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12,641 result(s) for "Gao, Cheng"
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Pivoting Isn’t Enough? Managing Strategic Reorientation in New Ventures
New ventures often experience deviations from their plans that oblige them to reorient in pursuit of a better fit between their evolving products and their target customers. Yet, research is largely silent on how managers explain such changes and justify their ventures in the wake of fundamental redirections in strategy. Ventures initially attain legitimacy and amass resources on the strength of aims that audiences find compelling; later, those early claims can complicate course corrections. To shed light on how ventures manage strategic reorientations, we conducted an inductive, comparative case study of ventures in a nascent financial-technology sector. The ventures pursued parallel reorientations and produced comparable end products but diverged conspicuously in managing audiences during transitions. Our process model, inspired by these differences, proposes a sequence of stratagems that may enable entrepreneurs to alter strategy while portraying faithfulness to enduring aims. Our theoretical framework posits that, for ventures, reorientation without penalty may depend on how they anticipate, justify, and stage changes to various audiences.
Overcoming Institutional Voids
Research summary: Emerging markets are characterized by underdeveloped institutions and frequent environmental shifts. Yet, they also contain many firms that have survived over generations. How are firms in weak institutional environments able to persist over time? Motivated by 69 interviews with leaders of emerging market firms with histories spanning generations, we combine induction and deduction to propose reputation as a meta‐resource that allows firms to activate their conventional resources. We conceptualize reputation as consisting of prominence, perceived quality, and resilience, and develop a process model that illustrates the mechanisms that allow reputation to facilitate survival in ways that persist over time. Building on research in strategy and business history, we thus shed light on an underappreciated strategic construct (reputation) in an undertheorized setting (emerging markets) over an unusual period (the historical long run). Managerial summary: Why are some firms able to persistently survive in challenging, uncertain, and underdeveloped business environments? To explore this question, we analyze in‐depth interviews with leaders of emerging market firms that have survived over decades and even centuries. We find that firm reputation is a key strategic driver, and propose new ideas about the ways through which reputation facilitates survival. We elaborate how a favorable reputation allows a firm to more fully utilize its existing resources by decreasing uncertainty. We also propose that reputation has offensive and defensive properties that make it valuable to firms during both positive and negative economic cycles. Finally, we discuss why a reputation‐based source of competitive advantage is hard to imitate, and outline three general approaches for building reputation. Copyright © 2017 John Wiley & Sons, Ltd. Video
NF‐κB signalling pathways in nucleus pulposus cell function and intervertebral disc degeneration
Intervertebral disc degeneration (IDD) is a common clinical degenerative disease of the spine. A series of factors, such as inflammation, oxidative stress and mechanical stress, promote degradation of the extracellular matrix (ECM) of the intervertebral discs (IVD), leading to dysfunction and structural destruction of the IVD. Nuclear factor‐κB (NF‐κB) transcription factor has long been regarded as a pathogenic factor of IDD. Therefore, NF‐κB may be an ideal therapeutic target for IDD. As NF‐κB is a multifunctional functional transcription factor with roles in a variety of biological processes, a comprehensive understanding of the function and regulatory mechanism of NF‐κB in IDD pathology will be useful for the development of targeted therapeutic strategies for IDD, which can prevent the progression of IDD and reduce potential risks. This review discusses the role of the NF‐κB signalling pathway in the nucleus pulposus (NP) in the process of IDD to understand pathological NP degeneration further and provide potential therapeutic targets that may interfere with NF‐κB signalling for IDD therapy. Intervertebral disc degeneration (IDD) is a common clinical degenerative disease of the spine. A series of factors, such as inflammation, oxidative stress, and mechanical stress, promote degradation of the extracellular matrix (ECM) of the intervertebral discs (IVD), leading to dysfunction and structural destruction of the IVD. Nuclear factor‐κB (NF‐κB) transcription factor has long been regarded as the pathogenic factor of IDD. Therefore, NF‐κB may be an ideal therapeutic target for IDD. As NF‐κB is a multifunctional functional transcription factor with roles in a variety of biological processes, a comprehensive understanding of the function and regulatory mechanism of NF‐κB in IDD pathology will be useful for the development of targeted therapeutic strategies for IDD, which can prevent the progression of IDD and reduce potential risks. This review discusses the role of the NF‐κB signalling pathway in the nucleus pulposus (NP) in the process of IDD to understand pathological NP degeneration further and provide potential therapeutic targets that may interfere with NF‐κB signalling for IDD therapy. ​
Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression through the circAMOTL1L-miR-193a-5p-Pcdha pathway
p53, circRNAs and miRNAs are important components of the regulatory network that activates the EMT program in cancer metastasis. In prostate cancer (PCa), however, it has not been investigated whether and how p53 regulates EMT by circRNAs and miRNAs. Here we show that a Amotl1-derived circRNA, termed circAMOTL1L, is downregulated in human PCa, and that decreased circAMOTL1L facilitates PCa cell migration and invasion through downregulating E-cadherin and upregulating vimentin, thus leading to EMT and PCa progression. Mechanistically, we demonstrate that circAMOTL1L serves as a sponge for binding miR-193a-5p in PCa cells, relieving miR-193a-5p repression of Pcdha gene cluster (a subset of the cadherin superfamily members). Accordingly, dysregulation of the circAMOTL1L-miR-193a-5p-Pcdha8 regulatory pathway mediated by circAMOTL1L downregulation contributes to PCa growth in vivo. Further, we show that RBM25 binds directly to circAMOTL1L and induces its biogenesis, whereas p53 regulates EMT via direct activation of RBM25 gene. These findings have linked p53/RBM25-mediated circAMOTL1L-miR-193a-5p-Pcdha regulatory axis to EMT in metastatic progression of PCa. Targeting this newly identified regulatory axis provides a potential therapeutic strategy for aggressive PCa.
Disease-induced changes in plant microbiome assembly and functional adaptation
Background The plant microbiome is an integral part of the host and increasingly recognized as playing fundamental roles in plant growth and health. Increasing evidence indicates that plant rhizosphere recruits beneficial microbes to the plant to suppress soil-borne pathogens. However, the ecological processes that govern plant microbiome assembly and functions in the below- and aboveground compartments under pathogen invasion are not fully understood. Here, we studied the bacterial and fungal communities associated with 12 compartments (e.g., soils, roots, stems, and fruits) of chili pepper ( Capsicum annuum L.) using amplicons (16S and ITS) and metagenomics approaches at the main pepper production sites in China and investigated how Fusarium wilt disease (FWD) affects the assembly, co-occurrence patterns, and ecological functions of plant-associated microbiomes. Results The amplicon data analyses revealed that FWD affected less on the microbiome of pepper reproductive organs (fruit) than vegetative organs (root and stem), with the strongest impact on the upper stem epidermis. Fungal intra-kingdom networks were less stable and their communities were more sensitive to FWD than the bacterial communities. The analysis of microbial interkingdom network further indicated that FWD destabilized the network and induced the ecological importance of fungal taxa. Although the diseased plants were more susceptible to colonization by other pathogenic fungi, their below- and aboveground compartments can also recruit potential beneficial bacteria. Some of the beneficial bacterial taxa enriched in the diseased plants were also identified as core taxa for plant microbiomes and hub taxa in networks. On the other hand, metagenomic analysis revealed significant enrichment of several functional genes involved in detoxification, biofilm formation, and plant-microbiome signaling pathways (i.e., chemotaxis) in the diseased plants. Conclusions Together, we demonstrate that a diseased plant could recruit beneficial bacteria and mitigate the changes in reproductive organ microbiome to facilitate host or its offspring survival. The host plants may attract the beneficial microbes through the modulation of plant-microbiome signaling pathways. These findings significantly advance our understanding on plant-microbiome interactions and could provide fundamental and important data for harnessing the plant microbiome in sustainable agriculture. DwWQb6Dg7ZT1-tarvfq632 Video abstract
What are Risk Factors of Postoperative Pneumonia in Geriatric Individuals after Hip Fracture Surgery: A Systematic Review and Meta‐Analysis
Postoperative pneumonia (POP) is a common postoperative complication. Negative consequences associated with POP included prolonged hospital length of stay, more frequent intensive care unit (ICU) stays, and a higher rate of sepsis, readmission, and mortality. This meta‐analysis aimed to assess the incidence and risk factors associated with POP after hip fracture surgery in elderly patients. PubMed, Web of Science, and Cochrane Library were searched (up to March 31, 2022). All studies on the risk factors for POP after hip fracture surgery in elderly patients, published in English, were reviewed. The qualities of the included studies were assessed using the Newcastle–Ottawa Scale. Data were pooled, and a meta‐analysis was performed. Ten studies, including 12,084 geriatric patients undergoing hip fracture surgery, were included. Of these 12,084 patients, POP occurred in 809 patients. The results indicated that age (mean difference [MD] = 4.95, 95% confidence interval [CI]: 3.22–6.69), male (odds ratio [OR] = 1.41, 95% CI: 1.02–1.93), the American Society of Anaesthesiologists classification ≥3 (OR = 3.48, 95% CI: 1.87–6.47), dependent functional status (OR = 5.23, 95% CI: 2.18–12.54, P = 0.0002), smoking (OR = 1.33, 95% CI: 1.07–1.65), chronic obstructive pulmonary disease (OR = 3.76, 95% CI: 2.07–6.81), diabetes mellitus (OR = 1.19, 95% CI: 1.01–1.40), coronary heart disease (OR = 1.74, 95% CI: 1.23–2.46), arrhythmia (OR = 1.47, 95% CI: 1.01–2.14), cerebrovascular disease (OR = 1.88, 95% CI: 1.56–2.27), dementia (OR = 2.36, 95% CI: 1.04–5.36), chronic renal failure (OR = 1.85, 95% CI: 1.29–2.67), hip arthroplasty (OR = 1.30, 95% CI: 1.08–1.56), delayed surgery (OR = 6.40, 95% CI: 3.00–13.68), preoperative creatinine (MD = 5.32, 95% CI: 0.55–10.08), and preoperative serum albumin (MD = −3.01, 95% CI: −4.21 – −1.80) were risk factors for POP. Related prophylactic measures should be provided in geriatric patients with the above‐mentioned risk factors to prevent POP after hip fracture surgery. We found that age, gender, ASA classification ≥ 3, dependent function status, smoking, COPD, diabetes mellitus, coronary heart disease, arrhythmia, cerebrovascular disease, dementia, chronic renal failure, hip arthroplasty, delayed surgery, preoperative creatinine, preoperative serum albumin were the risk factors of POP via meta‐analysis of 10 included studies.
Co-occurrence networks reveal more complexity than community composition in resistance and resilience of microbial communities
Plant response to drought stress involves fungi and bacteria that live on and in plants and in the rhizosphere, yet the stability of these myco- and micro-biomes remains poorly understood. We investigate the resistance and resilience of fungi and bacteria to drought in an agricultural system using both community composition and microbial associations. Here we show that tests of the fundamental hypotheses that fungi, as compared to bacteria, are (i) more resistant to drought stress but (ii) less resilient when rewetting relieves the stress, found robust support at the level of community composition. Results were more complex using all-correlations and co-occurrence networks. In general, drought disrupts microbial networks based on significant positive correlations among bacteria, among fungi, and between bacteria and fungi. Surprisingly, co-occurrence networks among functional guilds of rhizosphere fungi and leaf bacteria were strengthened by drought, and the same was seen for networks involving arbuscular mycorrhizal fungi in the rhizosphere. We also found support for the stress gradient hypothesis because drought increased the relative frequency of positive correlations. Fungi are expected to be more resistant and less resilient than bacteria to environmental disturbances. Here, the authors report complex responses by microbial co-occurrence networks to drought in an agricultural system, challenging simple predictions of fungal and bacterial drought responses.
Dexmedetomidine alleviates hepatic ischaemia‐reperfusion injury via the PI3K/AKT/Nrf2‐NLRP3 pathway
Hepatic ischaemia‐reperfusion (I/R) injury constitutes a tough difficulty in liver surgery. Dexmedetomidine (Dex) plays a protective role in I/R injury. This study investigated protective mechanism of Dex in hepatic I/R injury. The human hepatocyte line L02 received hypoxia/reoxygenation (H/R) treatment to stimulate cell model of hepatic I/R. The levels of pyroptosis proteins and inflammatory factors were detected. Functional rescue experiments were performed to confirm the effects of miR‐494 and JUND on hepatic I/R injury. The levels of JUND, PI3K/p‐PI3K, AKT/p‐AKT, Nrf2, and NLRP3 activation were detected. The rat model of hepatic I/R injury was established to confirm the effect of Dex in vivo. Dex reduced pyroptosis and inflammation in H/R cells. Dex increased miR‐494 expression, and miR‐494 targeted JUND. miR‐494 inhibition or JUND upregulation reversed the protective effect of Dex. Dex repressed NLRP3 inflammasome by activating the PI3K/AKT/Nrf2 pathway. In vivo experiments confirmed the protective effect of Dex on hepatic I/R injury. Overall, Dex repressed NLRP3 inflammasome and alleviated hepatic I/R injury via the miR‐494/JUND/PI3K/AKT/Nrf2 axis.