Research on online teaching platform system based on microservice architecture

The traditional online teaching adopts the single architecture to develop and implement the system, which facilitates the data sharing and testing of the system. However, due to the increasing complexity of the system's business functions, the system based on monolithic architecture has become increasingly complex, its scalability has deteriorated, and its concurrency performance has decreased. Based on these problems, this paper puts forward combining microservice architecture and online teaching platform, using microservice architecture independent deployment, concurrent performance characteristics such as high technology selection and flexible, the complex business function is divided into several small service module, solve the challenges faced by the traditional system, at the same time improve the efficiency of the use of online teaching platform and students' learning autonomy, The system function design, architecture design, safety design and so on are expounded to build an efficient and perfect online teaching platform

Research on copyright appointment registration microplatform system based on vue

With the rapid development of copyright industry, people’s copyright awareness of their own creation of software and works is constantly improving, the number of applications for software copyright registration and works copyright is increasing. Therefore, how to make copyright registration business becomes more convenient and efficient is imminent. Existing copyright registration system need to first fill through PC and then make an appointment through the phone to deal with relevant business. This model is not only complicated operations, but also poor user experience. Therefore, based on the analysis of multiple needs of users and enterprises, this paper proposes to use Vue,SpringBoot, MyBatis and other technologies to develop a copyright appointment registration system based on microplatform. The development of this system can not only for the user to create a more convenient way of operation, give users a better experience, but also can change, rich business approach, bring more profits

Effect of Heat Stress on Egg Production, Steroid Hormone Synthesis, and Related Gene Expression in Chicken Preovulatory Follicular Granulosa Cells

This study was conducted to elucidate the molecular mechanisms underlying heat stress (HS)-induced abnormal egg-laying in laying hens. Hy-Line brown laying hens were exposed to HS at 32 °C or maintained at 22 °C (control) for 14 days. In addition, granulosa cells (GCs) from preovulatory follicles were subjected to normal (37 °C) or high (41 °C or 43 °C) temperatures in vitro. Proliferation, apoptosis, and steroidogenesis were investigated, and the expression of estrogen and progesterone synthesis-related genes was detected. The results confirmed that laying hens reared under HS had impaired laying performance. HS inhibited proliferation, increased apoptosis, and altered the GC ultrastructure. HS also elevated progesterone secretion by increasing the expression of steroidogenic acute regulatory protein (StAR), cytochrome P450 family 11 subfamily A member 1 (CYP11A1), and 3b-hydroxysteroid dehydrogenase (3β-HSD). In addition, HS inhibited estrogen synthesis in GCs by decreasing the expression of the follicle-stimulating hormone receptor (FSHR) and cytochrome P450 family 19 subfamily A member 1 (CYP19A1). The upregulation of heat shock 70 kDa protein (HSP70) under HS was also observed. Collectively, laying hens exposed to high temperatures experienced damage to follicular GCs and steroidogenesis dysfunction, which reduced their laying performance. This study provides a molecular mechanism for the abnormal laying performance of hens subjected to HS

Recent Advances in g-C₃N₄-Based Photocatalysts for NO_x Removal

Nitrogen oxides (NOx) pollutants can cause a series of environmental issues, such as acid rain, ground-level ozone pollution, photochemical smog and global warming. Photocatalysis is supposed to be a promising technology to solve NOx pollution. Graphitic carbon nitride (g-C3N4) as a metal-free photocatalyst has attracted much attention since 2009. However, the pristine g-C3N4 suffers from poor response to visible light, rapid charge carrier recombination, small specific surface areas and few active sites, which results in deficient solar light efficiency and unsatisfactory photocatalytic performance. In this review, we summarize and highlight the recent advances in g-C3N4-based photocatalysts for photocatalytic NOx removal. Firstly, we attempt to elucidate the mechanism of the photocatalytic NOx removal process and introduce the metal-free g-C3N4 photocatalyst. Then, different kinds of modification strategies to enhance the photocatalytic NOx removal performance of g-C3N4-based photocatalysts are summarized and discussed in detail. Finally, we propose the significant challenges and future research topics on g-C3N4-based photocatalysts for photocatalytic NOx removal, which should be further investigated and resolved in this interesting research field

Non-canonical STING–PERK pathway dependent epigenetic regulation of vascular endothelial dysfunction via integrating IRF3 and NF-κB in inflammatory response

Inflammation-driven endothelial dysfunction is the major initiating factor in atherosclerosis, while the underlying mechanism remains elusive. Here, we report that the non-canonical stimulator of interferon genes (STING)–PKR-like ER kinase (PERK) pathway was significantly activated in both human and mice atherosclerotic arteries. Typically, STING activation leads to the activation of interferon regulatory factor 3 (IRF3) and nuclear factor-kappa B (NF-κB)/p65, thereby facilitating IFN signals and inflammation. In contrast, our study reveals the activated non-canonical STING–PERK pathway increases scaffold protein bromodomain protein 4 (BRD4) expression, which encourages the formation of super-enhancers on the proximal promoter regions of the proinflammatory cytokines, thereby enabling the transactivation of these cytokines by integrating activated IRF3 and NF-κB via a condensation process. Endothelium-specific STING and BRD4 deficiency significantly decreased the plaque area and inflammation. Mechanistically, this pathway is triggered by leaked mitochondrial DNA (mtDNA) via mitochondrial permeability transition pore (mPTP), formed by voltage-dependent anion channel 1 (VDAC1) oligomer interaction with oxidized mtDNA upon cholesterol oxidation stimulation. Especially, compared to macrophages, endothelial STING activation plays a more pronounced role in atherosclerosis. We propose a non-canonical STING–PERK pathway-dependent epigenetic paradigm in atherosclerosis that integrates IRF3, NF-κB and BRD4 in inflammatory responses, which provides emerging therapeutic modalities for vascular endothelial dysfunction

New clinical screening strategy to distinguish HNF1A variant-induced diabetes from young early-onset type 2 diabetes in a Chinese population

ObjectiveMaturity-onset diabetes of the young caused by hepatocyte nuclear factor-1 alpha (HNF1A) variants (HNF1A-MODY) is a common form of monogenetic diabetes. Although patients with HNF1A-MODY might specifically benefit from sulfonylurea treatment, available methods for screening this specific type of diabetes are not cost-effective. This study was designed to establish an optimized clinical strategy based on multiple biomarkers to distinguish patients with HNF1A-MODY from clinically diagnosed early-onset type 2 diabetes (EOD) for genetic testing in a Chinese population.Research design and methodsA case–control study including 125 non-related young patients with EOD and 15 probands with HNF1A-MODY (cohort 1) was conducted to evaluate reported biomarkers for HNF1A-MODY. A cut-off for the fasting insulin (Fins) level, the 97.5 percentile of 150 healthy subjects with normal components of metabolic syndrome (cohort 2), was used to filter out individuals with obvious insulin resistance (Fins <102 pmol/L). An optimized clinical screening strategy (HNF1A-CSS) was established, and its effectiveness was assessed in another group of 410 young patients with EOD (cohort 3).ResultsIn cohort 1, body mass index (BMI), serum high-density lipoprotein cholesterol (HDL-c) and high-sensitivity C reactive protein (hs-CRP) levels were confirmed to be useful for the differential diagnosis of HNF1A-MODY. In cohort 3, eight probands with HNF1A-MODY were identified. In cohort 3 and young relatives with HNF1A-MODY, meeting three of four criteria (BMI <28 kg/m2, hs-CRP <0.75 mg/L, Fins <102 pmol/L and HDL-c >1.12 mmol/L), the sensitivity and specificity of HNF1A-CSS were 100% and 69.3%, respectively. In the pooled analysis of all young patients, HNF1A-CSS displayed 90.5% sensitivity and 73.6% specificity for identifying patients with HNF1A-MODY among those with clinically diagnosed EOD.ConclusionOur HNF1A-CSS is useful for distinguishing patients with HNF1A-MODY from patients with EOD in a young Chinese population

Impairment on the lateral mobility induced by structural changes underlies the functional deficiency of the lupus-associated polymorphism FcγRIIB-T232.

FcγRIIB functions to suppress the activation of immune cells. A single-nucleotide polymorphism in the transmembrane (TM) domain of FcγRIIB, FcγRIIB-T232, is associated with lupus. In this study, we investigated the pathogenic mechanism of FcγRIIB-T232 at both functional and structural levels. Our results showed that FcγRIIB-T232 exhibited significantly reduced lateral mobility compared with FcγRIIB-I232 and was significantly less enriched into the microclusters of immune complexes (ICs) after stimulation. However, if sufficient responding time is given for FcγRIIB-T232 to diffuse and interact with the ICs, FcγRIIB-T232 can restore its inhibitory function. Moreover, substituting the FcγRIIB-T232 TM domain with that of a fast floating CD86 molecule restored both the rapid mobility and the inhibitory function, which further corroborated the importance of fast mobility for FcγRIIB to function. Mechanistically, the crippled lateral mobility of FcγRIIB-T232 can be explained by the structural changes of the TM domain. Both atomistic simulations and nuclear magnetic resonance measurement indicated that the TM helix of FcγRIIB-T232 exhibited a more inclined orientation than that of FcγRIIB-I232, thus resulting in a longer region embedded in the membrane. Therefore, we conclude that the single-residue polymorphism T232 enforces the inclination of the TM domain and thereby reduces the lateral mobility and inhibitory functions of FcγRIIB

Impairment on the lateral mobility induced by structural changes underlies the functional deficiency of the lupus-associated polymorphism FcγRIIB-T232

FcγRIIB functions to suppress the activation of immune cells. A single-nucleotide polymorphism in the transmembrane (TM) domain of FcγRIIB, FcγRIIB-T232, is associated with lupus. In this study, we investigated the pathogenic mechanism of FcγRIIB-T232 at both functional and structural levels. Our results showed that FcγRIIB-T232 exhibited significantly reduced lateral mobility compared with FcγRIIB-I232 and was significantly less enriched into the microclusters of immune complexes (ICs) after stimulation. However, if sufficient responding time is given for FcγRIIB-T232 to diffuse and interact with the ICs, FcγRIIB-T232 can restore its inhibitory function. Moreover, substituting the FcγRIIB-T232 TM domain with that of a fast floating CD86 molecule restored both the rapid mobility and the inhibitory function, which further corroborated the importance of fast mobility for FcγRIIB to function. Mechanistically, the crippled lateral mobility of FcγRIIB-T232 can be explained by the structural changes of the TM domain. Both atomistic simulations and nuclear magnetic resonance measurement indicated that the TM helix of FcγRIIB-T232 exhibited a more inclined orientation than that of FcγRIIB-I232, thus resulting in a longer region embedded in the membrane. Therefore, we conclude that the single-residue polymorphism T232 enforces the inclination of the TM domain and thereby reduces the lateral mobility and inhibitory functions of FcγRIIB