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为有效管控大豆浸出制油工艺的安全风险，消除事故隐患，预防安全事故，对大豆浸出制油工艺安全进行了辨识，对其工艺安全风险进行了评价，同时，梳理了安全风险与事故隐患的关系，并提出了工艺安全生产风险管控措施。大豆浸出制油工艺的安全生产风险较高，主要事故风险为坍塌、火灾、粉尘爆炸，主要风险点的风险等级为较大风险或重大风险。生产企业可通过建立并落实安全生产风险分级管控和生产安全事故排查治理双重预防工作机制，管控工艺安全生产风险，降低安全生产风险等级，减少隐患存量，确保生产装置和作业场所具备安全生产条件，同时可设置大豆粉尘抑爆系统，高温蒸汽泄漏紧急自动切断系统，正己烷、混合油泄漏紧急自动切断系统，提升工艺本质安全系数。In order to effectively control the safety risks during soybean leaching process, eliminate the hidden dangers and prevent safety accidents, the safety of soybean leaching technology was identified, its process safety risk was evaluated, the relationship between the safety production risks and the hidden dangers was sorted out, and control measures of the safety production were put forward. The safety production risk of the soybean leaching process is high. The main accident risks are collapse, fire and dust explosion, and the risk levels of the main risk points are greater risk or major risk. By establishing and implementing a dual prevention mechanism for the grading and control of production safety risks and the investigation and management of production safety accidents, production enterprises can control production safety risks, reduce the level of production safety risks, reduce the stock of hidden hazards, to ensure that production units and workplaces are equipped with safe production conditions. Meanwhile, enterprises can enhance the essential safety coefficient of the process by setting up soybean dust explosion suppression systems, automatic cut-off system of high temperature steam leakage emergency, automatic cut-off system of n-hexane and miscella oil leakage emergency.

Maintaining global ecological balance is inextricably linked to the effective governance of public resources. Previous studies have proposed the introduction of incentive mechanisms to mitigate the defection behavior within the scope of public resource management to facilitate sustainable utilization. However, these incentive strategies often present a considerable financial burden. Here, we first propose a two-threshold incentive scheme based on group state objectives, where the reward mechanism is triggered when the number of cooperators is below the threshold M , and the punishment mechanism is triggered when the number of cooperators is above the threshold Q. We further introduce an incentive mechanism by considering both resource and group thresholds, where incentives are implemented separately when the number of cooperators and the current quantity of resources meet thresholds. Our theoretical results reveal that introducing these two new mechanisms can effectively maintain cooperative behavior and sustainable resources while reducing management costs. However, if the initial resource level is low, the tragedy of the commons will still occur. It is recommended that the number of developers be reduced, the allocation be lowered, or the development simply suspended and the natural regeneration of resources be waited for. [ABSTRACT FROM AUTHOR]

Trust plays a crucial role in social and economic interactions, serving as the foundation for social stability and human cooperation. Previous studies have explored the evolution of trust between investors and trustees by constructing trust game models, incorporating factors such as network structure, reputation, and incentives. However, these studies often assume that investors consistently maintain their investment behavior, neglecting the potential influence of the investment environment on investment behavior. To address this gap, we introduce a loss assessment mechanism and construct a trust game model. Specifically, investors first allocate their investment amount to an assessment agency, which divides the amount into two parts according to a certain allocation ratio. One part is used for investment assessment, and the results are fed back to the investors. If the payoff from this portion exceeds the investors' expected value, the remaining amount is invested; otherwise, it is returned to the investors. The results indicate that investors with moderate expectations are more likely to form alliances with trustworthy trustees, thereby effectively promoting the evolution of trust. Conversely, lower or higher expectations yield opposite results. Additionally, we find that as investors' expected values increase, the corresponding allocation ratio should also increase to achieve higher payoffs. [ABSTRACT FROM AUTHOR]

The in situ metabolic profiling of the kidney is crucial to investigate the complex metabolic reprogramming underlying diabetic kidney disease (DKD) and to allow exploration of potential metabolic targets to improve kidney function. However, as the kidney is a highly heterogeneous organ, traditional metabolomic methods based on bulk analysis that produce an averaged measurement are inadequate. Herein, we employed an in situ metabolomics approach to discover alternations of DKD-associated metabolites and metabolic pathways. A series of histology-specific metabolic disturbances were discovered in situ using airflow-assisted desorption electrospray ionization mass spectrometry imaging (AFADESI–MSI). In combination with integrated metabolomics analysis, five dysfunctional metabolic pathways were identified and located in the kidneys of type-2 DKD mice simultaneously for the first time, including taurine metabolism, arginine and proline metabolism, histidine metabolism, biosynthesis of unsaturated fatty acids, and fatty acid degradation pathways. As crucial nodes of metabolic pathways, five dysregulated rate-limiting enzymes related to altered metabolic pathways were further identified. These findings reveal alternations from metabolites to enzymes at the molecular level in the progression of DKD and provide insights into DKD-associated metabolic reprogramming.

An arc fault is the leading cause of electrical fire. Aiming at the problems of difficulty in manually extracting features, poor generalization ability of models and low prediction accuracy in traditional arc fault detection algorithms, this paper proposes a fault arc detection method based on the fusion of channel attention mechanism and residual network model. This method is based on the channel attention mechanism to perform global average pooling of information from each channel of the feature map assigned by the residual block while ignoring the local spatial data to enhance the detection and recognition rate of the fault arc. This paper introduces a one-dimensional depth separable convolution (1D-DS) module to reduce the network model parameters and shorten the time of single prediction samples. The experimental results show that the F1 score of the network model for arc fault detection under mixed load conditions is 98.07%, and the parameter amount is reduced by 46.06%. The method proposed in this paper dramatically reduces the parameter quantity, floating-point number and time complexity of the network structure while ensuring a high recognition rate, which improves the real-time response ability to detect arc fault. It has a guiding significance for applying arc fault on the edge side. [ABSTRACT FROM AUTHOR]

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease, but the molecular mechanisms of disease remain not very clear and there is no curative therapeutic strategy so far. This study was carried out to identify the expression profile of circular RNA (circRNA) in human DKD and explore circRNA regulatory function in glomeruli and tubuli simultaneously. As a result, a total of 40 upregulated and 23 downregulated differentially expressed circRNAs (DEcircRNAs) were detected. Six candidate DEcircRNAs were verified by quantitative real-time polymerase chain reaction in high glucose-treated human mesangial cells and human proximal renal tubular epithelial cells, respectively. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that both in glomeruli and in tubuli the DEcircRNAs-targeted genes participated in many pathophysiological processes of DKD. Correlation analysis with renal function showed that expression level of DEcircRNA-targeted hub gene was related to renal function. In conclusion, this is the first study to report expression profiles of circRNAs in kidney of DKD patients, and further analysis demonstrated that circRNA probably played a significant regulatory role, providing help for understanding the pathogenesis of DKD and investigating novel diagnostic and therapeutic strategy. [ABSTRACT FROM AUTHOR]

Clinical characteristics of intestinal ulcers complicated with Epstein-Barr virus (EBV) infection remain poorly studied. This study is aimed at providing further insight into clinical features of this patient cohort. The presence of serum EBV DNA was assessed in 399 patients with colonic ulcers, of which 30 cases were positive. In EBV-positive patients, the EBV-encoded RNA (EBER) was detected in intestinal tissues of 13 patients (EBER-positive group). The test was negative in 17 patients (EBER-negative group). Acute EBV infection rate in patients with colonic ulcer was 7.52%. Age and sex differences between two groups were not statistically significant. Fever, abdominal lymph node enlargement, and crater-like gouged ulcer morphology were more common in the EBER-positive group (P < 0.05). The albumin level in the EBER-positive group was significantly lower compared to that in the EBER-negative group (P < 0.05). The copy count of EBV DNA in the blood of patients from the EBER-positive group was higher, and the prognosis was worse (P < 0.05). Clinical manifestations were more severe in the EBER-positive group. Endoscopic, histopathological, and biochemical findings were also more serious in this group of patients. The findings point to the importance of assessing the EBER expression in patients with intestinal ulcers of various etiology. EBER positivity should be viewed as a diagnostic marker of more severe condition requiring more aggressive treatment. [ABSTRACT FROM AUTHOR]

Renal tubulointerstitial fibrosis plays a significant role in the development of diabetic nephropathy (DN). SNAI1 is a main activator of epithelial-to-mesenchymal transition (EMT) in the process of fibrosis. This study aimed to investigate the effect of miR-30b-5p targeting SNAI1 on the EMT in DN. Bioinformatics and miRNAs microarray analyses were used to predict the candidate miRNA targeting SNAI1, that is miR-30b-5p. The db/db mice was as DN animal model and renal tissues of mice were stained with PAS. The miR-30b-5p expression in mouse and human renal tissue were examined by quantitative RT-PCR (qRT-PCR) and fluorescence in situ hybridization (FISH), while SNAI1 expression was determined by qRT-PCR and immunohistochemistry. Luciferase reporter gene assay was used to confirm miR-30b-5p directly target 3′-UTR of the SNAI1 mRNA. In vitro, HK-2 cells were treated with high glucose to establish hyperglycemia cell model and transfected with miR-30b-5p mimics to overexpress miR-30b-5p. Expression of miR-30b-5p, SNAI1 and EMT related indicators (E-cadherin, a-SMA and Vimentin) in HK-2 cells under different treatments were determined by qRT-PCR and/or western-blot. In addition, immunofluorescence was performed to evaluate a-SMA expression in HK-2 cells under different treatments. Bioinformatics analyses revealed miR-30b-5p had complementary sequences with SNAI1 mRNA and the seed region of miR-30b-5p was conserved in human and a variety of animals, including mice. Microarray analysis showed miR-30b expression decreased in DN mice, which was further verified in db/db mice by qRT-PCR and in human DN by FISH. Contrary to miR-30b-5p, SNAI1 expression level was upregulated in db/db mice. Correlation analysis suggested SNAI1 mRNA level was negatively with miR-30b-5p level in renal tissue of db/db mice. Luciferase reporter gene assay confirmed miR-30b-5p directly targeted SNAI1 mRNA. In high glucose induced HK-2 cells, expression levels of miR-30b-5p and E-cadherin were decreased, while SNAI1, a-SMA and Vimentin were increased. Overexpression miR-30b-5p in high glucose induced HK-2 cells could reverse that phenomenon to some extent. These findings suggest that miR-30b-5p play a protective role by targeting SNAI1 in renal EMT in DN. • EMT played a key role in tubulointerstitial fibrosis of DN. • SNAI1 is a main activator of EMT; SNAI1 participated in tubular lesion of DN. • miR-30b-5p regulated EMT of DN by directly targeting SNAI1. • Overexpression of miR-30b-5p alleviated high glucose-induced EMT in HK2 cells. [ABSTRACT FROM AUTHOR]

The present study investigated the role of the c-Jun N-terminal kinase (JNK)/transforming growth factor-β (TGF-β)/Smad3 pathway in endoplasmic reticulum stress (ERS)-mediated renal interstitial fibrosis, which would be beneficial for chronic kidney disease (CKD) therapy. In human renal biopsy tissue, the expression levels of glucose-regulated protein 78 (GRP78) and phosphorylated (p)-JNK were examined by immunohistochemical analysis. In renal tubular HK-2 cells, tunicamycin (TM) was used to induce ERS, and the cells were then treated with the chemical ERS inhibitor 4-phenylbutyrate (4-PBA) or the chemical JNK pathway inhibitor SP600125, respectively. Western blotting was then performed in the cells to determine the expression levels of GRP78 and p-JNK proteins, as well as TGF-β/Smad3 pathway-associated proteins, including TGF-β1, p-Smad3, connective tissue growth factor and α-smooth muscle actin. The results revealed that GRP78 and p-JNK were evidently expressed in the renal tissues of patients with CKD, and these expression levels were significantly higher in renal tissues with severe interstitial fibrosis compared with glomerular minor lesion tissues (P<0.01 and P<0.05, respectively). Furthermore, ERS and JNK pathway inhibition decreased the expression levels of TGF-β/Smad3 pathway signals in cells incubated with TM. ERS pathway inhibition also attenuated the expression levels of p-JNK in HK-2 cells. In conclusion, ERS was observed to serve an important role in the pathogenesis of CKD and may induce renal interstitial fibrosis via the JNK/TGF-β/Smad3 pathway. [ABSTRACT FROM AUTHOR]

Objective:To investigative clinical and pathological characteristics of IgA nephropathy with chronic renal failure. Method:Clinical and pathological findings from 65 cases of IgA nephropathy with chronic renal failure were reviewed. Pathological characteristics of all the cases were analyzed according to WHO definition and Oxford Classification. Evaluating the severity of pathological lesions by the KatafuchiRsemiquantitative scoring system, and analyzing their relationship with clinical indexes of renal function. Results:Of all 65 cases the male and female ratio was 1.4, and the mean age was 37 ± 13 years old. Levels of systolic pressure, mean arterial pressure (MAP), blood urea nitrogen (BUN), serum creatinine (Scr), uric acid (UA), album (Alb), serum IgG and 24 h urinary protein were related with eGRF level (p< 0.05, respectively). The most common pathological type was proliferative sclerosis glomerulonephritis (PSGN) and M1S1E0T0 according to WHO definition and Oxford Classification, respectively, and most of the 65 cases had glomerulosclerosis. Simple IgA deposition was the most common immunopathologic type. Of all the cases, 44.6% accompanied with C3 while 4.6% with C1q. Further analysis revealed there were no relationships between severity of pathological lesion and levels of clinical indexes (Scr and eGRF) (p > 0.05). Conclusion:IgA nephropathy with chronic renal failure usually occurred in young adults, and it had severe clinical condition and pathological changes, while there was no significant relationship between them. [ABSTRACT FROM AUTHOR]

Conclusions: Previous studies have stated the roles and correlation of the four TFs (Sox2, Atoh1, Neurog1, and Neurod1) in the development of neurosensory cells. but whether they are inherited pathogenic factors to cause non-syndromic sensorineural hearing loss is unknown so far. This is the first time for screening theSox2,Atoh1,Neurog1, andNeurod1genes in children with NSHL. The c.133A > G inNeurod1gene is a polymorphism, which is not associated with NSHL. Although these genes are the recognized TFs for modulating the development and transformation of NSCs, they may not be the inherited pathogenic factors to cause congenital severe or profound NSHL directly.Objective: To investigate the effect of the transcription factors (TFs) for the development of neurosensory cells (NSCs) and to explore the genetic etiology of congenital profound non-syndromic sensorineural hearing loss (NSHL).Methods: Children with NSHL, from multi-national and regional group, and control group were recruited to screen for the most common mutations for non-syndromic deafness among East Asian (mtDNA 12S rRNA: 1555A > G, 1494C > T; SLC26A4: IVS7-2 A > G, 2168 C > T). And mutational analysis of the coding regions inSox2,Atoh1andNeurog1,Neurod1genes were performed.Results: Only the c.133A > G (p. Ala45Thr) in theNeurod1gene was detected in this study. The allele frequencies of this variant were 88.00% and 84.88% in the inner ear malformation group and the normal inner ear group, respectively, while 90.85% of children in the control group carried c.133A > G. This variant existed in every group commonly and had no significant difference among them. No variant in the other two TFs was detected in this cohort. [ABSTRACT FROM PUBLISHER]

Inherited deafness has been shown to have high genetic heterogeneity. For many decades, linkage analysis and candidate gene approaches have been the main tools to elucidate the genetics of hearing loss. However, this associated study design is costly, time-consuming, and unsuitable for small families. This is mainly due to the inadequate numbers of available affected individuals, locus heterogeneity, and assortative mating. Exome sequencing has now become technically feasible and a cost-effective method for detection of disease variants underlying Mendelian disorders due to the recent advances in next-generation sequencing (NGS) technologies. In the present study, we have combined both the Deafness Gene Mutation Detection Array and exome sequencing to identify deafness causative variants in a large Chinese composite family with deaf by deaf mating. The simultaneous screening of the 9 common deafness mutations using the allele-specific PCR based universal array, resulted in the identification of the 1555A>G in the mitochondrial DNA (mtDNA) 12S rRNA in affected individuals in one branch of the family. We then subjected the mutation-negative cases to exome sequencing and identified novel causative variants in the MYH14 and WFS1 genes. This report confirms the effective use of a NGS technique to detect pathogenic mutations in affected individuals who were not candidates for classical genetic studies. [ABSTRACT FROM AUTHOR]

IgA nephropathy (IgAN) has become the most common form of primary glomerular disease worldwide. So far, it is still not very clear about the exact pathogenesis of IgAN, thus has no specific therapy. Generally mesangial deposition of IgA, especially polymeric IgA1 (pIgA1), suggests to be the initiating event in the pathogenesis of IgAN. In addition to decreased IgA clearance, IgA over production may also participate in the pathogenesis of IgAN. IgA class switching recombination (CSR) played key role during the process of IgA production. Stimulated with hemolytic streptococcus, tonsillar mononuclear cells (TMCs) of patients with IgAN presented with increased levels of Ia-Ca and activation-induced cytidine deaminase (AID), which are significant for IgA CSR. Human B cells and plasmacytoid dendritic cells express Toll-like receptor (TLR)-9, whose natural ligands are unmethylated cytosine-guanine dinucleotide (CpG) motifs characteristic of bacterial DNA (CpG-DNA). Unmethylated deoxycytidylic-deoxyguanosine oligodeoxynucleotide (CpG-ODN) is able to mimic the immunostimulatory activity of microbial DNA. Study found a significant increase in B cell activation factor (BAFF) production when tonsillar mononuclear cells stimulated with CpG-ODN in patients with IgAN. BAFF can induce germline Cα gene expression, AID expression, and IgA class switching in a CD40-independent manner. Therefore, it could be hypothesized that in IgAN there may exist TLR9-BAFF-IgA CSR axis, which induces excessive IgA production. If the hypothesis is correct, it could be of great significance for pathogenesis of IgAN elucidate and IgAN treatment. [ABSTRACT FROM AUTHOR]

Objective: In this study, we investigated the effect of small interfering RNA (siRNA) of connective tissue growth factor (CTGF) by pRetro-Super (PRS) retrovirus vector on the expression of CTGF and related extracellular matrix molecules in human renal proximal tubular cells (HKCs) induced by high glucose, to provide help for renal tubulointerstitial fibrosis therapy. Methods: HKCs were exposed to d-glucose to observe their dose and time effect, while the mannitol as osmotic control. Retrovirus producing CTGF siRNA were constructed from the inverted oligonucleotides and transferred into packaging cell line PT67 with lipofectamine, and the virus supernatant was used to infect HKC. The expression of CTGF, fibronectin (FN) and collagen-type I (col1) were measured by semi-quantitative RT-PCR and Western blot. Results: In response to high glucose, CTGF expression in HKCs was increased in a dose- and time-dependent manner, whereas the increase did not occur in the osmotic control. Introduction of PRS-CTGF-siRNA resulted in the significant reduction of CTGF, FN, col1 mRNA ( p < 0.01, respectively) and CTGF, col1 protein ( p < 0.05, respectively) expression, while PRS void vector group did not have these effects ( p > 0.05). Conclusions: CTGF siRNA therapy can effectively reduce the levels of CTGF, FN and col1 induced by high glucose in cultured HKCs, which suggested that it may be a potential therapeutic strategy to prevent the renal interstitial fibrosis in the future. [ABSTRACT FROM AUTHOR]

Autophagic/lysosomal dysfunction is a critical pathogenesis of neuronal injury after ischemic stroke. Trehalose has been validated to restore the impaired autophagy flux by boosting transcription factor EB (TFEB) nuclear translocation, but orally administrated trehalose can be greatly digested by intestinal trehalase before entering into brain. Melibiose (MEL), an analogue of trehalose, may thoroughly exert its pharmacological effects through oral administration due to absence of intestinal melibiase. The present study was to investigate whether melibiose could also confer a neuroprotection by the similar pharmacological mechanism as trehalose did after ischemic stroke. The rats were pretreated with melibiose for 7 days before middle cerebral artery occlusion (MCAO) surgery. Twenty-four hours following MCAO/reperfusion, the cytoplasmic and nuclear TFEB, and the proteins in autophagic/lysosomal pathway at the penumbra were detected by western blot and immunofluorescence, respectively. Meanwhile, the neurological deficit, neuron survival, and infarct volume were assessed to evaluate the therapeutic outcomes. The results showed that the neurological injury was significantly mitigated in MCAO+MEL group, compared with that in MCAO group. Meanwhile, nuclear TFEB expression in neurons at the penumbra was significantly promoted by melibiose. Moreover, melibiose treatment markedly enhanced autophagy flux, as reflected by the reinforced lysosomal capacity and reduced autophagic substrates. Furthermore, the melibiose-elicited neuroprotection was prominently counteracted by lysosomal inhibitor Bafilomycin A1 (Baf-A1). Contrarily, reinforcement of lysosomal capacity with EN6 further improved the neurological performance upon melibiose treatment. Our data suggests that melibiose-augmented neuroprotection may be achieved by ameliorating autophagy flux via facilitation of TFEB nuclear translocation in neurons after ischemic stroke. [ABSTRACT FROM AUTHOR]