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This study aims to investigate the current state of WeChat parent-child relationships among college students and their association with family factors. Using convenient sampling, 6159 students,age from 18 to 25,the participants were selected from colleges of Chengdu to complete a questionnaire survey on response and attitudes towards parents' WeChat friend requests, Family APGAR Index,Parental Management Scale,Family Conflict Scale,were used as measurement tools. Responses to parental WeChat friend requests showed significant positive correlations with higher levels of family function satisfaction (r = 0.10, P<0.01) and parental management (r = 0.11, P<0.01), and a significant negative correlation with family conflict (r = -0.03, P<0.05). This study reveals that Chinese college students generally accept their parents' WeChat friend requests, influenced by family dynamics and traditional values. Positive parental management, family harmony, and good marital relationships enhance students' willingness to connect with their parents on WeChat, indicating the complex interplay between digital interactions and traditional family concepts.This underscores the importance for parents to adopt modern and scientific parenting approaches, fostering a harmonious and nurturing family atmosphere rooted in trust and mutual respect for their children.

This investigation transcends traditional methodologies by providing a quantitative analysis of the dynamic relationship between visceral pathologies and neurogenic spots, employing an acute gastric mucosal injury (AGMI) rat model to map the somatotopic distribution of visceral sensitization. Through hydrochloric acid-induced plasma extravasation and Evans Blue dye (EB) marking, coupled with a geospatial grid system and multivariate statistical analysis, we identified Feature Regions (FRs) with distinct neurogenic responses. Notably, the right T10-13 dermatomere, or FR-11’, exhibited elevated levels of nociceptive neuropeptides and serotonin, indicative of its significant role in pain perception. The application of electroacupuncture at FR-11’ revealed enhanced therapeutic outcomes compared to the conventional acupoint BL-21, positioning it as a promising modality for the management of visceral pain. These findings contribute substantially to our understanding of the mechanisms underlying visceral-somatic pain and pave the way for innovative pain management interventions in clinical settings.

In recent years, bike-sharing has experienced rapid development; however, controversies about the externalities of bike-sharing programs have arisen as well. While bike-sharing programs have impacts on traffic, the environment, and public health, the social impacts, the management, and sustainable development of bike-sharing has also been of interest. The debate regards whether there are externalities, as well as whether and how such externalities can be determined. Based on the rapidly diffused bike-sharing in China, this paper quantitatively explores bike-sharing externalities. Specifically, this paper estimates the impacts of bike-sharing on the economy, energy use, the environment, and public health. The empirical results show that bike-sharing programs have significant positive externalities. The bike-sharing systems can provide urban residents with a convenient and time-saving travel mode. We find that the bike-sharing dramatically decreases traffic, reduces energy consumption, decreasing harmful gas emissions, improves public health generally, and promotes economic growth. This study contributes to a better comprehension of the externalities of bike-sharing and provides empirical evidence of the impacts of bike-sharing. Findings suggest that bike-sharing can play a critical role in the process of urban transportation development and provide information useful for urban transportation policies.

Mitophagy is an important metabolic mechanism that modulates mitochondrial quality and quantity by selectively removing damaged or unwanted mitochondria. BNIP3 (BCL2/adenovirus e1B 19 kDa protein interacting protein 3), a mitochondrial outer membrane protein, is a mitophagy receptor that mediates mitophagy under various stresses, particularly hypoxia, since BNIP3 is a hypoxia-responsive protein. However, the underlying mechanisms that regulate BNIP3 and thus mediate mitophagy under hypoxic conditions remain elusive. Here, we demonstrate that in hypoxia JNK1/2 (c-Jun N-terminal kinase 1/2) phosphorylates BNIP3 at Ser 60/Thr 66, which hampers proteasomal degradation of BNIP3 and drives mitophagy by facilitating the direct binding of BNIP3 to LC3 (microtubule-associated protein 1 light chain 3), while PP1/2A (protein phosphatase 1/2A) represses mitophagy by dephosphorylating BNIP3 and triggering its proteasomal degradation. These findings reveal the intrinsic mechanisms cells use to regulate mitophagy via the JNK1/2-BNIP3 pathway in response to hypoxia. Thus, the JNK1/2-BNIP3 signaling pathway strongly links mitophagy to hypoxia and may be a promising therapeutic target for hypoxia-related diseases.

A reduced removal of dysfunctional mitochondria is common to aging and age-related neurodegenerative pathologies such as Alzheimer’s disease (AD). Strategies for treating such impaired mitophagy would benefit from the identification of mitophagy modulators. Here we report the combined use of unsupervised machine learning (involving vector representations of molecular structures, pharmacophore fingerprinting and conformer fingerprinting) and a cross-species approach for the screening and experimental validation of new mitophagy-inducing compounds. From a library of naturally occurring compounds, the workflow allowed us to identify 18 small molecules, and among them two potent mitophagy inducers (Kaempferol and Rhapontigenin). In nematode and rodent models of AD, we show that both mitophagy inducers increased the survival and functionality of glutamatergic and cholinergic neurons, abrogated amyloid-β and tau pathologies, and improved the animals’ memory. Our findings suggest the existence of a conserved mechanism of memory loss across the AD models, this mechanism being mediated by defective mitophagy. The computational–experimental screening and validation workflow might help uncover potent mitophagy modulators that stimulate neuronal health and brain homeostasis. Two potent mitophagy inducers, identified and characterized via unsupervised machine learning and a cross-species screening approach, ameliorated the pathology of Alzheimer’s disease in worms and mice.

Magnetohydrodynamics (MHD) studies the dynamics of magnetic fields in electrically conducting fluids. In addition to the sound wave and electromagnetic wave behaviors, magneto-fluids also exhibit an interesting phenomenon: They can produce the Alfvén waves, which were first described in a physics paper by Hannes Alfvén in 1942. Subsequently, Alfvén was awarded the Nobel prize for his fundamental work on MHD with fruitful applications in plasma physics, in particular the discovery of Alfvén waves. This work studies (and constructs) global solutions for the three dimensional incompressible MHD systems (with or without viscosity) in strong magnetic backgrounds. We present a complete and self-contained mathematical proof of the global nonlinear stability of Alfvén waves. Specifically, our results are as follows: We obtain asymptotics for global solutions of the ideal system (i.e.,viscosity μ = 0 ) along characteristics; in particular, we have a scattering theory for the system. We construct the global solutions (for small viscosity μ ) and we show that as μ → 0 , the viscous solutions converge in the classical sense to the zero-viscosity solution. Furthermore, we have estimates on the rate of the convergence in terms of μ . We explain a linear-driving decay mechanism for viscous Alfvén waves with arbitrarily small diffusion. More precisely, for a given solution, we exhibit a time T n 0 (depending on the profile of the datum rather than its energy norm) so that at time T n 0 the H 2 -norm of the solution is small compared to μ (therefore the standard perturbation approach can be applied to obtain the convergence to the steady state afterwards). The results and proofs have the following main features and innovations: We do not assume any symmetry condition on initial data. The size of initial data (and the a priori estimates) does not depend on viscosity μ . The entire proof is built upon the basic energy identity. The Alfvén waves do not decay in time: the stable mechanism is the separation (geometrically in space) of left- and right-traveling Alfvén waves. The analysis of the nonlinear terms are analogous to the null conditions for non-linear wave equations. We use the (hyperbolic) energy method. In particular, in addition to the use of usual energies, the proof relies heavily on the energy flux through characteristic hypersurfaces. The viscous terms are the most difficult terms since they are not compatible with the hyperbolic approach. We obtain a new class of space-time weighted energy estimates for (weighted) viscous terms. The design of weights is one of the main innovations and it unifies the hyperbolic energy method and the parabolic estimates. The approach is ‘ quasi-linear ’ in nature rather than a linear perturbation approach: the choices of the coordinate systems, characteristic hypersurfaces, weights and multiplier vector fields depend on the solution itself. Our approach is inspired by Christodoulou–Klainerman’s proof of the nonlinear stability of Minkowski space-time in general relativity.

Inflammatory bowel disease (IBD) is a known medical burden in most developed countries and a significant cause of morbidity. The IBD label includes Crohn's disease (CD) and ulcerative colitis (UC). Pharmacological and surgical intervention are the two main management approaches for IBD. Some drugs have been developed for IBD therapy, but accessibility is limited due to high costs. Furthermore, these agents have demonstrated inactivity over long-term treatment courses. Therefore, an urgent need is present for new treatment options that are safe, able to sustain clinical remission, and improve mucosal gut healing. Seaweed has received much attention in the pharmacological field owing to its various biomedical properties, including the prolongation of blood clotting time, as well as antitumor, anti-inflammation, and antioxidant effects. This study therefore aimed to examine the effects of a dietary polysaccharide-rich extract obtained from Eucheuma cottonii (EC) on a model of colitis. Colitis was induced in male BALB/c mice by the administration of 2.5% (w/v) dextran sulfate sodium (DSS) for 7 days. DSS-induced mice were treated with either one of three different doses of EC extracts (0.35, 0.70, and 1.75 g/kg body weight) or curcumin as a positive control (0.10 g/kg). Mice were sacrificed post-treatment and blood samples were collected. The disease activity index (DAI) and inflammatory cytokine levels (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10) were measured. After treatment for 7 days, EC extract administration protected against weight loss and decreased the colon weight per length ratio. EC extract administration also decreased pro-inflammatory cytokine expression, increased IL-10 levels, and reduced colonic damage. Therefore, a dietary polysaccharide-rich extract from E. cottonii reduced DSS-induced bowel inflammation, thereby becoming a promising candidate for the treatment of colitis.

From the perspective of feminist translation, this study makes an analysis of the English version of Can Xue’s The Gloomy Mood of Ah Mei on a Sunny Day translated by Ronald R. Janssen and Zhang Jian. The conclusion shows that the translators adopt the two feminist translation strategies—supplementing and hijacking—in the process of translation. By these means, Ah Mei’s feelings, thoughts, and attitude to marriage are revealed. The translated works not only reproduces feminism presented in the source text, but also makes the implied feminist consciousness of the author obviously conveyed. It shows the creative rewriting of the translators, which enhances the value of the English translation and benefits its dissemination and acceptance in the English world.

Vildagliptin is an orally active, potent and selective dipeptidyl peptidase-4 (DPP-4) inhibitor, shown to be effective and well tolerated in patients with type 2 diabetes mellitus (T2DM) as either monotherapy or in combination with other anti-diabetic agents. Vildagliptin possesses several desirable pharmacokinetic properties that contribute to its lower variability and low potential for drug interaction. Following oral administration, vildagliptin is rapidly and well absorbed with an absolute bioavailability of 85%. An approximately dose-proportional increase in exposure to vildagliptin over the dose range of 25–200 mg has been reported. Food does not have a clinically relevant impact on the pharmacokinetics of vildagliptin, and it can be taken without regard to food. Vildagliptin is minimally bound to plasma proteins (9.3%) and, on the basis of a volume of distribution of 71 L, it is considered to distribute extensively into extra vascular spaces. Renal clearance of vildagliptin (13L/h) accounts for 33% of the total body clearance after intravenous administration (41 L/h). The primary elimination pathway is hydrolysis by multiple tissues/organs. The DPP-4 enzyme contributes to the formation of the major hydrolysis metabolite, LAY 151; therefore, vildagliptin is also a substrate of DPP-4. Vildagliptin has a low potential for drug interactions, as cytochrome P450 (CYP) enzymes are minimally (<1.6%) involved in the overall metabolism. Clinical pharmacokinetic studies have reported the lack of drug interaction with several drugs (metformin, pioglitazone, glyburide, simvastatin, amlodipine, valsartan, ramipril, digoxin and warfarin) that are likely to be frequently co-administered to patients with T2DM. In particular, vildagliptin does not affect the pharmacokinetics of pioglitazone, glyburide, warfarin and simvastatin; therefore, it is not expected to affect the pharmacokinetics of a drug that is a substrate for CYP2C8, CYP2C9 or CYP3A4. In the elderly, vildagliptin exposure increases by approximately 30%, which is considered to be mostly attributable to compromised renal function in the elderly population and is not considered to be clinically relevant. Vildagliptin has been demonstrated to be efficacious, safe and well tolerated in elderly patients with T2DM without dose adjustment. In subjects with varying degrees of renal impairment, vildagliptin exposure increases by approximately 2-fold; however, the increase in the exposure does not correlate with the severity of renal impairment. The lack of a clear correlation between the increased exposure and the severity of renal impairment is considered to be attributable to the fact that the kidneys contribute to both the excretion and the hydrolysis metabolism of vildagliptin. Hepatic impairment, gender, body mass index (BMI) and ethnicity do not have an influence on the pharmacokinetics of vildagliptin. These findings suggest that vildagliptin can be used in a diverse patient population without dose adjustment. Oral administration of vildagliptin to patients with T2DM completely inhibits DPP-4 activity at a variety of doses. The onset of DPP-4 inhibition is rapid, and the duration of DPP-4 inhibition is dose dependent. Vildagliptin is a potent inhibitor of the DPP-4 enzyme, with a concentration required to achieve 50% DPP-4 inhibition (IC 50 ) of 4.5 nmol/L in patients with T2DM. Similar potency of DPP-4 inhibition by vildagliptin has been reported in different ethnic groups, indicating that ethnicity does not affect the pharmacodynamics of vildagliptin. Vildagliptin significantly increases the active glucagon-like peptide 1 (GLP-1) levels by approximately 2- to 3-fold and glucose-dependent insulinotropic polypeptide (GIP) levels by approximately 5-fold, and significantly suppresses the postprandial glucagon levels in response to a meal or following an oral glucose tolerance test (OGTT) in patients with T2DM. Vildagliptin significantly reduces both fasting and postprandial glucose levels over the dose range of 50–100 mg daily (administered either once daily or twice daily), and there are no substantial additional benefits of doses greater than 50 mg twice daily. The primary clinical dosing regimen is 50 mg twice daily as monotherapy or in combination with metformin. Vildagliptin increases the insulin levels following an OGTT and an intravenous glucose tolerance test (IVGTT), and the stimulation of insulin secretion is glucose dependent. Vildagliptin has been shown to improve beta-cell function on the basis of pharmacodynamic modelling taking the reduced glucose levels into account. The improvement of beta-cell function by vildagliptin has been confirmed after chronic treatment with vildagliptin for up to 2 years. Reduction of the endogenous glucose production appears to contribute to the glucose-lowering effects. Unlike the GLP-1 receptor agonists, vildagliptin does not affect gastric emptying, and this is consistent with the favourable gastrointestinal safety profile. Vildagliptin improves the sensitivity of the alpha cell to glucose in patients with T2DM by enhancing the alpha-cell responsiveness to both suppressive effects of hyperglycaemia and stimulatory effects of hypoglycaemia. Consistently, a lower incidence of hypoglycaemic events with vildagliptin is reported when it is used as either monotherapy or in combination with other anti-diabetic agents, such as metformin or insulin, as compared with a sulphonylurea. Numerous long-term clinical trials of up to 2 years have demonstrated that vildagliptin 50 mg once daily or twice daily is effective, safe and well tolerated in patients with T2DM as either monotherapy or in combination with a variety of other anti-diabetic agents.

Metaheuristic algorithms, widely applied across various domains due to their simplicity and strong optimization capabilities, play a crucial role in problem-solving. While the Aquila Optimizer is recognized for its effectiveness, it often exhibits slow convergence rates and susceptibility to local optima in certain scenarios. To address these concerns, this paper introduces an enhanced version, termed Tent-enhanced Aquila Optimizer (TEAO). TEAO incorporates the Tent chaotic map to initialize the Aquila population, promoting a more uniform distribution within the solution space. To balance exploration and exploitation, novel formulas are proposed, accelerating convergence while ensuring precision. The effectiveness of the TEAO algorithm is validated through a comprehensive comparison with 14 state-of-the-art algorithms using 23 classical benchmark test functions. Additionally, to assess the practical feasibility of the approach, TEAO is applied to six constrained engineering problems and benchmarked against the performance of the same 14 algorithms. All experimental results consistently demonstrate that TEAO outperforms other advanced algorithms in terms of solution quality and stability, establishing it as a more competitive choice for optimization tasks.