discovery of PIEZO channel has generated great interests in its mechanotransduction. Many previous researches investigated PIEZO proteins by transcribing them in cells that originally have no response to mechanical stimulation, or by forming PIEZO-combined complexes in vitro, and few studied PIEZO protein’s natural characteristics in cells. In this study we show that MDA-MB-231, a malignant cell in human breast cancer cell line, expresses the mechanosensitive behavior of PIEZO in nature without extra treatment, and we report its characteristics in response to localized mechanical stimulation under an atomic force microscope, wherein a correlation between the force magnitude applied and the channel opening probability is observed. The results on PIEZO of MDA-MB-231 can help establish a basis of preventing and controlling of human breast cancer cell via mechanical forces.

Obesity is a worldwide epidemic that predisposes individuals to metabolic complications, such as type 2 diabetes mellitus and non-alcoholic fatty liver disease, all of which are related to an imbalance between food intake and energy expenditure. Identification of the pathogenic molecular mechanisms and effective therapeutic approaches are urgently needed. A well-accepted paradigm is that crosstalk between organs/tissues contributes to diseases. Endothelial dysfunction characterizes metabolic disorders and the related vascular complications. Over the past two decades, overwhelming studies have focused on mechanisms that lead to endothelial dysfunction. New investigations, however, have begun to appreciate the opposite direction of the crosstalk: endothelial regulation of metabolism, although the underlying mechanisms remain to be elucidated. This review summarizes the evidence that supports the concept of endothelial regulation of obesity and the associated insulin resistance in fat, liver, and skeletal muscles, the classic targets of insulin. Outstanding questions and future research directions are highlighted. Identification of the mechanisms of vascular endothelial regulation of metabolism may offer strategies for prevention and treatment of obesity and the related metabolic complications.

Carotid plaque echogenicity is associated with the risk of cardiovascular events. Gray-scale median (GSM) of the ultrasound image of carotid plaques has been widely used as an objective method for evaluation of plaque echogenicity in patients with atherosclerosis. We proposed a computer-aided method to evaluate plaque echogenicity and compared its efficiency with GSM.One hundred and twenty-five carotid plaques (43 echo-rich, 35 intermediate, 47 echolucent) were collected from 72 patients in this study. The cumulative probability distribution curves were obtained based on statistics of the pixels in the gray-level images of plaques. The area under the cumulative probability distribution curve (AUCPDC) was calculated as its integral value to evaluate plaque echogenicity.The classification accuracy for three types of plaques is 78.4% (kappa value, κ = 0.673), when the AUCPDC is used for classifier training, whereas GSM is 64.8% (κ = 0.460). The receiver operating characteristic curves were produced to test the effectiveness of AUCPDC and GSM for the identification of echolucent plaques. The area under the curve (AUC) was 0.817 when AUCPDC was used for training the classifier, which is higher than that achieved using GSM (AUC = 0.746). Compared with GSM, the AUCPDC showed a borderline association with coronary heart disease (Spearman r = 0.234, p = 0.050).Our experimental results suggest that AUCPDC analysis is a promising method for evaluation of plaque echogenicity and predicting cardiovascular events in patients with plaques.

The influence of a minor strontium (Sr) modifier on the microstructures and mechanical properties of 7075 Al alloys was investigated in this paper. The grain size of cast 7075 Al alloys was refined from 157 μm to 115 μm, 108 μm, and 105 μm after adding 0.05 wt. %, 0.1 wt. %, and 0.2 wt. % Sr, respectively. The extruded 7075 Al alloys was refined with different degrees of Sr modifier. The mechanical properties were optimum when adding 0.1 wt. % Sr. The ultimate tensile strength (σb) increased from 573 to 598 MPa and the elongation-to-failure (δf) was raised from 19.5% to 24.9%. The microhardness increased from 182 to 195 Hv. The tensile fracture surface via scanning electron microscopy (SEM) revealed a transition from brittle fracture to ductile fracture as Sr increased from 0 wt. % to 0.2 wt. %. The result in this paper proved that the modifier can improve the properties of 7075 Al alloy.

Atherosclerosis is a chronic and systemic disease and its developmental process involves the synergism of multiple risk factors such as hypertension, dyslipidemia, diabetes, obesity and smoking. The diagnosis of subclinical atherosclerosis is essential for strategic guidance towards suitable treatments and efficient prevention against acute cardiovascular events. This study employed ultrasound radiofrequency (RF) tracking technology to characterize human carotid arteries in vivo in terms of intima-media thickness (IMT) and artery stiffness, and evaluated the statistical correlation between carotid IMT and stiffness, and the number of risk factors for atherosclerosis.A total of 160 asymptomatic subjects were enrolled. Ultrasound RF-tracking technology was employed to acquire carotid IMT and stiffness parameters: maximum IMT ((MAX)IMT), RF Quality IMT ((RF)QIMT), distensibility coefficient (DC), compliance coefficient (CC), αindex, β index and local pulse wave velocity (PWVβ). The subjects were categorized in four groups in terms of the number of risk factors: 'zero', 'single', 'double', and 'multiple', and statistical analyses of carotid IMT and stiffness parameters were performed between these different groups.The subjects (n = 145) with (MAX)IMT smaller than 1.0 mm matched the IMT criteria for non-atherosclerosis and were named as NA-subjects. Spearman's rho correlation analysis of the whole group and the NA-subjects both showed that (MAX)IMT correlated positively with (RF)QIMT, α, β, and PWVβ, and negatively with DC and CC (p

BACKGROUND: Carotid intima-media thickness (IMT) and elasticity have been shown to be independent predictors of cardiovascular disease (CVD). Cardiovascular risk factors (CVRFs) includes hypertension, dyslipidemia, diabetes, overweight and smoking. The objective was to investigate whether the clustering of three or more components of CVRFs has a greater impact on carotid IMT and elasticity than individual components of CVRFs. METHODS: One hundred and seventy-three participants without clinical CVD were classified as the multiple CVRFs patients with three or more CVRFs (n = 55) and control group with two or less CVRFs (n = 118). Carotid IMT and elastic modulus were measured by B-mode ultrasound and vessel texture matching method (VTMM), respectively. RESULTS: The multiple CVRFs conferred a disproportionate increase in carotid IMT (43%, p

There is a strong research interest in identifying the surface roughness of the carotid arterial inner wall via texture analysis for early diagnosis of atherosclerosis. The purpose of this study is to assess the efficacy of texture analysis methods for identifying arterial roughness in the early stage of atherosclerosis. Ultrasound images of common carotid arteries of 15 normal mice fed a normal diet and 28 apoE(-/-) mice fed a high-fat diet were recorded by a high-frequency ultrasound system (Vevo 2100, frequency: 40 MHz). Six different texture feature sets were extracted based on the following methods: first-order statistics, fractal dimension texture analysis, spatial gray level dependence matrix, gray level difference statistics, the neighborhood gray tone difference matrix, and the statistical feature matrix. Statistical analysis indicates that 11 of 19 texture features can be used to distinguish between normal and abnormal groups (p

Blown-powder laser surface alloying was performed on the magnesium alloy AZ91D with Al–Si alloy powder to improve corrosion resistance. Characterization by scanning electron microscopy (SEM), energy dispersive spectroscopy (EDS) and x-ray diffraction (XRD) analysis revealed that intermetallic compounds (IMCs) of Mg2Si, Al12Mg17 and Al3Mg2 were formed in the matrix of α-Mg and Al solid solutions in Al–Si alloyed layers. The anodic polarization test in 3.5% NaCl aqueous solution showed that preferential corrosion occurred in the α-Mg matrix of the AZ91D base metal. The Al–Si alloyed layers exhibited a lower corrosion rate and a higher polarization resistance than AZ91D. The compactly dispersed dendritic Mg2Si phase, and the dendritic and angular phases of Al12Mg17 and Al3Mg2 in the alloyed microstructure were observed to be corrosion-resistant, constituting a barrier that retards corrosion. Corrosion initiated at the interface between IMCs and the solid solution matrix, and at substructures of the matrix, subsequently pervaded into the surrounding microstructure.

Thrombosis and inflammation are primary contributors to the onset and progression of ischemic stroke. The contactkinin pathway, initiated by plasma kallikrein (PK) and activated factor XII (FXIIa), functions bidirectionally with the coagulation and inflammation cascades, providing a novel target for therapeutic drug development in ischemic stroke. In this study, we identified a bat-derived oligopeptide from Myotis myotis (Borkhausen, 1797), designated LE6 (Leu-Ser-Glu-Glu-Pro-Glu, 702 Da), with considerable potential in stroke therapy due to its effects on the contact kinin pathway. Notably, LE6 demonstrated significant inhibitory effects on PK and FXIIa, with inhibition constants of 43.97 μmol/L and 6.37 μmol/L, respectively. In vitro analyses revealed that LE6 prolonged plasma recalcification time and activated partial thromboplastin time. In murine models, LE6 effectively inhibited carrageenan-induced mouse tail thrombosis, FeCl3-induced carotid artery thrombosis, and photochemically induced intracerebral thrombosis. Furthermore, LE6 significantly decreased inflammation and stroke injury in transient middle cerebral artery occlusion models. Notably, the low toxicity, hemolytic activity, and bleeding risk of LE6, along with its synthetic simplicity, underscore its clinical applicability. In conclusion, as an inhibitor of FXIIa and PK, LE6 offers potential therapeutic benefits in stroke treatment by mitigating inflammation and preventing thrombus formation. [ABSTRACT FROM AUTHOR]