134 research outputs found

    Research of Risk Identify of Accounts Receivable Financing Based on System Dynamics

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    Based on the analysis of operational mechanism and risk causes, this paper analyzes the financing risk, supply chain operation risk, financing operation risk, legal risk, macro system risk and market risk in six dimensions of SME accounts receivable financing in supply chain. This paper systematically studies the risk characteristics of SME accounts receivable financing, and build SD model of SME accounts receivable financing through the VENSIM simulation software to carry out risk identification, it could identify the risk dimension and risk boundary effectively , and it could dynamic identify the incentive of financing risk through feedback loops analysis of financing process, provides technical support for the further risk measurement and risk prevention of SME accounts receivable financing in supply chain

    The Differential Role of Human Cationic Trypsinogen (PRSS1) p.R122H Mutation in Hereditary and Nonhereditary Chronic Pancreatitis: A Systematic Review and Meta-Analysis.

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    Background:Environmental factors and genetic mutations have been increasingly recognized as risk factors for chronic pancreatitis (CP). The PRSS1 p.R122H mutation was the first discovered to affect hereditary CP, with 80% penetrance. We performed here a systematic review and meta-analysis to evaluate the associations of PRSS1 p.R122H mutation with CP of diverse etiology. Methods:The PubMed, EMBASE, and MEDLINE database were reviewed. The pooled odds ratio (OR) with 95% confidence intervals was used to evaluate the association of p.R122H mutation with CP. Initial analysis was conducted with all etiologies of CP, followed by a subgroup analysis for hereditary and nonhereditary CP, including alcoholic or idiopathic CP. Results:A total of eight case-control studies (1733 cases and 2415 controls) were identified and included. Overall, PRSS1 p.R122H mutation was significantly associated with an increased risk of CP (OR = 4.78[1.13-20.20]). Further analysis showed p.R122H mutation strongly associated with the increased risk of hereditary CP (OR = 65.52[9.09-472.48]) but not with nonhereditary CP, both alcoholic and idiopathic CP. Conclusions:Our study showing the differential role of p.R122H mutation in various etiologies of CP indicates that this complex disorder is likely influenced by multiple genetic factors as well as environmental factors

    AdaFuse: Adaptive Medical Image Fusion Based on Spatial-Frequential Cross Attention

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    Multi-modal medical image fusion is essential for the precise clinical diagnosis and surgical navigation since it can merge the complementary information in multi-modalities into a single image. The quality of the fused image depends on the extracted single modality features as well as the fusion rules for multi-modal information. Existing deep learning-based fusion methods can fully exploit the semantic features of each modality, they cannot distinguish the effective low and high frequency information of each modality and fuse them adaptively. To address this issue, we propose AdaFuse, in which multimodal image information is fused adaptively through frequency-guided attention mechanism based on Fourier transform. Specifically, we propose the cross-attention fusion (CAF) block, which adaptively fuses features of two modalities in the spatial and frequency domains by exchanging key and query values, and then calculates the cross-attention scores between the spatial and frequency features to further guide the spatial-frequential information fusion. The CAF block enhances the high-frequency features of the different modalities so that the details in the fused images can be retained. Moreover, we design a novel loss function composed of structure loss and content loss to preserve both low and high frequency information. Extensive comparison experiments on several datasets demonstrate that the proposed method outperforms state-of-the-art methods in terms of both visual quality and quantitative metrics. The ablation experiments also validate the effectiveness of the proposed loss and fusion strategy

    Mechanism of Electrochemical Delamination of Two-Dimensional Materials from Their Native Substrates by Bubbling

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    A capacitor-based circuit model is proposed to explain the electrochemical delamination of two-dimensional materials from their native substrates where produced gas bubbles squeeze into the interface. The delamination is actually the electric breakdown of the capacitor formed between the solution and substrate. To facilitate the procedure, the backside of the ubstrate has to be shielded so that the capacitor breakdown voltage can be reached. The screening effect can be induced either by nonreactive ions around the electrode or, more effectively, by an undetachable insulator. This mechanism serves as a guideline for the surface science and applications involving the bubbling delamination

    Attitude and Needs Toward MTM Applications of Chronic Disease in China: A Questionnaire Survey

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    ObjectiveChronic diseases are characterized by high incidence, long-term medication, and complex types of medication. There are also many corresponding medication therapy management (MTM) applications on the market, such as iCarea, and Medisafe. However, the existing research mainly focuses on how to choose high-quality MTM applications, and few researchers consider the expectations of MTM applications from potential users. The aims of this study were to investigate the demand, attitude, and expectations of the Chinese patients for the MTM applications to support.MethodsFrom August 2019 to December 2019, we created a questionnaire to have knowledge of user needs, preferences, and expectations for MTM applications among 302 chronic patients in Hunan, Guangdong, and other provinces in China. Logistic regression analysis was performed to analyze the risk factors of affecting patients' attitudes toward MTM applications. Then, respondents' expectations and preferences for MTM applications were statistically analyzed. The survey data were merged to provide information for the design of targeted chronic disease MTM applications.ResultsA total of 260 (86.09%) out of 302 patients the respondents were willing to use the MTM applications of chronic disease. The independent influencing factors for using the MTM applications were long-term medication history (OR = 4.45, P < 0.001), willing to learn about medicine knowledge (OR = 3.01, P = 0.04), and wanting to get more professional medication knowledge via Internet (OR = 2.86, P = 0.005). It was worth noting that among those willing to use MTM applications, 55.00% of respondents were willing to use the WeChat applet for MTM, while only 23.46% of respondents preferred other applications. As to the more prevalent WeChat applet for MTM, the majority of participants expected the inclusion of useful modules, such as medication log (62.81%), medication reminder (62.81%), and medication recommendations (57.79%).ConclusionThe participants are willing to use MTM applications of chronic disease, with a preference for the WeChat applet. Patients tended to use MTM applications if they had a long-term medication history or a desire for medical knowledge, especially if they want to get more professional medication knowledge via the Internet. Participants are expected to include in the WeChat applet as medication logs, medication reminders, and medication recommendations which should be taken into serious account for the further development of MTM applications

    Transcriptional and Functional Analysis of the Effects of Magnolol: Inhibition of Autolysis and Biofilms in Staphylococcus aureus

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    BACKGROUND: The targeting of Staphylococcus aureus biofilm structures are now gaining interest as an alternative strategy for developing new types of antimicrobial agents. Magnolol (MOL) shows inhibitory activity against S. aureus biofilms and Triton X-100-induced autolysis in vitro, although there are no data regarding the molecular mechanisms of MOL action in bacteria. METHODOLOGY/PRINCIPAL FINDINGS: The molecular basis of the markedly reduced autolytic phenotype and biofilm inhibition triggered by MOL were explored using transcriptomic analysis, and the transcription of important genes were verified by real-time RT-PCR. The inhibition of autolysis by MOL was evaluated using quantitative bacteriolytic assays and zymographic analysis, and antibiofilm activity assays and confocal laser scanning microscopy were used to elucidate the inhibition of biofilm formation caused by MOL in 20 clinical isolates or standard strains. The reduction in cidA, atl, sle1, and lytN transcript levels following MOL treatment was consistent with the induced expression of their autolytic repressors lrgA, lrgB, arlR, and sarA. MOL generally inhibited or reversed the expression of most of the genes involved in biofilm production. The growth of S. aureus strain ATCC 25923 in the presence of MOL dose-dependently led to decreases in Triton X-100-induced autolysis, extracellular murein hydrolase activity, and the amount of extracellular DNA (eDNA). MOL may impede biofilm formation by reducing the expression of cidA, a murein hydrolase regulator, to inhibit autolysis and eDNA release, or MOL may directly repress biofilm formation. CONCLUSIONS/SIGNIFICANCE: MOL shows in vitro antimicrobial activity against clinical and standard S. aureus strains grown in planktonic and biofilm cultures, suggesting that the structure of MOL may potentially be used as a basis for the development of drugs targeting biofilms

    Extracellular histones cause intestinal epithelium injury and disrupt its barrier function in vitro and in vivo.

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    Extracellular histones are cytotoxic to various cells and have been extensively proven a vital mediator of multiple organ injuries. However, the effect of extracellular histones on the intestine remains largely unknown. This study aimed to clarify the effect of extracellular histones on the intestine. IEC-6, a cell line of rat small intestinal epithelial crypt, and C57BL/6 or ICR mice were treated with histones. The IEC-6 cells treated with histones from 20 μg/mL to 200 μg/mL for 0-24 h displayed a decline of cell viability and an increase of cell death in a concentration- and time-dependent manner. Moreover, histones (100 μg/mL) induced IEC-6 apoptosis through activating caspase 3 and necroptosis through up-regulation of receptor-interacting serine/threonine protein kinase 1 and 3 (RIPK1 and RIPK3), phosphorylated mixed-lineage kinase domain-like protein (p-MLKL) along with the decrease of caspase-8. Histones treatment disturbed zonular occludens 1 (ZO-1) expression and increased permeability of IEC-6 cell monolayer. In vivo, histones 50 mg/kg injection caused mice intestinal edema, loss apex of villus, epithelial lifting down the sides of the villi, and increased neutrophil infiltration. Elevation of serum intestinal fatty acid binding protein (I-FABP), d-lactate, or Diamine oxidase (DAO) and loss of tight junction protein, ZO-1, at 3 h and 6 h after histones injection strongly indicated severe intestinal epithelium injury, which led to increased permeability of the intestine. In conclusion, extracellular histones cause intestinal epithelial damage via direct cytotoxicity. Consequently, intestinal epithelial tight junction and barrier integrity are disrupted, which may play pivotal roles in diverse diseases

    Hemoconcentration is associated with early faster fluid rate and increased risk of persistent organ failure in acute pancreatitis patients.

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    Background:Controversies existed surrounding the use of hematocrit to guide early fluid therapy in acute pancreatitis (AP). The association between hematocrit, early fluid therapy, and clinical outcomes in ward AP patients needs to be investigated. Methods:Data from prospectively maintained AP database and retrospectively collected details of fluid therapy were analyzed. Patients were stratified into three groups: Group 1, hematocrit 44% at 24 h; Group 3: hematocrit >44% on admission and decreased thereafter during first 24 h. "Early" means first 24 h after admission. Baseline characteristics, early fluid rates, and clinical outcomes of the three groups were compared. Results:Among the 628 patients, Group 3 had a higher hematocrit level, greater baseline predicted severity, faster fluid rate, and more fluid volume in the first 24 h compared with Group 1 or 2. Group 3 had an increased risk for persistent organ failure (POF; odds ratio 2, 95% confidence interval [1.1-3.8], P = 0.03) compared with Group 1 after adjusting for difference in baseline clinical severity scores, there was no difference between Group 2 and Group 3 or Group 1. Multivariate regression analyses revealed that hemoconcentration and early faster fluid rate were risk factors for POF and mortality (both P < 0.05). Conclusions:Hemoconcentration is associated with faster fluid rate and POF in ward AP patients. Randomized trials comparing standardized early fast and slow fluid management is warranted

    Transcriptomics and Network Pharmacology Reveal the Protective Effect of Chaiqin Chengqi Decoction on Obesity-Related Alcohol-Induced Acute Pancreatitis via Oxidative Stress and PI3K/Akt Signaling Pathway

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    Obesity-related acute pancreatitis (AP) is characterized by increasing prevalence worldwide and worse clinical outcomes compared to AP of other etiologies. Chaiqin chengqi decoction (CQCQD), a Chinese herbal formula, has long been used for the clinical management of AP but its therapeutic actions and the underlying mechanisms have not been fully elucidated. This study has investigated the pharmacological mechanisms of CQCQD in a novel mouse model of obesity-related alcohol-induced AP (OA-AP). The mouse OA-AP model was induced by a high-fat diet for 12 weeks and subsequently two intraperitoneal injections of ethanol, CQCQD was administered 2 h after the first injection of ethanol. The severity of OA-AP was assessed and correlated with changes in transcriptomic profiles and network pharmacology in the pancreatic and adipose tissues, and further docking analysis modeled the interactions between compounds of CQCQD and their key targets. The results showed that CQCQD significantly reduced pancreatic necrosis, alleviated systemic inflammation, and decreased the parameters associated with multi-organ dysfunction. Transcriptomics and network pharmacology analysis, as well as further experimental validation, have shown that CQCQD induced Nrf2/HO-1 antioxidant protein response and decreased Akt phosphorylation in the pancreatic and adipose tissues. In vitro, CQCQD protected freshly isolated pancreatic acinar cells from H2O2-elicited oxidative stress and necrotic cell death. The docking results of AKT1 and the active compounds related to AKT1 in CQCQD showed high binding affinity. In conclusion, CQCQD ameliorates the severity of OA-AP by activating of the antioxidant protein response and down-regulating of the PI3K/Akt signaling pathway in the pancreas and visceral adipose tissue
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