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With the increasing demand of security industry,abnormal crowd behavior detection has become a hot research issue in computer vision.Abnormal crowd behavior detection aims to model and analyze the behavior of pedestrians in surveillance videos,distinguish between normal and abnormal behaviors in the crowd,and discover disasters and accidents in time.A large number of algorithms for abnormal crowd behavior detection based on deep learning are summarized in this paper.First,abnormal crowd behavior detection task and its current research situation are briefly introduced.Second,the research progress of convolutional neural networks,auto-encoder and generative adversarial networks on abnormal crowd behavior detection are discussed separately.Then,some commonly used datasets are listed,and the performance of deep learning methods on UCSD pedestrian datasets are compared and analyzed.Finally,the development difficulties of abnormal crowd behavior detection tasks are summarized,and its future research directions are discussed.

With the explosive growth of multimedia data on the Internet,single-modal retrieval has been unable to meet the needs of users,and cross-modal retrieval has emerged.Cross-modal retrieval aims to retrieve related data of one modality with data of another modality.Its core task is to extract data features and measure data correlation between different modality.This paper summarizes the recent research progress in the field of cross-modal retrieval,and summarizes the research results in the field of cross-modal retrieval from the perspectives of traditional methods,deep learning methods,manual feature hash coding methods and deep learning hash coding methods.On this basis,the performance of various algorithms in cross-modal retrieval of commonly used standard data sets is compared and analyzed.Finally,the problems of cross-modal retrieval research are analyzed and the future development trend of the field is prospected.

BackgroundAcute pericardial tamponade (APT) is one of the most serious complications of catheter ablation for atrial fibrillation (AF-CA). Direct autotransfusion (DAT) is a method of reinjecting pericardial blood directly into patients through vein access without a cell-salvage system. Data regarding DAT for APT are rare and provide limited information. Our present study aims to further investigate the safety and feasibility of DAT in the management of APT during the AF-CA procedure.Methods and resultsWe retrospectively reviewed 73 cases of APT in the perioperative period of AF-CA from January 2014 to October 2021 at our institution, among whom 46 were treated with DAT. All included patients successfully received emergency pericardiocentesis through subxiphoid access guided by X-ray. Larger volumes of aspirated pericardial blood (658.4 ± 545.2 vs. 521.2 ± 464.9 ml), higher rates of bridging anticoagulation (67.4 vs. 37.0%), and surgical repair (6 vs. 0) were observed in patients with DAT than without. Moreover, patients with DAT were less likely to complete AF-CA procedures (32/46 vs. 25/27) and had a lower incidence of APT first presented in the ward (delayed presentation) (8/46 vs. 9/27). There was no difference in major adverse events (death/disseminated intravascular coagulation/multiple organ dysfunction syndrome and clinical thrombosis) (0/0/1/0 vs. 1/0/0/0), other potential DAT-related complications (fever/infection and deep venous thrombosis) (8/5/2 vs. 5/3/1), and length of hospital stay (11.4 ± 11.6 vs. 8.3 ± 4.7 d) between two groups.ConclusionDAT could be a feasible and safe method to deal with APT during AF-CA procedure.

Abstract Aims This study sought to compare healthcare quality and 30 day, 90 day, and 1 year mortality rates among patients admitted to secondary and tertiary hospitals for heart failure (HF) in Beijing. Methods and results This study retrospectively enrolled patients hospitalized with a primary discharge diagnosis of HF during January 2014 to December 2015, from five tertiary and four secondary hospitals, in Beijing, China. Mortality data were extracted from Beijing Death Surveillance Database. HF healthcare quality indices were used to evaluate in‐hospital care. Associations between hospital level and mortality rates were assessed using generalized linear mixed models, adjusting for patients' baseline characteristics and intra‐hospital correlation. Data from 1413 patients (median [interquartile range] age = 74 [65–80] years, 52.7% female) from secondary hospitals and 1250 patients (median [interquartile range] age = 72 [61–79] years, 43.3% female) from tertiary hospitals were collected. Rates of left ventricular ejection fraction assessment (73.2% vs. 90.1%) and combined use of β‐blockers and angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers (30.1% vs. 49.3%) were lower in secondary hospitals than those in tertiary hospitals, respectively. Patients admitted to secondary hospitals had a higher 90 day mortality [10.8% vs. 5.0%; adjusted odds ratio (OR): 2.06; 95% confidence interval (CI): 1.10–3.84, P = 0.024 and a higher 1 year mortality rate [21.0% vs. 12.1%; adjusted OR: 1.64; 95% CI: 1.02–2.62, P = 0.039], but 30 day mortality rates were not significantly different (5.5% vs. 3.0%; adjusted OR: 1.49; 95% CI: 0.63–3.52, P = 0.368). Conclusions Worse quality of care for patients with HF in secondary hospitals was associated with higher 90 day and 1 year mortality rates. Improving care quality in secondary hospitals is crucial to improve prognosis of patients they served.

Calpains are a family of calcium-dependent non-lysosomal cysteine proteases. In particular, calpains residing in the endothelial cells play important roles in angiogenesis. It has been shown that calpain activity can be increased in endothelial cells by growth factors, primarily vascular endothelial growth factor (VEGF). VEGF/VEGFR2 induces calpain 2 dependent activation of PI3K/AMPK/Akt/eNOS pathway, and consequent nitric oxide production and physiological angiogenesis. Under pathological conditions such as tumor angiogenesis, endothelial calpains can be activated by hypoxia. This review focuses on the molecular regulatory mechanisms of calpain activation, and the newly identified mechanistic roles and downstream signaling events of calpains in physiological angiogenesis, and in the conditions of pathological tumor angiogenesis and diabetic wound healing, as well as retinopathy and atherosclerosis that are also associated with an increase in calpain activity. Further discussed include the differential strategies of modulating angiogenesis through manipulating calpain expression/activity in different pathological settings. Targeted limitation of angiogenesis in cancer and targeted promotion of angiogenesis in diabetic wound healing via modulations of calpains and calpain-dependent signaling mechanisms are of significant translational potential. Emerging strategies of tissue-specific targeting, environment-dependent targeting, and genome-targeted editing may turn out to be effective regimens for targeted manipulation of angiogenesis through calpain pathways, for differential treatments including both attenuation of tumor angiogenesis and potentiation of diabetic angiogenesis.

Oxidative stress plays an important role in the formation of abdominal aortic aneurysm (AAA), and we have recently established a causal role of uncoupled eNOS in this severe human disease. We have also shown that activation of NADPH oxidase (NOX) lies upstream of uncoupled eNOS. Therefore, identification of the specific NOX isoforms that are required for eNOS uncoupling and AAA formation would ultimately lead to novel therapies for AAA. In the present study, we used the Ang II infused hph-1 mice to examine the roles of NOX isoforms in the development of AAA. We generated double mutants of hph-1-NOX1, hph-1-NOX2, hph-1-p47phox, and hph-1-NOX4. After two weeks of Ang II infusion, the incidence rate of AAA substantially dropped from 76.5% in Ang II infused hph-1 mice (n=34) to 11.1%, 15.0%, 9.5% and 0% in hph-1-NOX1 (n=27), hph-1-NOX2 (n=40), hph-1-p47phox (n=21), and hph-1-NOX4 (n=33) double mutant mice, respectively. The size of abdominal aortas of the four double mutant mice, determined by ultrasound analyses, was significantly smaller than the hph-1 mice. Aortic nitric oxide and H4B bioavailabilities were markedly improved in the double mutants, while superoxide production and eNOS uncoupling activity were substantially diminished. These effects seemed attributed to an endothelial specific restoration of dihydrofolate reductase expression and activity, deficiency of which has been shown to induce eNOS uncoupling and AAA formation in both Ang II-infused hph-1 and apoE null animals. In addition, over-expression of human NOX4 N129S or T555S mutant newly identified in aneurysm patients increased hydrogen peroxide production, further implicating a relationship between NOX and human aneurysm. Taken together, these data indicate that NOX isoforms 1, 2 or 4 lies upstream of dihydrofolate reductase deficiency and eNOS uncoupling to induce AAA formation. These findings may promote development of novel therapeutics for the treatment of the disease by inhibiting NOX signaling.

Restenosis after angioplasty is a serious clinical problem that can result in re-occlusion of the coronary artery. Although current drug-eluting stents have proved to be more effective in reducing restenosis, they have drawbacks of inhibiting reendothelialization to promote thrombosis. New treatment options are in urgent need. We have shown that netrin-1, an axon-guiding protein, promotes angiogenesis and cardioprotection via production of nitric oxide (NO). The present study examined whether and how netrin-1 attenuates neointimal formation in a femoral wire injury model. Infusion of netrin-1 into C57BL/6 mice markedly attenuated neointimal formation following wire injury of femoral arteries, measured by intimal to media ratio (from 1.94 ± 0.55 to 0.45 ± 0.86 at 4 weeks). Proliferation of VSMC in situ was largely reduced. This protective effect was absent in DCC+/- animals. NO production was increased by netrin-1 in both intact and injured femoral arteries, indicating netrin-1 stimulation of endogenous NO production from intact endothelium and remaining endothelial cells post-injury. VSMC migration was abrogated by netrin-1 via a NO/cGMP/p38 MAPK pathway, while timely EPC homing was induced. Injection of netrin-1 preconditioned wild-type EPCs, but not EPCs of DCC+/- animals, substantially attenuated neointimal formation. EPC proliferation, NO production, and resistance to oxidative stress induced apoptosis were augmented by netrin-1 treatment. In conclusion, our data for the first time demonstrate that netrin-1 is highly effective in reducing neointimal formation following vascular endothelial injury, which is dependent on DCC, and attributed to inhibition of VSMC proliferation and migration, as well as improved EPC function. These data may support usage of netrin-1 and netrin-1 preconditioned EPCs as novel therapies for post angioplasty restenosis.Key messageNetrin-1 attenuates neointimal formation following post endothelial injury via DCC and NO. Netrin-1 inhibits VSMC proliferation in situ following endothelial injury. Netrin-1 inhibits VSMC migration via a NO/cGMP/p38 MAPK pathway. Netrin-1 augments proliferation of endothelial progenitor cells (EPCs) and EPC eNOS/NO activation. Netrin-1 enhances resistance of EPCs to oxidative stress, improving re-endothelialization following injury.

The VEGF/VEGFR2/Akt/eNOS/NO pathway is essential to VEGF-induced angiogenesis. We have previously discovered a novel role of calpain in mediating VEGF-induced PI3K/AMPK/Akt/eNOS activation through Ezrin. Here, we sought to identify possible feedback regulation of VEGFR2 by calpain via its substrate protein phosphotyrosine phosphatase 1B (PTP1B), and the relevance of this pathway to VEGF-induced angiogenesis, especially in diabetic wound healing. Overexpression of PTP1B inhibited VEGF-induced VEGFR2 and Akt phosphorylation in bovine aortic endothelial cells, while PTP1B siRNA increased both, implicating negative regulation of VEGFR2 by PTP1B. Calpain inhibitor ALLN induced VEGFR2 activation, which can be completely blocked by PTP1B overexpression. Calpain activation induced by overexpression or Ca/A23187 resulted in PTP1B cleavage, which can be blocked by ALLN. Moreover, calpain activation inhibited VEGF-induced VEGFR2 phosphorylation, which can be restored by PTP1B siRNA. These data implicate calpain/PTP1B negative feedback regulation of VEGFR2, in addition to the primary signaling pathway of VEGF/VEGFR2/calpain/PI3K/AMPK/Akt/eNOS. We next examined a potential role of PTP1B in VEGF-induced angiogenesis. Endothelial cells transfected with PTP1B siRNA showed faster wound closure in response to VEGF. Aortic discs isolated from PTP1B siRNA-transfected mice also had augmented endothelial outgrowth. Importantly, PTP1B inhibition and/or calpain overexpression significantly accelerated wound healing in STZ-induced diabetic mice. In conclusion, our data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-induced angiogenesis. Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment of impaired wound healing in diabetes.

Inflammation is one of the main causes of impaired health in livestock and some of its processes weaken animal productivity and impact human health. The present study was conducted to evaluate the effect of echinacea extract (cichoric acid – CA) on yak peripheral blood mononuclear cells (PBMCs), inflammatory-related factors, and the toll-like receptor (TLR)4 signalling pathway induced by lipopolysaccharide (LPS) in these PBMCs.

The CCCH(C3H) transcription factor is an important transcription factor in plants in the process of plant development, hormone regulation and under stress. Rose is one of the most important commercial flower crops worldwide. However, there are few reports about the C3H gene of rose and Rosa chinensis Jacq. The reference genome sequence becomes a valuable source of data for the C3H genes in rose (RcC3Hs). We identified 31 encoding members in total, which were distributed on seven chromosomes and clustered into 11 subgroups in R. chinensis. Each subgroup has similar group-specific features including motifs, gene structure, cis-acting elements and collinearity in R. chinensis and two other species (Arabidopsis thaliana and Oryza sativa L). The RcC3Hs’tissue-specific expression by quantitative real-time PCR (qRT-PCR) showed that the expression of RcC3Hs was higher in roots and leaves compared with other tissues. These results provide a theoretical basis for the follow-up exploration of the functions of RcC3Hs and the molecular breeding of rose. Supplemental data for this article is available online at https://doi.org/10.1080/13102818.2021.1901609 .

Background: Interleukin 24 (IL-24) has been implicated in the nociceptive signaling. However, direct evidence and the precise molecular mechanism underlying IL-24's role in peripheral nociception remain unclear. Methods: Using patch clamp recording, molecular biological analysis, immunofluorescence labeling, siRNA-mediated knockdown approach and behavior tests, we elucidated the effects of IL-24 on sensory neuronal excitability and peripheral pain sensitivity mediated by T-type Ca2+ channels (T-type channels). Results: IL-24 enhances T-type channel currents (T-currents) in trigeminal ganglion (TG) neurons in a reversible and dose-dependent manner, primarily by activating the interleukin-22 receptor 1 (IL-22R1). Furthermore, we found that the IL-24-induced T-type channel response is mediated through tyrosine-protein kinase Lyn, but not its common downstream target JAK1. IL-24 application significantly activated protein kinase A; this effect was independent of cAMP and prevented by Lyn antagonism. Inhibition of PKA prevented the IL-24-induced T-current response, whereas inhibition of protein kinase C or MAPK kinases had no effect. Functionally, IL-24 increased TG neuronal excitability and enhanced pain sensitivity to mechanical stimuli in mice, both of which were suppressed by blocking T-type channels. In a trigeminal neuropathic pain model induced by chronic constriction injury of the infraorbital nerve, inhibiting IL-22R1 signaling alleviated mechanical allodynia, which was reversed by blocking T-type channels or knocking down Cav3.2. Conclusion: Our findings reveal that IL-24 enhances T-currents by stimulating IL-22R1 coupled to Lyn-dependent PKA signaling, leading to TG neuronal hyperexcitability and pain hypersensitivity. Understanding the mechanism of IL-24/IL-22R1 signaling in sensory neurons may pave the way for innovative therapeutic strategies in pain management. [ABSTRACT FROM AUTHOR]

In order to clarify the influence of key cultivation measures on rapeseed oil quality, a single factor field experiments of sowing date, planting density, and nitrogen rate were carried out in Wuhan and Lanzhou with "Xiangzayou 518 (XZY518)" and "Dadi 199 (DD199)" as the experimental materials. The rapeseed was harvested at maturity stage, followed by cold pressing and oil content, oil extraction efficiency, color of rapeseed oil, peroxide value, total polar phenols, and phytosterol content were assessed, and rapeseed oil quality was evaluated comprehensively under each treatment. The results showed that sowing date, density, and nitrogen rate all significantly affected the key quality indexes of rapeseed oil, and the pattern of change of each index was not the same between the two varieties from two sites. Two varieties from two sites had higher oleic acid content in rapeseed oil under early sowing conditions, and as the sowing date was delayed, rapeseed oil color deepened, chlorophyll content increased, and the comprehensive quality decreased. The XZY518 from two sites at D2 density (4.5x105 hm-2) had a lower acid value, higher total polar phenol, total phytosterol, and total tocopherol contents, and better comprehensive quality. The DD 199 from two sites with increasing density, the chlorophyll content of rapeseed oil increased, the color deepened, the linoleic acid content decreased, and the comprehensive quality also decreased. Two varieties from two sites had higher oil content and oil extraction efficiency under low nitrogen (120 kg hm-2). With the increase of nitrogen rate, rapeseed oil color deepened, comprehensive quality declined. Principal component analysis showed that the effect of sowing date on the comprehensive quality of rapeseed oil was greater than that of planting density and nitrogen rate treatments, and that acid value, chlorophyll, total polar phenols, antioxidant power and total phytosterols were key quality indicators affecting rapeseed oils. Correlation analysis showed that seed oil content was significantly positively correlated with oil extraction efficiency, chlorophyll, carotenoids, and rapeseed oil color were all significantly positively correlated, and total polar phenols were significantly positively correlated with antioxidant power. In summary, early sowing at an appropriate date, reducing nitrogen fertilizer rate, and lowering planting density in production can improve the quality of pressed rapeseed oil. The findings of this study offer technical assistance to produce high-quality rapeseed oil raw materials. [ABSTRACT FROM AUTHOR]

Objective: Rece nt studies ha ve revealed that hemoglobin beta (HBB) plays an important role not only in blood disorders but also in malignancies. The aim of this study is to investigate the clinical significance, diagnostic value, and biological function of HBB in lung cancer. Methods: HBB expression was examined in lung cancer tissues and plasma samples using quantitative real-time polymerase chain reaction, and its relationship with clinical pathological characteristics was analyzed. Receiver operating characteristic (ROC) curves were constructed to evaluate the diagnostic value of HBB in lung cancer. The proliferation of A549 and SPCA1 cells was analyzed using a cell counting kit-8 assay and protein expressions were detected by western blot. Results: The expressions of HBB were found to be down-regulated in both lung cancer tissues and plasma samples. Notably, plasma HBB levels were significantly elevated in postoperative samples when compared to their preoperative counterparts. Across 66 cases of lung cancer tissues, a correlation was observed between HBB levels and both gender and tumor, node, metastasis staging. ROC curve analysis further confirmed the high diagnostic potential of HBB expression in lung cancer. Moreover, the combination of HBB and carcinoembryonic antigen (CEA) had greater significance than HBB or CEA alone in the diagnosis of lung cancer. Knocking out or overexpressing HBB could affect lung cancer cell proliferation through the ERK1/2 signaling pathway. Conclusion: HBB can serve as a novel biomarker for the diagnosis and monitoring of lung cancer, regulating cell proliferation via the ERK1/2 pathway and playing a pivotal role in the oncogenesis and progression of the disease. [ABSTRACT FROM AUTHOR]

Background: Left bundle branch block (LBBB) and atrial fibrillation (AF) are commonly coexisting conditions. The impact of LBBB on catheter ablation of AF has not been well determined. This study aims to explore the long‐term outcomes of patients with AF and LBBB after catheter ablation. Methods: Forty‐two patients with LBBB of 11,752 patients who underwent catheter ablation of AF from 2011 to 2020 were enrolled as LBBB group. After propensity score matching in a 1:4 ratio, 168 AF patients without LBBB were enrolled as non‐LBBB group. Late recurrence and a composite endpoint of stroke, all‐cause mortality, and cardiovascular hospitalization were compared between the two groups. Results: Late recurrence rate was significantly higher in the LBBB group than that in the non‐LBBB group (54.8% vs. 31.5%, p =.034). Multivariate analysis showed that LBBB was an independent risk factor for late recurrence after catheter ablation of AF (hazard ratio [HR] 2.19, 95% confidence interval [CI] 1.09–4.40, p =.031). LBBB group was also associated with a significantly higher incidence of the composite endpoint (21.4% vs. 6.5%, HR 3.98, 95% CI 1.64–9.64, p =.002). Conclusions: LBBB was associated with a higher risk for late recurrence and a higher incidence of composite endpoint in the patients underwent catheter ablation. [ABSTRACT FROM AUTHOR]