In recent years, escalating geopolitical tensions between the United States and China, together with the rise of technological protectionism, have accelerated the process of technological decoupling. This study investigates the impact of U.S. sanctions—specifically the Entity List designation—on the innovation performance of Chinese firms. Drawing on institutional theory, we argue that sanctioned firms adjust their innovation strategies through coercive isomorphism, thereby improving innovation outcomes. Moreover, this institutional shock extends beyond directly sanctioned firms and diffuses across the technological domain through imitative isomorphism, generating positive innovation spillovers for firms operating within the same technological domain. We further examine the moderating role of government support. For sanctioned firms, government assistance—particularly through strategic and emerging industry initiatives—strengthens the positive effect of sanctions on innovation performance. In contrast, for non-sanctioned firms operating within the same technological domain, such support may attenuate these positive spillover effects. Finally, we propose that firms with stronger technological capabilities are better positioned to manage external resource dependencies, enabling them to achieve greater improvements in innovation performance when facing sanctions.

Purpose Total factor productivity (TFP) is a central driver of firms' high-quality development. The rapid expansion of the digital economy has fundamentally reshaped production processes and organizational structures, creating substantial potential for TFP enhancement. This study aims to investigate the key determinants, configurational pathways, and dynamic evolutionary trajectories through which firms achieve high TFP in the context of digital transformation. Design/methodology/approach Grounded in the technology–organization–environment (TOE) framework and a configurational perspective, this study employs panel data from Chinese A-share listed firms. Using stage-based dynamic fuzzy-set qualitative comparative analysis (fsQCA), we identify multiple equifinal configurations associated with high firm-level TFP and examine their temporal evolution. Findings The results reveal six equifinal configurational pathways leading to high TFP. No single antecedent condition is necessary; rather, high TFP emerges from complementary alignments among technological, organizational, and environmental conditions. The findings further reveal a dynamic evolutionary shift in TFP-enhancing pathways as external environments transition from stable to turbulent conditions. In addition, the productivity-enhancing effects of digital technology adoption are contingent upon firm-specific endowments and external environmental conditions. Originality/value Unlike prior research emphasizing the net effects of isolated determinants, this study adopts a configurational perspective to demonstrate how multi-level factor combinations jointly shape firm-level TFP. By integrating the TOE framework with stage-based dynamic fsQCA, the study provides a novel explanation of how digital transformation translates into productivity gains and offers new insights into the contingent and evolutionary nature of TFP enhancement.

With the increasing prevalence of cooperative research and development (R&D) in artificial intelligence (AI) among companies, the performance implications of these collaborations remain underexplored. This study examines the financial impact of AI-related R&D collaborations, focusing on how AI type, partnerships with top-tier technology companies, and digitalization capabilities moderate their effects on firm value. Analyzing announcements from Chinese firms between 2016 and 2023, we find a positive association between AI-related R&D collaborations and firm value, with this effect being particularly strong for collaborations on language/text understanding and with top-tier technology partners. However, this positive effect diminishes as firms’ digitalization capabilities increase. This research provides empirical evidence of the benefits of AI-related R&D collaborations and offers insights into how firms can maximize the value of such partnerships.

Stress triggers disorders in accelerated peristalsis, with corticotropin releasing factor receptor 1 (CRF-R1) playing a pivotal role. Enteric glia cells (EGCs) and glial Cx43 are known to influence gastrointestinal motility, yet their involvement in colonic motor responses to stress remains unclear. Using immunofluorescence and single-cell RNA sequencing data, we identified CRF-R1 expression in EGCs. Male C57BL/6 mice subjected to wrap restraint stress (WRS) revealed stress-induced colonic motility changes. By employing Fluoroacetate, NBI 27914, and Gap26, we elucidated the impact of glial CRF-R1/Cx43 on stress-induced colonic motor responses. Our study demonstrated CRF-R1 expression in EGCs of the small intestine and colon, along with elevated CRF levels and upregulated CRF-R1 in the distal colon under stress. Antagonizing CRF-R1 and disrupting EGC function made mice resistant to colonic stress responses. Mechanistically, increased glial Cx43 expression and activity influenced colonic motor responses in a CRF-R1-dependent manner. Our findings highlight the role of EGC-derived CRF-R1 in stress-induced colonic motor responses via Cx43 activation. Targeting CRF-R1/Cx43 signaling in EGCs may offer a promising approach to mitigate stress-induced colonic transit changes.

Purpose This study investigates the impact of supplier dependence on suppliers’ exploitative and exploratory innovations. Drawing on resource dependence theory, this research demonstrates that two governance mechanisms, relationship tenure and board interlocks with customers, can be used to manage supplier dependence. Design/methodology/approach Using 1,825 observations from listed Chinese firms from 2008 to 2020, we established a unique dataset of buyer–supplier dyads. The hypotheses were tested using zero-inflated negative binomial regression analysis. Findings The findings indicate that greater supplier dependence on major customers has distinct impacts on suppliers’ exploitative and exploratory innovations. We demonstrate that the strategic management of relationship tenure and board interlocks with customers can serve as mechanisms countervailing the negative impact of supplier dependence on exploitative and exploratory innovations. Originality/value These results provide insights into the complex relationship between supplier dependence and innovation, offering practical recommendations for companies to alleviate resource dependence.

PurposeThis study aims to examine the performance implications of blockchain implementation in the supply chain and explore how blockchain functions and supply chain processes of blockchain implementation moderate the effect on firm performance.Design/methodology/approachUsing 220 blockchain implementations announced between January 2015 and December 2022, we use the event study methodology to estimate the effects of blockchain implementation on the firm value. Regression analyses are conducted to examine the moderating effects of blockchain functions and supply chain processes.FindingsFirst, there is a positive and statistically significant relationship between blockchain implementation in the supply chain and firm value. Second, we find that abnormal returns from blockchain implementation are higher when used with blockchain’s contract automation function and applied in downstream processes, supporting the moderation effects.Originality/valueThe study provides empirical evidence on the effects of the blockchain implementation on firm performance, taking into account the complexity of blockchain functions and supply chain processes. It enriches the current understanding of how blockchain implementation in the supply chain contributes to firm value.

OBJECTIVE:Cognitive impairment (CI) is highly prevalent in subarachnoid hemorrhage (SAH) patients. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays a critical role in neuronal survival in a variety of central nervous system injuries. This study aimed to determine whether electroacupuncture (EA) at Yintang and LI20 ameliorates SAH-CI in a rat model and to examine whether it modulates the PI3K/AKT pathway by administering a PI3K inhibitor (LY294002) versus dimethyl sulfoxide (DMSO) vehicle. METHODS:Notably, 129 male Sprague-Dawley rats were divided into Blank, Sham, SAH and SAH + EA groups (Experiment 1, n = 54) and SAH, SAH + EA, SAH + LY294002, SAH + EA + LY294002 and SAH + EA + DMSO groups (Experiment 2, n = 75). Garcia scoring was used to evaluate neurological function. The moisture content of the rat brain was determined by dry‒wet method. The Morris water maze was used to assess learning and memory function. Pathological changes in neurons in the hippocampus were observed via hematoxylin-eosin (H&E) staining. The number of surviving neurons and the percentage of apoptotic cells in the hippocampus were detected via Nissl and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. The expression of PI3K/AKT pathway-related proteins was detected via Western blotting. RESULTS:The results indicated that EA intervention after SAH reduced brain water content, enhanced Garcia scores, improved neurological function and behavioral markers of CI, and increased the number of surviving neurons in the hippocampus. Moreover, EA significantly increased the expression of AKT, phosphorylated (p)-AKT, PI3K, p-PI3K, glycogen synthase kinase (GSK)-3β, p-GSK-3β and B cell lymphoma (Bcl)-2 proteins, and decreased the expression of Bcl-2-associated X (Bax) and caspase-3. In addition, the effects of EA were abolished by LY294002. CONCLUSION:EA appeared to improve CI in a rat model of SAH through the activation of the PI3K/AKT pathway.

Firms are increasingly adopting blockchain technology to enhance risk management strategies. Nevertheless, the extent to which blockchain adoption influences firm resilience and its broader spectrum of stakeholders remains uncertain. Our study investigates how a focal firm's adoption of blockchain in the supply chain affects its resilience, encompassing both financial stability and operational flexibility. We then explore the spillover effects of the focal firm's use of blockchain on the resilience of both suppliers and customers, and further examine the moderating effects of supply chain diversification. Drawing on data from Chinese listed manufacturers and their supply chain partners, the empirical results reveal that blockchain significantly improves the financial stability of focal firms while its relationship with operational flexibility follows an inverted U-shaped pattern. In terms of supply chain spillover effects, the blockchain adoption of focal firms is linked to decreased financial stability for customers, but it concurrently boosts the operational flexibility of suppliers and customers. Supply chain diversification moderates the relationship between blockchain adoption and the operational flexibility of both suppliers and customers. These insights illuminate the trade-offs introduced by blockchain for supply chain resilience, providing a nuanced understanding of how supply chain members are influenced by the focal firm's blockchain adoption.

Diabetes-associated cognitive dysfunction (DACD) has ascended to become the second leading cause of mortality among diabetic patients. Phosphoserine phosphatase (PSPH), a pivotal rate-limiting enzyme in L-serine biosynthesis, has been documented to instigate the insulin signaling pathway through dephosphorylation. Concomitantly, CD38, acting as a mediator in mitochondrial transfer, is activated by the insulin pathway. Given that we have demonstrated the beneficial effects of exogenous mitochondrial supplementation on DACD, we further hypothesized whether astrocytic PSPH could contribute to improving DACD by promoting astrocytic mitochondrial transfer into neurons. In the Morris Water Maze (MWM) test, our results demonstrated that overexpression of PSPH in astrocytes alleviated DACD in db/db mice. Astrocyte specific-stimulated by PSPH lentivirus/ adenovirus promoted the spine density both in vivo and in vitro. Mechanistically, astrocytic PSPH amplified the expression of CD38 via initiation of the insulin signaling pathway, thereby promoting astrocytic mitochondria transfer into neurons. In summation, this comprehensive study delineated the pivotal role of astrocytic PSPH in alleviating DACD and expounded upon its intricate cellular mechanism involving mitochondrial transfer. These findings propose that the specific up-regulation of astrocytic PSPH holds promise as a discerning therapeutic modality for DACD.

Despite the vital role of astrocytes in preserving blood-brain barrier (BBB) integrity, their therapeutic potential as targets in ischemic stroke-induced barrier disruption remains underexplored. We previously reported externalization of phosphatidylserine (PS) on astrocytic membranes concurrent with the emergence of PS externalization in neurons. PS externalization of astrocytes induced microglial phagocytosis of astrocytes, resulting in reduced astrocyte-vascular coupling and subsequent BBB breakdown. Annexin A5 (ANXA5) belongs to the superfamily of calcium (Ca2+)- and phospholipid-binding proteins. Here, we report two X-ray structures of human ANXA5, including monomeric ANXA5 (1.42 Å) and dimeric ANXA5 (1.80 Å). Through the combination of molecular docking and functional analysis, we explored the mechanism of action of ANXA5 in stroke treatment. In addition, we observed a clear increase in therapeutic efficacy corresponding to the increased affinity of ANXA5 for PS. In summary, the phagocytosis of PS-externalized astrocytes by microglia has emerged as a critical mechanism driving BBB breakdown after ischemia. Our findings offer valuable structural insight into ANXA5 as an innovative pharmacological target for safeguarding blood-brain barrier integrity after cerebral ischemia. These insights may facilitate the development of novel PS-targeting medications aimed at achieving enhanced efficacy with minimal side effects.

Purpose This study examines the firm-level financial consequences caused by supply chain disruptions during COVID-19 and explores how firms' supply chain diversification strategies, including diversified suppliers, customers and products, moderate the negative effect on firm performance. Design/methodology/approach Based on data drawn from 222 publicly traded firms in China, the authors use event study methodology to estimate the effects of supply chain disruptions on the financial performance of affected firms. Regression analyses are conducted to examine the moderating effects of supply chain diversification. Findings Firms affected by supply chain disruptions during COVID-19 experienced a significant decline in shareholder value in two weeks and a subsequent decrease in operating performance in one year. Diversified suppliers, customers and products act as shock absorbers to alleviate the negative effects. Further regression shows a substitution effect between customer and product diversification. Cross-industry comparisons reveal that service firms experienced more loss than manufacturing firms. Customer diversification mitigates the adverse effects of supply chain disruptions for both manufacturing and service firms. Supplier diversification exerts a noteworthy role in manufacturing firms, while product diversification is beneficial for service firms. Originality/value The study provides empirical evidence on the magnitude of financial consequences of supply chain disruptions during COVID-19 in both the short term and long term and enriches the current understanding of how to build resilience from the supply chain diversification perspective.

Social memory has been developed in humans and other animals to recognize familiar conspecifics and is essential for their survival and reproduction. Here, we demonstrated that parvalbumin-positive neurons in the sensory thalamic reticular nucleus (sTRNPvalb) are necessary and sufficient for mice to memorize conspecifics. sTRNPvalb neurons receiving glutamatergic projections from the posterior parietal cortex (PPC) transmit individual information by inhibiting the parafascicular thalamic nucleus (PF). Mice in which the PPCCaMKII→sTRNPvalb→PF circuit was inhibited exhibited a disrupted ability to discriminate familiar conspecifics from novel ones. More strikingly, a subset of sTRNPvalb neurons with high electrophysiological excitability and complex dendritic arborizations is involved in the above corticothalamic pathway and stores social memory. Single-cell RNA sequencing revealed the biochemical basis of these subset cells as a robust activation of protein synthesis. These findings elucidate that sTRNPvalb neurons modulate social memory by coordinating a hitherto unknown corticothalamic circuit and inhibitory memory engram.

目的 糖尿病小鼠可表现出学习记忆功能障碍,探究 Sigma-1 受体激动剂 PRE-084 对 1 型糖尿病小鼠海马区神经元及认知损伤的影响.方法 将 20 只 8～10 周龄链脲佐菌素诱导的 1 型糖尿病小鼠和 20 只对照小鼠随机分为4 组(CON+Vehicle、CON+PRE-084、T1 DM+Vehicle和T1 DM+PRE-084 组);分别用添加 PRE-084 及对照溶剂的高糖培养基培养小鼠原代神经元.监测并记录各组小鼠的体质量、饮食饮水量及空腹血糖水平,利用新物体识别实验检测小鼠的学习记忆能力,透射电镜检测小鼠海马CA1 区神经元MAM结构的变化,生化试剂盒检测小鼠海马区 ATP、活性氧(ROS)的表达水平;利用 CCK8 和细胞 ROS 试剂盒检测原代神经元的细胞活力和 ROS 水平.结果 PRE-084 可降低糖尿病小鼠体质量、饮食饮水量和血糖.PRE-084 明显缓解 1 型糖尿病小鼠的学习记忆障碍,改善糖尿病小鼠海马CA1 区神经元 MAM结构的变化,升高糖尿病小鼠海马区 ATP的水平,降低糖尿病小鼠海马区及高糖条件下神经元中 ROS表达水平.结论 Sigma-1 受体激动剂PRE-084 改善 1 型糖尿病小鼠学习记忆障碍可能与海马区神经元 MAM结构变化、ATP产量增加及 ROS生成减少相关.

By integrating the dynamic capability perspective and service-dominant logic (SDL), this study empirically investigates the distinct roles of internal and external knowledge integration capabilities in the relationship between value co-creation orientation and radical service innovation. Based on survey data from a sample of 200 service innovation projects from IT and Internet-related industries in China, this study uses structural equation modeling (SEM) and a bootstrapping approach to test the hypothesized relationships in the conceptual model. The results show that external knowledge integration capability mediates the relationship between value co-creation orientation and radical service innovation. In addition, internal and external knowledge integration capability jointly play a serial mediating role between value co-creation orientation and radical service innovation. These findings contribute to the growing literature on value co-creation in radical service innovation, and offer service managers meaningful implications that reveal how to convert multiple sources of knowledge resources into superior radical service innovation.

The microbiome-gut-brain axis plays a crucial role in many neurological diseases, including mild cognitive impairment. Sleep deprivation (SD) induces cognitive decline accompanied by alterations in the gut microbiota. However, the role of gut microbiota alterations in SD-induced cognitive dysfunction and the underlying mechanisms remain unclear. Here, we found that dysbiosis of the gut microbiota following pretreatment with broad-spectrum antibiotics worsens SD-induced cognitive impairment in mice. Fecal microbiota transplantation from SD mice to healthy mice induced cognitive impairment. Additionally, the abundance of Akkermansia muciniphila (A. muciniphila) in the mouse gut microbiota was significantly reduced after 7 days of SD. A. muciniphila pretreatment alleviated cognitive dysfunction and prevented synaptic reduction in the hippocampus in SD mice. A. muciniphila pretreatment inhibited extensive microglial activation and synaptic engulfment in the hippocampus of SD mice. Metabolomics analysis revealed that A. muciniphila pretreatment increased the serum acetate and butanoic acid levels in SD mice. Finally, pretreatment with short-chain fatty acids (SCFAs) inhibited microglial synaptic engulfment and prevented neuronal synaptic loss in SD mice and primary microglia-neuron co-culture following LPS stimulation. Together, our findings illustrate that gut dysbiosis plays an essential role in SD-induced cognitive impairment by activating microglial engulfment at synapses. A. muciniphila supplementation may be a novel preventative strategy for SD-induced cognitive dysfunction, by increasing SCFAs production and maintaining microglial homeostasis.

The prevalence of diabetes-associated cognitive dysfunction (DACD) has increased to 13.5%. Dementia, as the most severe DACD, is the second leading cause of death in patients with diabetes mellitus. Hence, the potential mechanisms of DACD for slowing or halting its progression need to be urgently explored. Given that the sigma-1 receptor (Sig-1R), a chaperone protein located in the endoplasmic reticulum (ER)-mitochondrion contact membranes to regulate ER stress (ERS), is associated with cognitive outcomes in neurodegenerative diseases, this study aimed to investigate the role of astrocytic Sig-1R in DACD and its underlying mechanism. Here, we examined the levels of ERS and complement component 3/3a (C3/C3a) from primary astrocytes with different concentrations of glucose and treatment. Subsequently, HT22 neurons were cultured in different astrocyte-conditioned medium, and the expression of synaptic proteins was detected. We constructed type 1 diabetes mellitus (T1DM) model to evaluate the astrocytic Sig-1R mechanism on synapse and cognitive function changes. In vitro, high glucose concentration downregulated Sig-1R and aggravated ERS in astrocytes, resulting in synapse deficits. PRE-084, a high-affinity and selective Sig-1R agonist, inhibited astrocytic ERS and complement cascades and restored synaptic damage, while the Sig-1R antagonist displayed the opposite results. Moreover, C3a receptor antagonist (C3aRA) could mimic the effect of PRE-084 and exerted neuroprotective effects. In vivo, PRE-084 substantially reduced ER-mitochondrion contact, activation of ERS, and C3/C3a secretion in mice with T1DM. Additionally, the synaptic loss and neurobehavioral dysfunction of mice with T1DM were less pronounced in both the PRE-084 and C3aRA treatment groups. These findings demonstrated that Sig-1R activation reduced the astrocytic ER-mitochondrion contact, ERS activation, and complement-mediated synaptic damage in T1DM. This study suggested the mechanisms and potential therapeutic approaches for treating DACD.