安徽医科大学

Structure and dynamical prediction are two core tasks in multiplex network research, yet they are often investigated separately. However, in real-world scenarios, the structural and dynamical information is typically simultaneously available but incomplete, which makes these tasks more challenging. Therefore, a natural idea to utilize such incomplete information for collaborative modeling of the two tasks. To address these challenges, we propose a data-driven collaborative learning framework (Multi-CoLF) that integrates incomplete structural and dynamical information for predicting network structure and dynamical evolutions of multiplex networks. The framework consists of a structure prediction learner and a dynamical prediction learner. Specifically, the structure prediction learner employs the Gumbel-Softmax technique to infer missing links in each layer and constructs an extended graph. Based on this extended graph, the dynamical prediction learner develops an extended graph neural network to model spreading dynamics and capture the underlying evolution rules. An alternating optimization strategy is further designed to enable collaborative optimization between the two learners, facilitating collaborative prediction of structure and dynamics. Experiments on three synthetic and five real-world networks demonstrate that our method outperforms baseline approaches on both tasks under different types of spreading dynamics, with structure prediction accuracy improving by more than 10% on certain datasets. Moreover, extensive experimental results reveal that the structure and spreading dynamics in multiplex networks are complementary: the learned network structure enhances the accuracy of dynamical prediction, while the learned spreading dynamical rules improve the accuracy of structure prediction.

Zn-0.4 Sr and Zn-0.8 Sr (wt%) alloys (denoted ZS0.4 and ZS0.8) were processed by a single-pass friction stir processing (FSP) using a non-shouldered spiral tool (10 mm diameter, 2° tilt angle) at 1300 rpm, 200 mm/min traverse speed, and ∼1 mm plunge depth at room temperature. Mechanical properties were evaluated using tensile testing, nanoindentation, and Vickers and Brinell hardness measurements. Corrosion and degradation behaviors were assessed via electrochemical polarization and 30-day immersion in Hanks' solution and DMEM + FBS. Tribocorrosion resistance was examined by reciprocating friction tests under dry conditions and in liquid-wetted environments of Hanks' solution and DMEM + FBS. Biological performance was assessed using MC3T3-E1, MG-63, and hBMSC cultures, along with a rat subcutaneous implantation model. The horizontally tested ZS0.8 exhibited an exceptional strength-elongation product of 4.1 GPa%, with an ultimate tensile strength of 258 MPa, a yield strength of 210 MPa, an elongation of 15.9%, and a nanoindentation hardness of 2.6 GPa for the SrZn13 phase, compared with 0.7 GPa for the α-Zn matrix. Electrochemical corrosion rates of ZS0.8 were 388 μm/y in Hanks' and 216 μm/y in DMEM + FBS, while 30-day degradation rates were 44.9 μm/y and 27.2 μm/y, respectively. ZS0.8 also exhibited superior tribocorrosion resistance. Biologically, 25% and 50% extracts of ZS0.8 enhanced MC3T3-E1 and MG-63 viability, promoted hBMSC osteogenic differentiation and mineralization, showed potent anti-Staphylococcus aureus activity both in vitro and in vivo, and maintained good biosafety. These findings demonstrate a favorable balance of mechanical, degradation, and biological properties for load-bearing bone-fixation applications.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading chronic liver condition affecting nearly 40

Both platelet-rich plasma (PRP) and exosomes derived from bone marrow mesenchymal stem cells (BMSCs) exhibit therapeutic potential for spinal cord injury (SCI). However, the combined application of PRP and BMSCs-derived exosome (PRP-primed BMSCs-EXO, PRP-BMSCs-EXO) has not been reported. This study aimed to investigate whether the combined use confers superior therapeutic effects and to explore the underlying molecular mechanisms. First, we examined the effects of PRP priming on the proliferation and exosome secretion of BMSCs. High-throughput sequencing and RT-qPCR were used to analyze the differential miRNA expression profiles between exosomes from PRP- primed BMSCs (PRP-BMSCs-EXO) and naive BMSCs (BMSCs-EXO). Subsequently, a series of in vitro SCI models were established to evaluate the therapeutic effects of PRP-BMSCs-EXO on SCI. TargetScan, RNAhybrid, GO, KEGG, dual-luciferase reporter assay, RT-qPCR, western blotting (WB), and rescue experiments were performed to explore the roles of miRNAs in PRP-BMSCs-EXO and the associated signaling regulatory mechanisms in SCI. Finally, a series of in vivo SCI models were used to verify the therapeutic efficacy and mechanisms of PRP-BMSCs-EXO in vivo. PRP priming promoted the proliferation and exosome secretion of BMSCs. High-throughput sequencing and RT-qPCR revealed that multiple miRNAs were highly expressed in PRP-BMSCs-EXO compared with BMSCs-EXO, among which miR-29a-3p was the most abundant. In in vitro SCI models, PRP-BMSCs-EXO exerted better therapeutic effects than BMSCs-EXO and PRP. Mechanistically, PRP-BMSCs-EXO may enhance the viability and migration and inhibit the apoptosis and autophagy of pheochromocytoma 12 (PC12) cells by delivering miR-29a-3p, thereby promoting nerve regeneration and SCI repair. Bioinformatic analysis and luciferase assays indicated that PTEN may be a downstream target gene of miR-29a-3p. Rescue experiments confirmed that the miR-29a-3p/PTEN/PI3K/Akt/mTOR axis may mediate the regulatory effects of PRP-BMSCs-EXO on neuronal apoptosis, autophagy, and nerve regeneration in SCI. These findings were further validated in in vivo SCI models. Compared with PRP and BMSC-derived exosomes alone, PRP-primed BMSC-derived exosomes provide superior neuroprotective effects against SCI. PRP-BMSCs-EXO inhibits neuronal apoptosis and autophagy and promotes nerve regeneration via the miR-29a-3p/PTEN/PI3K/Akt/mTOR axis, representing a promising and effective therapeutic strategy for SCI.

Alcohol-related liver disease (ALD) is increasingly affecting younger populations globally and has become the leading cause of rising liver-related morbidity and mortality. Chronic alcohol exposure over a long period of time has been shown to result in a continuum of pathological processes including liver inflammation, fibrosis, and hepatocellular carcinoma (HCC). However, the therapeutic options for ALD are still limited due to its multifactorial morbidity mechanisms and treatment resistance. This review focuses on the critical regulatory role of the P2X4-P2X7 purinergic axis in ALD pathogenesis, and elucidates that extracellular ATP (eATP), a damage-associated molecular pattern (DAMP) released from alcohol-injured hepatocytes, activates this axis to drive ALD progression. The interaction between P2X4 and P2X7 receptors, including functional synergy and intracellular signal crosstalk, amplifies inflammatory signaling, promotes hepatic stellate cell (HSC) activation, and fosters an immunosuppressive microenvironment during fibrogenesis, ultimately leading to malignant transformation and impaired immunotherapeutic efficacy. Therefore, targeting the P2X4-P2X7 axis through selective receptor antagonism or combining antifibrotic with immunotherapeutic approaches may be a potential strategy to limit fibrosis and improve immunotherapeutic resistance. By synthesizing recent preclinical evidence, this review summarizes the pathogenic role of the P2X4-P2X7 axis in ALD and discusses the prospects of novel axis-based therapies to address unmet clinical needs in ALD management. Notably, most preclinical studies in this field lack standardized blank/sham control groups, which limits the causal inference of purinergic signaling in ALD progression.