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This study presents a comprehensive analysis of vehicle ownership, energy consumption, and carbon emissions in Guangdong Province, China, from 2020 to 2035 under different scenarios. Key findings highlight the province's pursuit of carbon peak goals and provide valuable insights into strategies to achieve them. Vehicle ownership in Guangdong is projected to exceed 48 million by 2035, which represents a doubling from 2020. Under both scenarios, internal combustion engine vehicle ownership will peak around 2030 and then gradually decline, while under the enhanced scenario, electric vehicle ownership will exceed 40% by 2035. Enhanced vehicle energy efficiency and reduced annual mileage will lead to a 17% reduction in gasoline and diesel consumption by 2035 in both scenarios. At the same time, there will be a substantial five- to six-fold increase in electricity consumption for vehicles compared to 2020. Both scenarios peak in carbon emissions before 2030, with the enhanced scenario achieving this peak a year earlier. The enhanced scenario outperforms the baseline, reducing carbon emissions by about 21.2% from the peak and 8% relative to 2020. Pure electric vehicles exhibit a significant advantage in reducing carbon emissions per vehicle compared to their internal combustion engine counterparts. Encouraging new energy vehicles, especially pure electric ones, accelerates the carbon emissions peak and lowers overall peak emissions. Accelerating the adoption of electric vehicles, reducing per-vehicle fuel consumption and annual average mileage, and optimizing transportation modes are crucial for carbon peaking from the vehicle fuel cycle. Policy recommendations focus on promoting new energy vehicles, optimizing transportation, and advancing research and technology. [ABSTRACT FROM AUTHOR]

Complications related to wound healing pose substantial obstacle in the management of colorectal cancer (CRC), specifically in the field of anorectal medicine. Biosimilars of bevacizumab have emerged as crucial therapeutic agents in the management of these complications. With the particular emphasis on effects of Bevacizumab Biosimilar Plus on wound healing among patients diagnosed with CRC, this review underscores the potential of this anorectal medication to improve patient outcomes and was aimed to assess the safety and efficacy of Bevacizumab Biosimilar Plus in relation to complications associated with wound healing in patients with CRC. The assessment centers on its therapeutic potential and safety profile within the domain of anorectal medicine. In accordance with the PRISMA guidelines, a comprehensive literature search was performed, resulting in the identification of 19 pertinent studies out of an initial 918. Priority was given to assessing the safety and adverse effects of Bevacizumab Biosimilar Plus in conjunction with its effectiveness in wound healing. The extracted data comprised the following: study design, patient demographics, comprehensive treatment regimens, wound healing‐specific outcomes and adverse effects. The evaluation of study quality was conducted utilizing the instruments provided by the Cochrane Collaboration and the Newcastle‐Ottawa Scale (NOS). Bevacizumab Biosimilar Plus demonstrates efficacy in the management of wound healing complications among patients with CRC, with a safety and efficacy profile similar to that of the original Bevacizumab, according to the analysis. Notably, several studies reported improved rates of wound healing in relation to the biosimilar. The safety profiles exhibited similarities to the anticipated anti‐VEGF agent effects. In wound management, the biosimilar also demonstrated advantages in terms of prolonged efficacy. In addition, analyses of cost‐effectiveness suggested that the use of biosimilars could result in cost reductions. Bevacizumab Biosimilar Plus exhibited potential as an anorectal medication for the effective management of wound healing complications in patients with CRC. This has substantial ramifications for improving the quality of patient care, encompassing the affordability and effectiveness of treatments. [ABSTRACT FROM AUTHOR]

A hypoglossal nerve stimulator (HGNS) is an invasive device that is used to treat obstructive sleep apnea (OSA) through electrical stimulation. The conventional implantable HGNS device consists of a stimuli generator, a breathing sensor, and electrodes connected to the hypoglossal nerve via leads. However, this implant is bulky and causes significant trauma. In this paper, we propose a minimally invasive HGNS based on an electrocardiogram (ECG) sensor and wireless power transfer (WPT), consisting of a wearable breathing monitor and an implantable stimulator. The breathing external monitor utilizes an ECG sensor to identify abnormal breathing patterns associated with OSA with 88.68% accuracy, achieved through the utilization of a convolutional neural network (CNN) algorithm. With a skin thickness of 5 mm and a receiving coil diameter of 9 mm, the power conversion efficiency was measured as 31.8%. The implantable device, on the other hand, is composed of a front-end CMOS power management module (PMM), a binary-phase-shift-keying (BPSK)-based data demodulator, and a bipolar biphasic current stimuli generator. The PMM, with a silicon area of 0.06 mm 2 (excluding PADs), demonstrated a power conversion efficiency of 77.5% when operating at a receiving frequency of 2 MHz. Furthermore, it offers three-voltage options (1.2 V, 1.8 V, and 3.1 V). Within the data receiver component, a low-power BPSK demodulator was ingeniously incorporated, consuming only 42 μ W when supplied with a voltage of 0.7 V. The performance was achieved through the implementation of the self-biased phase-locked-loop (PLL) technique. The stimuli generator delivers biphasic constant currents, providing a 5 bit programmable range spanning from 0 to 2.4 mA. The functionality of the proposed ECG- and WPT-based HGNS was validated, representing a highly promising solution for the effective management of OSA, all while minimizing the trauma and space requirements. [ABSTRACT FROM AUTHOR]

In this paper, amino-carboxymethyl chitosan (ACC) was prepared through amino carboxymethylation, which introduces -COOH and -NH2 groups to the chitosan (CS) chains. Meanwhile, dialdehyde starch (DAS) was produced by oxidizing corn starch using sodium periodate. To attain the optimal loading and long-time release of ε-polylysine (ε-PL), the ACC/DAS hydrogels were synthesized through the Schiff base reaction between the amino group on ACC and the aldehyde group in DAS. The molecular structure, microcosmic properties, loading capacity, and bacteriostatic properties of the four types of hydrogels containing different mass concentrations of ACC were investigated. The results showed that the dynamic imine bond C=N existed in the ACC/DAS hydrogels, which proved that the hydrogels were formed by the cross-linking of the Schiff base reaction. With the increasing mass concentration of the ACC, the cross-sectional morphology of the hydrogel became smoother, the thermal stability increased, and the swelling behavior was gradually enhanced. The tight network structure improved the ε-PL loading efficiency, with the highest value of 99.2%. Moreover, the loading of ε-PL gave the hydrogel good antibacterial properties. These results indicate that ACC/DAS hydrogel is potential in food preservation. [ABSTRACT FROM AUTHOR]

Introduction: Sjögren's disease (SjD) is a chronic autoimmune disease characterized by the loss of the secretory function of the exocrine glands. At present, drugs that can both correct the immune imbalance and improve exocrine gland function are needed. Meanwhile, vasoactive intestinal peptide (VIP) has been reported as a candidate with anti‐inflammatory and immunoregulatory properties for treating autoimmune diseases. Methods: Nonobese diabetic (NOD) mice and the primary splenic lymphocyte cells (SPLCs) were used to construct the SS model. The therapeutic effects of VIP for SjD by evaluating water consumption, histopathology, T cell subsets, and related cytokines. RT‐qPCR and Western blot analysis were used to identify the expression of the PTEN/PI3K/AKT pathway. Results: We found that VIP therapy in NOD mice could increase the expression of PTEN and VIP/VPAC1 receptor, as well as decrease the PI3K/AKT pathway. In vitro, the results showed that the PTEN knockdown decreased the Treg/Th17 ratio and enhanced the phosphorylated PI3K/AKT pathway, which were reversed with VIP treatment. Conclusions: VIP exerts potential therapeutic action in SjD by upregulating PTEN through the PI3K/AKT pathway and Treg/Th17 cell balance. [ABSTRACT FROM AUTHOR]

Interstitial lung disease (ILD) is associated with substantial morbidity and mortality, which is one of the key systematic manifestations of connective tissue disease (CTD). Tripterygium wilfordii, known as Leigongteng in Chinese, has been applied to treat connective tissue disease-related interstitial lung disease (CTD-ILD) for many years. Triptolide is a key effective component from Tripterygium wilfordii. But the molecular mechanism of Triptolide for treating CTD-ILD is not yet clear. Gaining insight into the molecular mechanism of Triptolide intervention CTD-ILD, we used the method of network pharmacology. And then we conducted drug-target networks to analyse the potential protein targets between Triptolide and CTD-ILD. Finally, AutoDock Vina was selected for molecular docking. By analysing the interaction genes between Triptolide and CTD-ILD, 242 genes were obtained. The top 10 targets of the highest enrichment scores were STAT3, AKT1, MAPK1, IL6, TP53, MAPK3, RELA, TNF, JUN, JAK2. GO and KEGG enrichment analysis exhibited that multiple signalling pathways were involved. PI3K-Akt, multiple virus infections, cancer signalling, chemokine, and apoptosis signalling pathway are the main pathways for Triptolide intervention CTD-ILD. And it is related to various biological processes such as inflammation, infection, cell apoptosis, and cancer. Molecular docking shows Triptolide can bind with its target protein in a good bond by intermolecular force. This study preliminarily reveals the internal molecular mechanism of Triptolide interfere with CTD-ILD through multiple targets, multiple access, validated through molecular docking. Triptolide intervention CTD-ILD, which are related to various biological processes such as inflammation, infection, cell apoptosis, and cancer. PI3K-Akt, multiple virus infections, and apoptosis signalling pathway are the main pathways for Triptolide intervention CTD-ILD. Triptolide can bind with related target protein in a good bond by Intermolecular force, exhibiting a good docking activity. [ABSTRACT FROM AUTHOR]

This study draws upon organizational psychology and platform labor research to investigate how socio‐psychological factors affect the mental well‐being of platform workers and help them cope with the challenges of work. Based on a survey study of 500 food‐delivery workers ('riders') in China, we provide quantitative evidence of workers' ambivalent subjective experiences that complements the predominantly qualitative account in the extant literature. In particular, we assess the complex relationships between meaningfulness of work, autonomy at work, self‐perceived competence, and workers' subjective well‐being. Our data also show that the stress‐buffering effect of social support mainly comes from the riders' familial contact and their online group chat with other workers. Overall, despite the well‐documented precarity and stress in platform work, the riders in our sample appear to be able to mobilize inner and relational resources to achieve a relatively high‐level mental well‐being. [ABSTRACT FROM AUTHOR]

Background: Proficient mismatch repair (pMMR) colorectal adenocarcinoma (CRAC) metastasizes to a greater extent than MMR-deficient CRAC. Prognostic biomarkers are preferred in clinical practice. However, traditional biomarkers screened directly from sequencing are often not robust and thus cannot be confidently utilized. Methods: To circumvent the drawbacks of blind screening, we established a new strategy to identify prognostic biomarkers in the conserved and specific oncogenic pathway and its regulatory RNA network. We performed RNA sequencing (RNA-seq) for messenger RNA (mRNA) and noncoding RNA in six pMMR CRAC patients and constructed a glycosylation-related RNA regulatory network. Biomarkers were selected based on the network and their correlation with the clinicopathologic information and were validated in multiple centers (n = 775). Results: We constructed a competing endogenous RNA (ceRNA) regulatory network using RNA-seq. Genes associated with glycosylation pathways were embedded within this scale-free network. Moreover, we further developed and validated a seven-glycogene prognosis signature, GlycoSig (B3GNT6 , GALNT3 , GALNT8 , ALG8 , STT3B , SRD5A3 , and ALG6) that prognosticate poor-prognostic subtype for pMMR CRAC patients. This biomarker set was validated in multicenter datasets, demonstrating its robustness and wide applicability. We constructed a simple-to-use nomogram that integrated the risk score of GlycoSig and clinicopathological features of pMMR CRAC patients. Conclusions: The seven-glycogene signature served as a novel and robust prognostic biomarker set for pMMR CRAC, highlighting the role of a dysregulated glycosylation network in poor prognosis. [ABSTRACT FROM AUTHOR]

Late Mesozoic magmatic rocks of the Zhangbaling Uplift (ZBU) in eastern China, which comprises the northern Zhangbaling area and the southern Feidong area, can provide insights into the deep crustal processes and tectonic affinity of the massif. These rocks are dominated by granitoids with formation ages of 132–120 Ma and a peak at 129 Ma. The Shankouling dyke (120.4 ± 1.1 Ma) and the Zhuyuanzhang quartz monzodiorite (129.0 ± 2.2 Ma) crop out sporadically in the Feidong area. These rocks show adakitic signatures of high Al2O3 and Sr contents, high Sr/Y, (La/Yb)N, and (Dy/Yb)N ratios, and low Y and YbN contents. They have enriched (87Sr/86Sr)i ratios, negative εNd(t) and εHf(t) values, and unradiogenic Pb isotopic compositions that resemble those of coeval high Sr/Y granitoids in the Dabie Orogen. These ZBU rocks can be divided into two groups: low-Mg granitoids with more enriched Sr–Nd isotopic signatures and low Mg# values (<50), and high-Mg granitoids with weakly enriched Sr–Nd isotopic signatures and high Mg# values (mostly >50). Combining their geochemical features with previous results of experimental melts, we conclude that the low-Mg granitoids were derived from fluid-absent partial melting of in situ thickened lower continental crust, resulted from Triassic continental subduction and collision in this area, whereas the high-Mg granitoids were derived from delaminated eclogitic lower crust followed by interaction with mantle peridotites during magma ascent. Isotopic compositions show that these granitoids could have been derived from ancient crust of the Yangtze Block via re-melting of Neoarchean and Paleoproterozoic lower continental crust. The great depth of the Tan–Lu Fault Zone enabled delamination of the thickened eclogitic mountain root beneath the ZBU, which resulted in the formation and emplacement of the high-Mg rocks, followed by uplift of the Zhangbaling massif associated with rollback of the subducting Paleo-Pacific (Izanagi) Plate. [ABSTRACT FROM AUTHOR]

MG53 is an important membrane repair protein and partially protects bone marrow multipotent adult progenitor cells (MAPCs) against oxidized low‐density lipoprotein (ox‐LDL). The present study was to test the hypothesis that the limited protective effect of MG53 on MAPCs was due to ox‐LDL‐induced reduction of MG53. MAPCs were cultured with and without ox‐LDL (0‐20 μg/mL) for up to 48 hours with or without MG53 and antioxidant N‐acetylcysteine (NAC). Serum MG53 level was measured in ox‐LDL‐treated mice with or without NAC treatment. Ox‐LDL induced significant membrane damage and substantially impaired MAPC survival with selective inhibition of Akt phosphorylation. NAC treatment effectively prevented ox‐LDL‐induced reduction of Akt phosphorylation without protecting MAPCs against ox‐LDL. While having no effect on Akt phosphorylation, MG53 significantly decreased ox‐LDL‐induced membrane damage and partially improved the survival, proliferation and apoptosis of MAPCs in vitro. Ox‐LDL significantly decreased MG53 level in vitro and serum MG53 level in vivo without changing MG53 clearance. NAC treatment prevented ox‐LDL‐induced MG53 reduction both in vitro and in vivo. Combined NAC and MG53 treatment significantly improved MAPC survival against ox‐LDL. These data suggested that NAC enhanced the protective effect of MG53 on MAPCs against ox‐LDL through preventing ox‐LDL‐induced reduction of MG53. [ABSTRACT FROM AUTHOR]