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Context Ulcerative colitis has been clinically treated with Qing Hua Chang Yin (QHCY), a traditional Chinese medicine formula. However, its precise mechanisms in mitigating chronic colitis are largely uncharted.Objective To elucidate the therapeutic efficiency of QHCY on chronic colitis and explore its underlying molecular mechanisms.Materials and methods A total ion chromatogram fingerprint of QHCY was analysed. Chronic colitis was induced in male C57BL/6 mice using 2% dextran sodium sulphate (DSS) over 49 days. Mice were divided into control, DSS, DSS + QHCY (0.8, 1.6 and 3.2 g/kg/d dose, respectively) and DSS + mesalazine (0.2 g/kg/d) groups (n = 6). Mice were intragastrically administered QHCY or mesalazine for 49 days. The changes of disease activity index (DAI), colon length, colon histomorphology and serum pro-inflammatory factors in mice were observed. RNA sequencing was utilized to identify the differentially expressed transcripts (DETs) in colonic tissues and the associated signalling pathways. The expression of endoplasmic reticulum (ER) stress-related protein and NF-κB signalling pathway-related proteins in colonic tissues was detected by immunohistochemistry staining.Results Forty-seven compounds were identified in QHCY. Compared with the DSS group, QHCY significantly improved symptoms of chronic colitis like DAI increase, weight loss, colon shortening and histological damage. It notably reduced serum levels of IL-6, IL-1β and TNF-α. QHCY suppressed the activation of PERK–ATF4–CHOP pathway of ER stress and NF-κB signalling pathways in colonic tissues.Discussion and conclusions The findings in this study provide novel insights into the potential of QHCY in treating chronic colitis patients.

Abstract Recombinant adeno-associated viruses (rAAVs) have emerged as promising gene therapy vectors due to their proven efficacy and safety in clinical applications. In non-human primates (NHPs), rAAVs are administered via suprachoroidal injection at a higher dose. However, high doses of rAAVs tend to increase additional safety risks. Here, we present a novel AAV capsid (AAVv128), which exhibits significantly enhanced transduction efficiency for photoreceptors and retinal pigment epithelial (RPE) cells, along with a broader distribution across the layers of retinal tissues in different animal models (mice, rabbits, and NHPs) following intraocular injection. Notably, the suprachoroidal delivery of AAVv128-anti-VEGF vector completely suppresses the Grade IV lesions in a laser-induced choroidal neovascularization (CNV) NHP model for neovascular age-related macular degeneration (nAMD). Furthermore, cryo-EM analysis at 2.1 Å resolution reveals that the critical residues of AAVv128 exhibit a more robust advantage in AAV binding, the nuclear uptake and endosome escaping. Collectively, our findings highlight the potential of AAVv128 as a next generation ocular gene therapy vector, particularly using the suprachoroidal delivery route.

Abstract Background Carthamus tinctorius L., a traditional herbal medicine used for atherosclerosis (AS), lacks a clear understanding of its therapeutic mechanisms. This study aimed to investigate the therapeutic effects and mechanisms of Carthamus tinctorius L.-derived nanovesicles (CDNVs) in AS treatment. Methods CDNVs were isolated and characterized using improved isolation methods. Transmission electron microscopy, nanoparticle tracking analysis, and protein analysis confirmed their morphology, size, and protein composition. Small RNA sequencing was performed to identify the miRNA profile of CDNVs, and bioinformatics analysis was used to determine their potential biological roles. In vivo biodistribution and toxicity studies were conducted in mice to assess the stability and safety of orally administered CDNVs. The anti-atherosclerotic effects of CDNVs were evaluated in ApoE-/- mice through plaque burden analysis. The protective effects of CDNVs on ox-LDL-treated endothelial cells were assessed through proliferation, apoptosis, reactive oxygen species activation, and monocyte adhesion assays. miRNA and mRNA sequencing of CDNV-treated endothelial cells were performed to explore their regulatory effects and potential target genes. Results CDNVs were successfully isolated and purified from Carthamus tinctorius L. tissue lysates. They exhibited a saucer-shaped or cup-shaped morphology, with an average particle size of 142.6 ± 0.7 nm, and expressed EV markers CD63 and TSG101. CDNVs contained proteins, small RNAs, and metabolites, including the therapeutic compound HSYA. Small RNA sequencing identified 95 miRNAs, with 10 common miRNAs accounting for 72.63% of the total miRNAs. These miRNAs targeted genes involved in cell adhesion, apoptosis, and cell proliferation, suggesting their relevance in cardiovascular disease. Orally administered CDNVs were stable in the gastrointestinal tract, absorbed into the bloodstream, and accumulated in the liver, lungs, heart, and aorta. They significantly reduced the burden of atherosclerotic plaques in ApoE-/- mice and exhibited superior effects compared to HSYA. In vitro studies demonstrated that CDNVs were taken up by HUVECs, promoted proliferation, attenuated ox-LDL-induced apoptosis and ROS activation, and reduced monocyte adhesion. CDNV treatment resulted in significant changes in miRNA and mRNA expression profiles of HUVECs, with enrichment in inflammation-related genes. CXCL12 was identified as a potential direct target of miR166a-3p. Conclusion CDNVs isolated from Carthamus tinctorius L. tissue lysates represent a promising oral therapeutic option for cardiovascular diseases. The delivery of miRNAs by CDNVs regulates inflammation-related genes, including CXCL12, in HUVECs, suggesting their potential role in modulating endothelial inflammation. These findings provide valuable insights into the therapeutic potential of CDNVs and their miRNAs in cardiovascular disease.

Diazotrophic communities contribute inorganic nitrogen for the primary productivity of the marine environment by biological nitrogen fixation (BNF). They play a vital role in the biogeochemical cycle of nitrogen in the marine ecological environment. However, there is still an incomplete understanding of BNF and diazotrophs in artificial seaweed farms. Therefore, this study comprehensively investigated the temporal variations of BNF associated with Gracilariopsis lemaneiformis, as well as the diazotrophic communities associated with macroalgae and its surrounding seawater. Our results revealed that a total of 13 strains belonging to Proteobacteria and Bacteroidetes were identified as N2-fixing bacteria using azotobacter selective solid medium and nifH gene cloning. Subsequently, BNF and diazotrophic communities were characterized using the acetylene reduction method and high-throughput sequencing of the nifH gene, respectively. The results showed that nitrogenase activity and nifH gene abundance of epiphytic bacteria on G. lemaneiformis varied significantly among four different cultivation periods, i.e., Cultivation Jan. (CJ), Cultivation Feb. (CF), Cultivation Mar. (CM), Cultivation Apr. (CA). Among them, the nitrogenase activity and nifH gene abundance of epiphytic bacteria on G. lemaneiformis in CM were significantly higher than those in CJ, CF, and CA, indicating that the BNF of eiphytic bacteria on G. lemaneiformis was markedly enhanced. Combined with the data on environmental factors, it was found that the low concentration of nitrogen and phosphorus in CM might considerably boost the BNF of epiphytic bacteria in G. lemaneiformis. The sequencing results of the nifH gene showed that the α-diversity of diazotrophic communities associated with G. lemaneiformis and seawater in CM was higher than that in other cultivation periods. In addition, the diazotrophic communities on G. lemaneiformis were significantly different in CJ, CF, CM, and CA, and they were significantly diverse from diazotrophic communities in seawater. LEfSe analysis indicated that Rhodobacterales, Hyphomonadaceae, Robiginitomaculum, and Robiginitomaculum antarcticum within α-proteobacteria played a remarkable role in BNF in response to nitrogen nutrient deficiency. Taken together, these results provide a unique insight into the interaction between macroalgae and its epiphytic bacteria and lay a foundation for further research on the mechanism of action of nitrogen-cycling microorganisms associated with macroalgae.

Slow transit constipation (STC) is a common and debilitating condition characterized by delayed colonic transit and difficulty in fecal expulsion, significantly impacting patients’ physical and mental wellbeing as well as their overall quality of life. This study investigates the therapeutic potential of Liqi Tongbian Decoction (LTD) in the treatment of STC, especially in cases involving the context of Qi stagnation, through a multifaceted approach involving the modulation of intestinal flora and short-chain fatty acids (SCFAs). We employed a rat model of STC with Qi Stagnation Pattern, established using the “loperamide + tail-clamping provocation method,” to explore the effects of LTD on fecal characteristics, intestinal motility, and colonic pathology. Importantly, LTD exhibited the ability to increase the richness, diversity, and homogeneity of intestinal flora while also modulating the composition of microorganisms. It significantly increased the production of SCFAs, especially butyric acid. Moreover, LTD exerted a substantial influence on the synthesis of serotonin (5-HT) by modulating the expression of tryptophan hydroxylase (TPH) and interacting with the 5-HT4 receptor (5-HT4R), resulting in enhanced colonic motility. Correlation analyses revealed a positive correlation between certain bacterial genera, such as Lachnospiraceae_NK4A136 spp. and Clostridiales spp. and the concentrations of butyric acid and 5-HT. These results suggest a mechanistic link between microbiome composition, SCFAs production, and 5-HT synthesis. These findings highlight the potential of LTD to alleviate STC by facilitating a beneficial interplay among intestinal flora, SCFAs production, and 5-HT-mediated colonic motility, providing novel insights into the management of STC with Qi Stagnation Pattern.

Background This study investigated whether gCTRP9 (globular C1q/tumor necrosis factor–related protein‐9) could restore high‐glucose (HG)‐suppressed endothelial progenitor cell (EPC) functions by activating the endothelial nitric oxide synthase (eNOS). Methods and Results EPCs were treated with HG (25 mmol/L) and gCTRP9. Migration, adhesion, and tube formation assays were performed. Adiponectin receptor 1, adiponectin receptor 2, and N‐cadherin expression and AMP‐activated protein kinase, protein kinase B, and eNOS phosphorylation were measured by Western blotting. eNOS activity was determined using nitrite production measurement. In vivo reendothelialization and EPC homing assays were performed using Evans blue and immunofluorescence in mice. Treatment with gCTRP9 at physiological levels enhanced migration, adhesion, and tube formation of EPCs. gCTRP9 upregulated the phosphorylation of AMP‐activated protein kinase, protein kinase B, and eNOS and increased nitrite production in a concentration‐dependent manner. Exposure of EPCs to HG‐attenuated EPC functions induced cellular senescence and decreased eNOS activity and nitric oxide synthesis; the effects of HG were reversed by gCTRP9. Protein kinase B knockdown inhibited eNOS phosphorylation but did not affect gCTRP9‐induced AMP‐activated protein kinase phosphorylation. HG impaired N‐cadherin expression, but treatment with gCTRP9 restored N‐cadherin expression after HG stimulation. gCTRP9 restored HG‐impaired EPC functions through both adiponectin receptor 1 and N‐cadherin‐mediated AMP‐activated protein kinase /protein kinase B/eNOS signaling. Nude mice that received EPCs treated with gCTRP9 under HG medium showed a significant enhancement of the reendothelialization capacity compared with those with EPCs incubated under HG conditions. Conclusions CTRP9 promotes EPC migration, adhesion, and tube formation and restores these functions under HG conditions through eNOS‐mediated signaling mechanisms. Therefore, CTRP9 modulation could eventually be used for vascular healing after injury.

H. perforatum, as one of the Traditional Chinese Medicinal materials, possesses a variety of pharmacological activities and high medicinal value. However, in recent years, the wild resources of H. perforatum have been severely depleted due to global climate change and human activities, and artificial cultivation faces problems such as unstable yield and active ingredient content. This poses a serious obstacle to the development and utilization of its resources. Therefore, this experiment took H. perforatum as the research object and used 894 distribution records of H. perforatum and 36 climatic environmental factors, using the MaxEnt model and GIS technology to explore the main climatic factors affecting the distribution of H. perforatum. Additionally, by utilizing the principles of ecological niche theory, the potential suitable distribution regions of H. perforatum across past, present, and future timelines were predicted, which can ascertain the dynamics of its spatial distribution patterns and the trend of centroid migration. The results indicate that the main environmental factors affecting the geographical distribution of H. perforatum are solar radiation in April (Srad4), solar radiation in September (Srad9), mean temperature of driest quarter (Bio9), solar radiation in November (Srad11), annual mean temperature (Bio1), and annual precipitation (Bio12). Under future climate scenarios, there is a remarkable trend of expansion in the suitable distribution areas of H. perforatum. The centroid migration indicates a trend of migration towards the northwest direction and high-altitude areas. These results can provide a scientific basis for formulating conservation and sustainable use management strategies for H. perforatum resources.

Background: Qing Hua Chang Yin (QHCY) is a famous formula of traditional Chinese medicine (TCM) and has been proven to have protective effect on ulcerative colitis. However, its protective effect and potential therapeutic mechanisms in chronic colitis remain unclear. The purpose of this study is to explore the effects and underlying mechanisms of QHCY on dextran sulfate sodium (DSS)-induced chronic colitis mice model.Methods: The chronic colitis model was established by administration of 2% DSS for three consecutive cycles of 7 days with two intervals of 14 days for recovery by drinking water. The experiment lasted 49 days. The DSS + QHCY group received QHCY administration by oral gavage at doses of 1.6 g/kg/d, DSS + Mesalazine group was administrated Mesalazine by oral gavage at doses of 0.2 g/kg/d. The control and DSS group were given equal volume of distilled water. The body weight, stool consistency and blood in stool were monitored every 2 days. The disease activity index (DAI) was calculated. The colon length was measured after the mice were sacrificed. The histomorphology of colonic tissues was checked by the HE and PAS staining. Immunohistochemistry was performed to detect the expressions of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), tight junction proteins (ZO-1, occludin) and Mucin2 (MUC2). 16S rRNA sequencing analysis was conducted to study the diversity and abundance of gut microbiota changes.Results: QHCY treatment not only significantly attenuated DSS-induced the weight loss, DAI score increase, colon shortening and histological damage in mice, but also decreased the expression of pro-inflammatory cytokines in colonic tissues and increased the expression of ZO-1, occludin, and MUC2. Furthermore, QHCY enhanced the diversity of gut microbes and regulated the structure and composition of intestinal microflora in mice with chronic colitis.Conclusion: QHCY has a therapeutic effect on a murine model of chronic colitis. It can effectively reduce the clinical and pathological manifestations of colitis and prevent alterations in the gut microbiota.

Abstract Dynamic change of mitochondrial morphology and distribution along neuronal branches are essential for neural circuitry formation and synaptic efficacy. However, the underlying mechanism remains elusive. We show here that Pink1 knockout (KO) mice display defective dendritic spine maturation, reduced axonal synaptic vesicles, abnormal synaptic connection, and attenuated long-term synaptic potentiation (LTP). Drp1 activation via S616 phosphorylation rescues deficits of spine maturation in Pink1 KO neurons. Notably, mice harboring a knockin (KI) phosphor-null Drp1 S616A recapitulate spine immaturity and synaptic abnormality identified in Pink1 KO mice. Chemical LTP (cLTP) induces Drp1S616 phosphorylation in a PINK1-dependent manner. Moreover, phosphor-mimetic Drp1S616D restores reduced dendritic spine localization of mitochondria in Pink1 KO neurons. Together, this study provides the first in vivo evidence of functional regulation of Drp1 by phosphorylation and suggests that PINK1-Drp1S616 phosphorylation coupling is essential for convergence between mitochondrial dynamics and neural circuitry formation and refinement.

Abstract Background Percutaneous transluminal coronary angioplasty (PTCA) represents an efficient therapeutic method for atherosclerosis but conveys a risk of causing restenosis. Endothelial colony-forming cell-derived exosomes (ECFC-exosomes) are important mediators during vascular repair. This study aimed to investigate the therapeutic effects of ECFC-exosomes in a rat model of atherosclerosis and to explore the molecular mechanisms underlying the ECFC-exosome-mediated effects on ox-LDL-induced endothelial injury. Methods The effect of ECFC-exosome-mediated autophagy on ox-LDL-induced human microvascular endothelial cell (HMEC) injury was examined by cell counting kit-8 assay, scratch wound assay, tube formation assay, western blot and the Ad-mCherry-GFP-LC3B system. RNA-sequencing assays, bioinformatic analysis and dual-luciferase reporter assays were performed to confirm the interaction between the miR-21-5p abundance of ECFC-exosomes and SIPA1L2 in HMECs. The role and underlying mechanism of ECFC-exosomes in endothelial repair were explored using a high-fat diet combined with balloon injury to establish an atherosclerotic rat model of vascular injury. Evans blue staining, haematoxylin and eosin staining and western blotting were used to evaluate vascular injury. Results ECFC-exosomes were incorporated into HMECs and promoted HMEC proliferation, migration and tube formation by repairing autophagic flux and enhancing autophagic activity. Subsequently, we demonstrated that miR-21-5p, which is abundant in ECFC-exosomes, binds to the 3’ untranslated region of SIPA1L2 to inhibit its expression, and knockout of miR-21-5p in ECFC-exosomes reversed ECFC-exosome-decreased SIPA1L2 expression in ox-LDL-induced HMEC injury. Knockdown of SIPA1L2 repaired autophagic flux and enhanced autophagic activity to promote cell proliferation in ox-LDL-treated HMECs. ECFC-exosome treatment attenuated vascular endothelial injury, regulated lipid balance and activated autophagy in an atherogenic rat model of vascular injury, whereas these effects were eliminated with ECFC-exosomes with knockdown of miR-21-5p. Conclusions Our study demonstrated that ECFC-exosomes protect against atherosclerosis- or PTCA-induced vascular injury by rescuing autophagic flux and inhibiting SIAP1L2 expression through delivery of miR-21-5p. Video Abstract.

N-acyl homoserine lactones (AHLs) are small, diffusible chemical signal molecules that serve as social interaction tools for bacteria, enabling them to synchronize their collective actions in a density-dependent manner through quorum sensing (QS). The QS activity from epiphytic bacteria of the red macroalgae Porphyra haitanensis, along with its involvement in biofilm formation and regulation, remains unexplored in prior scientific inquiries. Therefore, this study explores the AHL signal molecules produced by epiphytic bacteria. The bacterium isolated from the surface of P. haitanensis was identified as Pseudoalteromonas galatheae by 16s rRNA gene sequencing and screened for AHLs using two AHL reporter strains, Agrobacterium tumefaciens A136 and Chromobacterium violaceum CV026. The crystal violet assay was used for the biofilm-forming phenotype. The inferences revealed that P. galatheae produces four different types of AHL molecules, i.e., C4-HSL, C8-HSL, C18-HSL, and 3-oxo-C16-HSL, and it was observed that its biofilm formation phenotype is regulated by QS molecules. This is the first study providing insights into the QS activity, diverse AHL profile, and regulatory mechanisms that govern the biofilm formation phenotype of P. galatheae. These findings offer valuable insights for future investigations exploring the role of AHL producing epiphytes and biofilms in the life cycle of P. haitanensis.

Accumulating evidence suggests that gut microbiota as a critical mediator of gut-brain axis plays an important role in human health. Altered gut microbial profiles have been implicated in increasing the vulnerability of psychiatric disorders, such as autism, depression, and schizophrenia. However, the cellular and molecular mechanisms underlying the association remain unknown. Here, we modified the gut microbiome with antibiotics in newborn mice, and found that gut microbial alteration induced behavioral impairment by decreasing adult neurogenesis and long-term potentiation of synaptic transmission, and altering the gene expression profile in hippocampus. Reconstitution with normal gut flora produced therapeutic effects against both adult neurogenesis and behavioral deficits in the dysbiosis mice. Furthermore, our results show that circulating metabolites changes mediate the effect of gut dysbiosis on hippocampal plasticity and behavior outcomes. Elevating the serum 4-methylphenol, a small aromatic metabolite produced by gut bacteria, was found to induce autism spectrum disorder (ASD)-like behavior impairment and hippocampal dysfunction. Together our finding demonstrates that early-life gut dysbiosis and its correlated metabolites change contribute to hippocampal dysfunction and behavior impairment, hence highlight the potential microbiome-mediated therapies for treating psychiatric disorders.

Corneal neovascularization (CoNV) leads to visual impairment, affecting over 1.4 million people in the United States per year. It is caused by a variety of pathologies, such as inflammation, hypoxia, and limbal barrier dysfunction. Injection of the anti-vascular endothelial growth factor (VEGF) drug KH902 (conbercept) can inhibit CoNV but requires repeated dosing that produces associated side effects, such as cornea scar. To explore more efficacious and long-lasting treatment of CoNV, we employed recombinant adeno-associated virus (rAAV)2 and rAAV8 vectors to mediate KH902 expression via a single intrastromal injection and investigated its anti-angiogenic effects and safety in both alkali-burn- and suture-induced CoNV mouse models. Our results showed that rAAV-mediated KH902 mRNA expression in the cornea was sustained for at least 3 months after a single intrastromal injection. Moreover, the expression level of rAAV8-KH902 far exceeded that of rAAV2-KH902. A single-dose rAAV8-KH902 treatment at 8 × 108 genome copies (GCs) per cornea dramatically inhibited CoNV for an extended period of time in mouse CoNV models without adverse events, whereas the inhibition of CoNV by a single intrastromal administration of the conbercept drug lasted for only 10−14 days. Overall, our study demonstrated that the treatment of CoNV with a single dose of rAAV8-KH902 via intrastromal administration was safe, effective, and long lasting, representing a novel therapeutic strategy for CoNV.

Abstract In the field of automatic driving, identifying vehicles and pedestrians is the starting point of other automatic driving techniques. Using the information collected by the camera to detect traffic targets is particularly important. The main bottleneck of traffic object detection is due to the same category of targets, which may have different scales. For example, the pixel‐level of cars may range from 30 to 300 px, which will cause instability of positioning and classification. In this paper, a multi‐dimension feature pyramid is constructed in order to solve the multi‐scale problem. The feature pyramid is built by developing a U‐shaped module and using a cascade‐method. In order to verify the effectiveness of the U‐shaped module, we also designed a new one‐shot detector U‐FPNDet. The model first extracts the basic feature map by using the basic network and constructs the multi‐dimension feature pyramid. Next, a pyramid pooling module is used to get more context information from the scene. Finally, the detection network is run on each level of the pyramid to obtain the final result by NMS. By using this method, a state‐of‐the‐art performance is achieved on both detection and classification on commonly used benchmarks.

Abstract Background Annexin A1 (ANXA1) exerts anti-nociceptive effect through ANXA1 receptor formyl peptide receptor 2 (FPR2/ALX (receptor for lipoxin A4), FPR2) at the dorsal root ganglia (DRG) level. However, the mechanisms remain elucidated. By using radiant heat, hot/cold plate, tail flick, von Frey, and Randall-Selitto tests to detect nociception in intact and chemical (capsaicin, menthol, mustard oil, formalin or CFA) injected AnxA1 conditional knockout (AnxA1 −/−) mice, applying calcium imaging and patch clamp recordings in cultured DRG neurons to measure neuronal excitability, conducting immunofluorescence and western blotting to detect the protein levels of TRPV1, FPR2 and its downstream molecules, and performing double immunofluorescence and co-immunoprecipitation to investigate the interaction between Calmodulin (CaM) and TRPV1; we aim to uncover the molecular and cellular mechanisms of ANXA1’s role in antinociception. Results AnxA1 −/− mice exhibited significant sensitivity to noxious heat (mean ± SD, 6.2 ± 1.0 s vs. 9.9 ± 1.6 s in Hargreaves test; 13.6 ± 1.5 s vs. 19.0 ± 1.9 s in hot plate test; n = 8; P

Inflammatory immune response is apparently one of the determinants of progressive exacerbation of valvular atrial fibrillation(VAF). Ferroptosis, an iron-dependent modality of regulated cell death, is involved in the immune regulation of cardiovascular disease. However, the relevant regulatory mechanisms of immune infiltration and ferroptosis in VAF have been less studied. In the current study, a highly efficient system for screening immunity- and ferroptosis-related biomarkers and immunomodulatory ability of herbal ingredients has been developed with the integration of intelligent data acquisition, data mining, network pharmacology, and computer-assisted target fishing. VAF patients showed higher infiltration of neutrophils and resting stage dendritic cells, while VSR patients showed higher infiltration of follicular helper T cells. In addition, six (e.g., PCSK2) and 47 (e.g., TGFBR1) ImmDEGs and one (SLC38A1) and four (TGFBR1, HMGB1, CAV1, and CD44) FerDEGs were highly expressed in patients with valvular sinus rhythm (VSR) and VAF, respectively. We further identified a core subnetwork containing 34 hub genes, which were intersected with ImmDEGs and FerDEGs to obtain the key gene TGFBR1. Based on TGFBR1, 14 herbs (e.g., Fructus zizyphi jujubae, Semen Juglandis, and Polygonum cuspidatum) and six herbal ingredients (curcumin, curcumine, D-glucose, hexose, oleovitamin A, and resveratrol) were predicted. Finally, TGFBR1 was found to dock well with curcumin and resveratrol, and it was further verified that curcumin and resveratrol could significantly reduce myocardial fibrosis. We believe that herbs rich in curcumin and resveratrol such as Rhizoma curcumae longae and Curcuma kwangsiensis, mitigate myocardial fibrosis to improve VAF by modulating the TGFβ/Smad signaling pathway. This strategy provides a prospective approach systemically characterizing phenotype-target-herbs relationships based on the tissue-specific biological functions in VAF and brings us new insights into the searching lead compounds from Chinese herbs.

Synthetic aperture radar (SAR) is an advanced active microwave sensor widely used in marine surveillance. As part of typical marine surveillance missions, ship classification in synthetic aperture radar (SAR) images is a significant task for the remote sensing community. However, fully utilizing polarization information to enhance SAR ship classification remains an unresolved issue. Thus, we proposed a dual-polarization information-guided network (DPIG-Net) to solve it. DPIG-Net utilizes available dual-polarization information from the Sentinel-1 SAR satellite to adaptively guide feature extraction and feature fusion. We first designed a novel polarization channel cross-attention framework (PCCAF) to model the correlations of different polarization information for feature extraction. Then, we established a novel dilated residual dense learning framework (DRDLF) to refine the polarization characteristics for feature fusion. The results on the open OpenSARShip dataset indicated DPIG-Net’s state-of-the-art classification accuracy compared with eleven other competitive models, which showed the potential of DPIG-Net to promote effective and sufficient utilization of SAR polarization data in the future.

BackgroundThe present study aims to explore risk factors related to in-stent restenosis (ISR) in elderly patients with coronary heart disease and type 2 diabetes within 2 years after the first drug-eluting stent (DES) implantation.MethodsThis case-control study retrospectively analyzed the clinical data of patients with coronary heart disease and diabetes undergoing percutaneous coronary intervention (PCI) in Shenzhen Sun Yat-sen Cardiovascular Hospital between January 2010 and March 2020. Univariate and multivariate models were used to assess independent factors for DES-ISR. Categorical principal component analysis of clinical variables was performed to determine important components for DES-ISR. Nomogram was constructed to quantitatively predict the probability of DES-ISR development. The diagnostic potential of clinical variables was determined by receiver operating characteristic curve.ResultsIn the derivation cohort, 1,741 cases were included in this study, and a total of 227 pairs of cases and controls were generated by propensity score matching. In the validation cohort, 102 cases were included with 19 cases (18.6%) with DES-ISR. Glomerular filtration rate

Abstract Chronic atrophic gastritis (CAG) is well-known related with multiple pathogenic factors and normally therapies comprised by western or Chinese medicines. The present study was designed to identify the bacterial community characterized by 16S rRNA amplicon sequencing and determine the modulate affection of bacterial composition response western and Chinese medicine Qinghuayin (QHY) as well as antibiotic on model rats. The result shown the overall structure alteration of bacterial appeared under medicine intervened, antibiotic caused a marked depletion in bacterial diversity and richness. The enrichments of Firmicutes (85.1–90.7%) in antibiotic-free converts into Bacteroidetes (30.7–34.6%) in antibiotic-added model rat were demonstrated. Firmicutes as the most dominant phylum in antibiotic-free treatments and significantly decreased till 21.9–68.5% in antibiotic-added treatments. Especially QHY-treated rats showed highest RA of Firmicutes (90.7%) and the amelioration of CAG using QHY attributed by beneficial bacterial enrichment, especially Ruminococcus, Lactobacillus and Bifidobacterium. In addition, alpha and beta diversity analysis also demonstrated the clear dispersion and aggregation that revealed the alteration and steady of bacterial community structures. In summary, QHY has potential application value in the treatment of CAG, which attributed to close relation with the modulatory of internal bacterial communities.

Abstract Background HIIT has recently been widely used for health promotion in healthy people and patients with chronic diseases. Exercise can help SUD reduce drug cravings, enhance mental health and return to normal life. However, whether HIIT can bring better physical rehabilitation benefits to individuals with SUD than MICT is unclear. The study aimed to compare the effects of HIIT versus MICT on the physical fitness of individuals with SUD. Methods One hundred twenty individuals with amphetamine-type stimulant dependence voluntarily participated in this study. They were randomly assigned to the HIIT group and MICT group. Both groups received training three times a week. The intervention lasted from January 2019 to December 2019. Physical fitness was assessed at the baseline, 3 months, 6 months, 9 months and 12 months, including blood pressure (BP), vital capacity(VC), hand grip, push-up, sit-and-reach, one-leg standing with eyes closed and choice reaction time. The craving level was assessed using the Visual Analog Scale at baseline, 6 months and 12 months to see any change along with the improvement in physical fitness. Two-way repeated measures ANOVA was applied to analyse the differences in change by group (HIIT and MICT) and time (baseline, 3 months, 6 months, 9 months and 12 months). Results The within-group factor displayed significant changes in the HIIT and MICT groups in terms of systolic BP (F (4,336) = 12.799, P

This paper discusses new approaches to parameter estimation of gamma distribution based on representative points. In the first part, the existence and uniqueness of gamma mean squared error representative points (MSE-RPs) are discussed theoretically. In the second part, by comparing three types of representative points, we show that gamma MSE-RPs perform well in parameter estimation and simulation. The last part proposes a new Harrel–Davis sample standardization technique. Simulation studies reveal that the standardized samples can be used to improve estimation performance or generate MSE-RPs. In addition, a real data analysis illustrates that the proposed technique yields efficient estimates for gamma parameters.

Ship instance segmentation in synthetic aperture radar (SAR) images can provide more detailed location information and shape information, which is of great significance for port ship scheduling and traffic management. However, there is little research work on SAR ship instance segmentation, and the general accuracy is low because the characteristics of target SAR ship task, such as multi-scale, ship aspect ratio, and noise interference, are not considered. In order to solve these problems, we propose an idea of scale in scale (SIS) for SAR ship instance segmentation. Its essence is to establish multi-scale modes in a single scale. In consideration of the characteristic of the targeted SAR ship instance segmentation task, SIS is equipped with four tentative modes in this paper, i.e., an input mode, a backbone mode, an RPN mode (region proposal network), and an ROI mode (region of interest). The input mode establishes multi-scale inputs in a single scale. The backbone mode enhances the ability to extract multi-scale features. The RPN mode makes bounding boxes better accord with ship aspect ratios. The ROI mode expands the receptive field. Combined with them, a SIS network (SISNet) is reported, dedicated to high-quality SAR ship instance segmentation on the basis of the prevailing Mask R-CNN framework. For Mask R-CNN, we also redesign (1) its feature pyramid network (FPN) for better small ship detection and (2) its detection head (DH) for a more refined box regression. We conduct extensive experiments to verify the effectiveness of SISNet on the open SSDD and HRSID datasets. The experimental results reveal that SISNet surpasses the other nine competitive models. Specifically, the segmentation average precision (AP) index is superior to the suboptimal model by 4.4% on SSDD and 2.5% on HRSID.

Abstract In this study, the self-extracted constipation treatment of traditional Chinese medicine extracts was applied to constipated rats. To explore the mechanism and role of the Chinese medicine for the treatment of constipation, the 16S rRNA sequencing and qRT-PCR technology were used to analyze the intestinal flora. We found that the relative abundance of Firmicutes with constipation was significantly higher accounted for 86.7%, while the gut microbiota was significantly changed after taking a certain dose of Chinese medicine, greatly increased the relative abundance of Lactobacillus accounted for 23.1%, enhanced the symbiotic relationships of Lactobacillus with other intestinal flora. The total copies of intestinal bacteria in the constipated rats decreased after taking the traditional Chinese medicine. Finally, this study results provides a theoretical basis for the treatment and understand the mechanism and effect of traditional Chinese medicine on rate constipation.

Qing-Chang-Hua-Shi (QCHS) is a Chinese herbal formula, which is composed of 11 herbs. Studies have also shown that QCHS granules can alleviate colitis in animal models by preventing inflammatory responses and suppressing apoptosis through the MEK/ERK signaling pathway. To determine the efficacy and safety of QCHS granules in patients with moderately active UC. We performed a multicenter, randomized, placebo-controlled, double-blind study of patients with moderately active UC who did not respond to 4 weeks of mesalazine therapy at the maximum dose. Patients were randomly assigned to groups and administered QCHS granules (125 g/day, n = 59) or an identical placebo, which was similar to the QCHS granules in color and taste (125 g/day, n = 60), with continued 5-ASA 4 g/d therapy for 12 weeks. The primary outcome was the rate of clinical response and clinical remission at week 12. The secondary outcomes were health-related quality of life, endoscopic response rate, and mucosal healing rate. Any changes in mucus/bloody stool and diarrhea were recorded. Out of the 119 enrolled patients at 10 different centers in China, 102 patients completed the trial. Clinical remission and clinical response were seen in 31.48% and 92.59% of QCHS-treated patients, and 12.50% and 72.92% of placebo-treated patients, respectively. There was a significant difference between the two treatment groups. More patients receiving QCHS granules vs. placebo achieved remission of mucus/bloody stool (70.37% vs. 47.92%, P = 0.0361). Adverse event rates were similar (QCHS granules 38.33%; placebo 25.42%). In conclusion, QCHS granules were superior to the placebo in introducing clinical remission and mucosal healing, as well as in relieving mucus/blood stool in patients with moderately active and 5-ASA-refractory UC.

BackgroundIschemia/reperfusion-mediated myocardial infarction (MIRI) is a major pathological factor implicated in the progression of ischemic heart disease, but the key factors dysregulated during MIRI have not been fully elucidated, especially those essential non-coding factors required for cardiovascular development.MethodsA murine MIRI model and RNA sequencing (RNA-seq) were used to identify key lncRNAs after myocardial infarction. qRT-PCR was used to validate expression in cardiac muscle tissues and myocardial cells. The role of Gm18840 in HL-1 cell growth was determined by flow cytometry experiments in vitro. Full-length Gm18840 was identified by using a rapid amplification of cDNA ends (RACE) assay. The subcellular distribution of Gm18840 was examined by nuclear/cytoplasmic RNA fractionation and qRT-PCR. RNA pulldown and RNA immunoprecipitation (RIP)-qPCR assays were performed to identify Gm18840-interacting proteins. Chromatin isolation by RNA purification (ChIRP)-seq (chromatin isolation by RNA purification) was used to identify the genome-wide binding of Gm18840 to chromatin. The regulatory activity of Gm18840 in transcriptional regulation was examined by a luciferase reporter assay and qRT-PCR.ResultsGm18840 was upregulated after myocardial infarction in both in vivo and in vitro MIRI models. Gm18840 was 1,471 nt in length and localized in both the cytoplasm and the nucleus of HL-1 cells. Functional studies showed that the knockdown of Gm18840 promoted the apoptosis of HL-1 cells. Gm18840 directly interacts with histones, including H2B, highlighting a potential function in transcriptional regulation. Further ChIRP-seq and RNA-seq analyses showed that Gm18840 is directly bound to the cis-regulatory regions of genes involved in developmental processes, such as Junb, Rras2, and Bcl3.ConclusionGm18840, a novel transcriptional regulator, promoted the apoptosis of myocardial cells via direct transcriptional regulation of essential genes and might serve as a novel therapeutic target for MIRI.

Background: A risk assessment of in-stent restenosis (ISR) patients is critical for providing adequate treatment. Nevertheless, the prognostic value of high-sensitivity CRP (hs-CRP) levels on ISR has not been consistently demonstrated in clinical studies. In the current meta-analysis, we aim to assess the predictive role of hs-CRP in patients treated with stenting. Methods: We searched PubMed, Web of Science, Embase, and the Cochrane Registry through May 2022. We selected random control trials that compared the effects of different interventions, and that revealed the effects of hs-CRP. Two reviewers independently screened the articles, extracted the data, and assessed the quality of the studies according to the PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). The data were pooled using a random-effects meta-analysis. Results: Nine articles were included in the meta-analysis. A total of 1.049 patients received stent implantation, and 185 ISR events were recorded during the 1–12-month follow-up period. Baseline hs-CRP levels were not associated with the prediction of ISR among patients receiving stent implantation. The OR of hs-CRP for ISR was 1.81 (0.92–2.69). In the subgroup analysis, 6–12-month hs-CRP levels, diabetes mellitus (DM), and age ≥60(years)were associated with a higher risk of ISR. Conclusions: This meta-analysis shows that higher levels of baseline hs-CRP are not associated with an increased risk of ISR in stented patients. However, an increased risk of ISR was associated with hs-CRP levels at 6 to 12 months of follow-up, which is higher in studies with diabetes mellitus patients and the elderly.

Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Endothelial progenitor cell (EPC)-derived exosomes have been found to be effective in alleviating MI, while the detailed mechanisms remain unclear. The present study aimed to determine the protective effects of EPC-derived exosomal miR-1246 and miR-1290 on MI-induced injury and to explore the underlying molecular mechanisms. The exosomes were extracted from EPCs; gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot and immunofluorescence staining, respectively. The angiogenesis and proliferation of human cardiac fibroblasts (HCFs) were determined by tube formation assay and immunofluorescence staining of PKH67, respectively. Luciferase reporter, CHIP, and EMSA assays determined the interaction between miR-1246/1290 and the targeted genes (EFL5 and SP1). The protective effects of miR-1246/1290 on MI were evaluated in a rat model of MI. EPC-derived exosomes significantly upregulated miR-1246 and miR-1290 expression and promoted phenotypic changes of fibroblasts to endothelial cells, angiogenesis, and proliferation in HCFs. Exosomes from EPCs with miR-1246 or miR-1290 mimics transfection promoted phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs, while exosomes from EPCs with miR-1246 or miR-1290 knockdown showed opposite effects in HCFs. Mechanistically, miR-1246 and miR-1290 from EPC-derived exosomes induced upregulation of ELF5 and SP1, respectively, by targeting the promoter regions of corresponding genes. Overexpression of both ELF5 and SP1 enhanced phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs pretreated with exosomes from EPCs with miR-1246 or miR-1290 mimics transfection, while knockdown of both EFL5 and SP1 exerted the opposite effects in HCFs. Both ELF5 and SP1 can bind to the promoter of CD31, leading to the upregulation of CD31 in HCFs. Furthermore, in vivo animal studies showed that exosomes from EPCs with miR-1246 or miR-1290 overexpression attenuated the MI-induced cardiac injury in the rats and caused an increase in ELF5, SP1, and CD31 expression, respectively, but suppressed α-SMA expression in the cardiac tissues. In conclusion, our study revealed that miR-1246 and miR-1290 in EPC-derived exosomes enhanced in vitro and in vivo angiogenesis in MI, and these improvements may be associated with amelioration of cardiac injury and cardiac fibrosis after MI.

Abstract Background Myocardial fibrosis is a common pathophysiological change in cardiovascular disease, which can cause cardiac dysfunction and even sudden death. Excessively activated fibroblasts proliferate and secret excessive extracellular matrix (ECM) components, resulting in normal cardiac structural damage and cardiac fibrosis. We previously found that human endothelial progenitor cell (EPC)-derived exosomes, after hypoxia/reoxygenation (H/R) induction, could significantly increase the mesenchymal-endothelial transition (MEndoT) compared to normal culture EPC-derived exosomes. Exosomes have been shown to carry different nucleic acids, including microRNAs. However, the effects of microRNAs in EPC-derived exosomes on MEndoT and myocardial fibrosis remain unknown. Methods EPCs were isolated from human peripheral blood, and fibroblasts were isolated from rat hearts, then transfected with miR-133 inhibitor, si-YBX-1, and ov-YBX-1 into EPCs. After H/R induction for 48 h, isolation and characterization of exosomes derived from human EPCs were performed. Finally, fibroblasts were treated by exosome at 48 h. The expression of miR-133 was measured by qRT-PCR; YBX-1 expression was measured by qRT-PCR and western blot. Angiopoiesis was measured by tube formation assay. Endothelial markers and fibrosis markers were measured by western blot. Results H/R treatment promoted miR-133 expression in EPCs and EPC-derived exosomes. miR-133 could be incorporated into exosomes and transmitted to cardiac fibroblasts, increasing the angiogenesis and MEndoT of cardiac fibroblasts. miR-133 silencing in H/R-induced EPCs could inhibit miR-133 expression in EPCs and EPCs-derived exosomes. miR-133 silencing in H/R-induced EPCs could inhibit the angiogenesis and MEndoT of cardiac fibroblasts and reverse the effect of H/R treatment. Additionally, miR-133 was specially sorted into H/R-induced EPC-derived exosomes via YBX-1. YBX-1 silencing inhibited miR-133 transfer and reduced fibroblast angiogenesis and MEndoT. Conclusion miR-133 was specially sorted into H/R-induced EPC-derived exosomes via YBX-1 to increase fibroblast angiogenesis and MEndoT.

Introduction Myocardial ischemia/reperfusion (I/R) injury is a leading cause of cardiac dysfunction. Circular RNAs (circRNAs) are involved in the pathogenesis of myocardial I/R injury. However, the functions and underlying mechanisms are unclear. The present study determined the role of circ-RHOJ.1 in regulating myocardial cell proliferation and apoptosis after I/R injury. Material and methods Myocardial cells isolated from Sprague-Dawley rats were identified with an immunofluorescence assay using cardiac troponin T antibody. Expression of circ-RHOJ.1, miR-124-3p and neuregulin-1 (NRG1) mRNA was assessed with real-time quantitative polymerase chain reaction. NRG1 protein expression was evaluated with western blot and immunofluorescence assays. Dual-luciferase reporter assay was performed to confirm interaction between miR-124-3p and circ-RHOJ.1, and miR-124-3p and NRG1. Effects of circ-RHOJ.1 overexpression or miR-124-3p inhibition on cell proliferation and apoptosis were evaluated using cell counting kit (CCK)-8 assay and flow cytometry. Cytokines levels were analyzed with an enzyme-linked immunosorbent assay. Results Myocardial cells were successfully isolated and had down-regulated expression of circ-RHOJ.1 and NRG1, and up-regulated expression of miR-124-3p after I/R injury. circ-RHOJ.1 acted as a sponge for miR-124-3p, and NRG1 served as a target gene of miR-124-3p. circ-RHOJ.1 overexpression or miR-124-3p inhibition increased interleukin (IL)-10 levels and reduced IL-2, IL-6, and tumor necrosis factor-a levels in myocardial cells after I/R injury. Functional assay results illustrated that circ-RHOJ.1 overexpression or miR-124-3p inhibition enhanced proliferation and inhibited apoptosis of myocardial cells after I/R injury. Conclusions Circ-RHOJ.1 served as a molecular marker of myocardial I/R injury via regulation of miR-124-3p and NRG1 expression.

Introduction Our previous study showed that naringin (NRG) protects cardiomyocytes against high glucose (HG)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK). Leptin induces hypertrophy in rat cardiomyocytes via p38/MAPK activation. The present study aimed to test the hypothesis that leptin-Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3), which are responsible for leptin’s functions, are involved in HG-induced injuries and cardioprotective effects of NRG in cardiomyocytes. Material and methods H9c2 cells were exposed to HG for 24 h to establish a cardiomyocyte injury model. Cells were pretreated with NRG and other drugs before exposure to HG. Protein expression was measured by western blot analysis. Cell viability was detected by Cell Counting Kit-8 assay. Apoptotic cells were assessed by Hoechst 33258 staining assay. Intracellular reactive oxygen species levels were determined by dichlorofluorescein diacetate staining. Mitochondrial membrane potential was evaluated using JC-1. An enzyme-linked immunosorbent assay was performed to determine the inflammatory cytokines. Results NRG significantly attenuated HG-induced increases in leptin and Ob-R expression. Pretreatment with either a leptin antagonist (LA) or NRG markedly ameliorated HG-induced elevation of phosphorylated (p)-JAK2 and p-STAT3, respectively. Pretreatment with NRG, LA, Ob-R antagonist, or AG490 clearly alleviated HG-induced injuries and inflammation. Conclusions This study provides new evidence of the NRG protective effects of H9c2 cells against HG-induced injuries possibly via modulation of the leptin-JAK2/STAT3 pathway.

Numerous stereoscopic image saliency detection algorithms have been presented to detect the salient objects in a stereoscopic image. However, they typically fail to uniformly highlight all the objects when the image contains multiple objects or complex backgrounds. In this paper, we propose a multi-cue-driven optimization (MCDO) for stereoscopic image saliency detection. MCDO leverages multiple cues, including depth, color, and spatial position to optimize the saliency maps generated by existing saliency detection algorithms. Fully connected conditional random field is used to integrate the depth, color, and spatial cues from the input stereoscopic image to ensure that pixels with similar depth, color, and/or spatial position have similar saliency values. Compared with original saliency maps, the optimized saliency maps have more uniformly highlighted salient objects, whose boundaries are more precise, and fewer incorrectly detected background regions. The experimental results on three datasets demonstrate that the proposed MCDO method can effectively improve the performance of stereoscopic and 2-D image saliency detection algorithms.

One-shot video-based person re-identification exploits the unlabeled data by using a single-labeled sample for each individual to train a model and to reduce the need for laborious labeling. Although recent works focusing on this task have made some achievements, most state-of-the-art models are vulnerable to misalignment, pose variation and corrupted frames. To address these challenges, we propose a one-shot video-based person re-identification model based on pose-guided spatial alignment and KFS. First, a spatial transformer sub-network trained using pose-guided regression is employed to perform the spatial alignment. Second, we propose a novel training strategy based on KFS. Key frames with abruptly changing poses are deliberately identified and selected to make the network adaptive to pose variation. Finally, we propose a frame feature pooling method by incorporating long short-term memory with an attention mechanism to reduce the influence of corrupted frames. Comprehensive experiments are presented based on the MARS and DukeMTMC-VideoReID datasets. The mAP values for these datasets reach 46.5% and 68.4%, respectively, demonstrating that the proposed model achieves significant improvements over state-of-the-art one-shot person re-identification methods.

Semantic segmentation plays a critical role in image understanding. Recently, Fully Convolutional Network (FCN)-based models have made significant progress in semantic segmentation. However, achieving the full utilization of contextual information and recovery of lost spatial details remains a huge challenge. In this paper, we present a semantic segmentation model based on pyramid context contrast and a subpixel-aware dense decoder. We propose first using the pyramid context contrast to exploit the capability of contextual information by aggregating multi-scale foreground representations in different background regions via the pyramid context contrast module. Then, we add a subpixel-aware dense decoder architecture to reuse features extracted from different decoder levels by pixel shuffle, which can reasonably resolve resolution inconsistency between feature maps. Next, we refine the boundary by utilizing spatial visual information about low-level features via a boundary refinement branch with addition of auxiliary supervision. The presented model was evaluated using the PASCAL VOC 2012 semantic segmentation benchmark and achieved a performance of 86.9%, demonstrating that the proposed model achieves considerable improvement over most state-of-the-art models.

2D image quality assessment (IQA) and stereoscopic 3D IQA are considered as two different tasks in the literature. In this paper, we present an index for both no-reference 2D and 3D IQA. We propose to transform the IQA task into a task of quality comparison between images. By generating image pairs, the amount of training data reaches the square of the original amount of data, effectively solving the lacking of training samples. We also propose a learning to rank model using Siamese convolutional neural networks (LRSN) for quality comparison. The presented LRSN has two branches that have the same structure, share weights with each other, and take two image patches as inputs. The goal of LRSN is learning to rank the quality scores between the two input image patches. The relative quality score of a test image is obtained by first comparing its image patches with many image patches of other images and counts the number of times that its image patches are ranked superior to other patches. The experimental results on three 2D (LIVE, CSIQ, and TID2013) and three 3D (LIVE 3D Phase-I, LIVE 3D Phase-II, and NBU) IQA databases demonstrate that the proposed LRSN model works well for both 2D and 3D IQA and outperforms the state-of-the-art no-reference 2D and 3D IQA metrics.

Synthetic aperture radar (SAR) is an advanced microwave sensor, which has been widely used in ocean surveillance, and its operation is not affected by light and weather. SAR ship instance segmentation can provide not only the box-level ship location but also the pixel-level ship contour, which plays an important role in ocean surveillance. However, most existing methods are provided with limited box positioning ability, hence hindering further accuracy improvement of instance segmentation. To solve the problem, we propose a global context boundary-aware network (GCBANet) for better SAR ship instance segmentation. Specifically, we propose two novel blocks to guarantee GCBANet’s excellent performance, i.e., a global context information modeling block (GCIM-Block) which is used to capture spatial global long-range dependences of ship contextual surroundings, enabling larger receptive fields, and a boundary-aware box prediction block (BABP-Block) which is used to estimate ship boundaries, achieving better cross-scale box prediction. We conduct ablation studies to confirm each block’s effectiveness. Ultimately, on two public SSDD and HRSID datasets, GCBANet outperforms the other nine competitive models. On SSDD, it achieves 2.8% higher box average precision (AP) and 3.5% higher mask AP than the existing best model; on HRSID, they are 2.7% and 1.9%, respectively.

The present study was undertaken to examine the association between intermittent hypoxia and left ventricular (LV) remodeling and explore which parameter of intermittent hypoxia is most relevant to LV remodeling in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). Two hundred eighty six patients underwent polysomnographic examination were enrolled. Based on apnea-hypoxia index (AHI), patients were divided into no, mild, moderate and severe OSAHS groups. Between-group differences in LV remodeling and the association between parameters of intermittent hypoxia and LV remodeling was evaluated. Patients with severe OSAHS were more likely to have hypertension, and higher values of LV mass (LVM) and LVM index (LVMI). In univariate regression analysis, male, body mass index (BMI), systolic and diastolic blood pressure (BP), statins, antihypertensive drugs, creatinine, and parameters of intermittent hypoxia (AHI, obstructive apnea index [OAI], lowest oxygen saturation [LSpO2], oxygen desaturation index [ODI], time spent below oxygen saturation of 90% [TS90%], and mean nocturnal oxygen saturation [MSpO2]) were associated with LVMI. After multivariate regression analyses, only male gender, BMI, systolic BP, creatinine, and ODI remained significantly associated with LVMI. Compared to those without LV hypertrophy (LVH), patients with LVH had higher ODI. Compared to patients with normal LV, concentric remodeling and eccentric LVH, those with concentric LVH had higher ODI. In conclusion, intermittent hypoxia was significantly associated with left ventricular remodeling; and among various parameters of intermittent hypoxia, ODI was the most relevant to LV remodeling.

Background: This study aimed to evaluate the role of Semen Brassicae, a common Traditional Chinese Medicine, in the treatment of hypertension. Methods: Spontaneously hypertensive rats (SHRs) were divided into five groups and were gavaged with either distilled water, water-decocted solution from Semen Brassicae (0.5, 1 or 2 g/kg), or nifedipine (2.7 mg/kg). Normal rats gavaged with distilled water were used as a control. Systolic (SBP) and diastolic blood pressure (DBP) were measured using a non-invasive method. After 8 weeks of administration, all animals were anesthetized. Abdominal aortic serum was collected to measure serum factors; the thoracic aorta was collected for hematoxylin and eosin staining and western blot analysis. Results: Both SBP and DBP were significantly decreased after Semen Brassicae treatment. Endothelin-1 and angiotensin II levels in abdominal aortic serum, as well as the levels of inflammatory factors interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha, were significantly decreased after Semen Brassicae treatment. The wall thickness of the thoracic aorta was significantly reduced after Semen Brassicae treatment. Nitric oxide level and the activity of superoxide dismutase and glutathione peroxidase were significantly increased, and malondialdehyde level was significantly decreased in the abdominal aortic serum after Semen Brassicae treatment. Semen Brassicae treatment increased the levels of peroxisome proliferator-activated receptor gamma and IκB-α and decreased the levels of intercellular adhesion molecule 1, monocyte chemoattractant protein-1, von Willebrand factor, p-IκB-α and p-p65 NF-κB. Conclusions: In conclusion, water-decocted solution from Semen Brassicae can decrease blood pressure, improve vascular remodeling, and attenuate oxidative stress and inflammation in SHRs.

In view of the observation that saliency maps generated by saliency detection algorithms usually show similarity imperfection against the ground truth, the authors propose an optimisation algorithm based on clustering and fitting (CF) for saliency detection. The algorithm uses a fitting model to represent the quantitative relationship between ground truth and algorithm‐generated saliency maps. The authors use the K‐means method to cluster the images into k clusters according to the similarities among images. Image similarity is measured in terms of scene and colour by using the GIST and colour histogram features, after which the fitting model for each cluster is calculated. The saliency map of a new image is optimised by using one of the fitting models which correspond to the cluster to which the image belongs. Experimental results show that their CF‐based optimisation algorithm improves the performance of various single image saliency detection algorithms. Moreover, the improvement achieved by their algorithm when using both CF strategies is greater than the improvement achieved by the same algorithm when not using the clustering strategy. In addition, their proposed optimisation algorithm can also effectively optimise co‐saliency detection algorithms which already consider multiple similar images simultaneously to improve saliency of single images.