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"Zhang, Yu"
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The source of innovation in China : highly innovative human systems
\"Given the popular belief that China's comparative advantage is its low labour cost, The Source of Innovation in China argues that the fundamental source for Chinese economic growth is its innovation. Based on qualitative case studies and quantitative surveys of 600 firms, this research describes the competitive advantages of successful Chinese enterprises and builds a theoretical framework for innovative firms and empirically tests the resulting hypothesis. The authors explore the general features of Chinese enterprise and innovation, hypothesizing that the rapid economic development in China is based on innovation. This innovation is not only about technological innovation, but also process and strategy innovation. Cases are drawn from technological innovative firms and from traditional labour-intensive industries. Moreover, the underlying source of Chinese innovation is centred on its people, and the authors discuss this by looking at the philosophical, linguistic and culture influences. They take a broad stakeholder perspective and employ social network theory to explain that, by extension, innovative people surround the organization and create organizational values. At the organizational level, they propose a theoretical framework of a High-Innovative Human System, by integrating both Western and Chinese management systems. \"-- Provided by publisher.
Book
Sleep quality, APOE ε4, and Alzheimer’s disease: associations from two prospective cohort studies and mechanisms by plasma proteomic analysis
Background
The relationship between sleep quality and Alzheimer's disease (AD), and its interaction with genetic susceptibility, remains unclear. Our study explores the complex association between sleep quality and AD risk, focusing on the moderating role of the
APOE
ε4 allele.
Methods
Linear regression models, linear mixed-effects models, and Cox proportional hazard models were conducted in 321,905 non-demented participants from UK Biobank (UKB, mean age = 56.49, mean follow-up: 12.3 years) and 1,598 non-demented participants (mean age = 73.19, mean follow-up: 3.90 years) from Alzheimer's Disease Neuroimaging Initiative (ADNI). The interaction terms of sleep by
APOE
ε4 status were added in all analyses and stratified analyses were further performed. Proteomic and bioinformatic analyses were conducted to explore the biological mechanisms by which sleep and its interaction with
APOE
ε4 influence the development of AD.
Results
Poor sleep quality was significantly associated with worse cognition, faster hippocampal atrophy, and increased AD risk (HR = 1.05 in UKB and HR = 1.37 in ADNI). Notably, these associations were intensified in
APOE
ε4 carriers. Proteomic analyses identified eleven proteins linked to both poor sleep and AD risk (
P
< 1.72 × 10
–5
). These proteins were enriched mainly in inflammatory and metabolic pathways. Growth differentiation factor 15 was identified as the bridge linking poor sleep and AD risk specifically in
APOE
ε4 carriers.
Conclusions
Poor sleep is associated with increased risk of AD, possibly by dysregulating peripheral inflammatory responses and metabolic pathways. The interaction between poor sleep and
APOE
ε4 may further enhance AD risk. Future studies are warranted to test whether this interaction was driven by neuroinflammation.
Journal Article
صناعة السفن والمعدات البحرية في الصين
يحدثنا تشاويا هوي، كما تشير الدار في بيانها الصحفي، عن القدرة التنافسية للصين في مجال صناعة السفن البحرية ولا سيما ناقلات النفط وغيرها من سفن الأبحاث العلمية، وزوارق اختراق الأمواج، وعبارات القطارات، وسفن الاستطلاع البحرية، وسفن الصيد البحرية، يستعرض تشاويا هوي في كتابه بالأرقام مراحل الإنتاج والتوزيع في السوق العالمية بدءا من السفن الصغيرة والبسيطة، وصولا إلى السفن الكبيرة والمتطورة ويذكر أهم الشركات الرائدة في هذا المجال من خلال تقديم معلومات مكتوبة ومصورة.
BOOK
Pain regulation by non-neuronal cells and inflammation
Acute pain is protective and a cardinal feature of inflammation. Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated with chronic neuroinflammation, a local inflammation in the peripheral or central nervous system. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We review how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain. Recent studies also suggest that bacterial infections regulate pain through direct actions on sensory neurons, and specific receptors are present in nociceptors to detect danger signals from infections. We also discuss new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
Journal Article
Prediction and analysis of essential genes using the enrichments of gene ontology and KEGG pathways
Identifying essential genes in a given organism is important for research on their fundamental roles in organism survival. Furthermore, if possible, uncovering the links between core functions or pathways with these essential genes will further help us obtain deep insight into the key roles of these genes. In this study, we investigated the essential and non-essential genes reported in a previous study and extracted gene ontology (GO) terms and biological pathways that are important for the determination of essential genes. Through the enrichment theory of GO and KEGG pathways, we encoded each essential/non-essential gene into a vector in which each component represented the relationship between the gene and one GO term or KEGG pathway. To analyze these relationships, the maximum relevance minimum redundancy (mRMR) was adopted. Then, the incremental feature selection (IFS) and support vector machine (SVM) were employed to extract important GO terms and KEGG pathways. A prediction model was built simultaneously using the extracted GO terms and KEGG pathways, which yielded nearly perfect performance, with a Matthews correlation coefficient of 0.951, for distinguishing essential and non-essential genes. To fully investigate the key factors influencing the fundamental roles of essential genes, the 21 most important GO terms and three KEGG pathways were analyzed in detail. In addition, several genes was provided in this study, which were predicted to be essential genes by our prediction model. We suggest that this study provides more functional and pathway information on the essential genes and provides a new way to investigate related problems.
Journal Article
Single-cell tumor heterogeneity landscape of hepatocellular carcinoma: unraveling the pro-metastatic subtype and its interaction loop with fibroblasts
Background
Tumor heterogeneity presents a formidable challenge in understanding the mechanisms driving tumor progression and metastasis. The heterogeneity of hepatocellular carcinoma (HCC) in cellular level is not clear.
Methods
Integration analysis of single-cell RNA sequencing data and spatial transcriptomics data was performed. Multiple methods were applied to investigate the subtype of HCC tumor cells. The functional characteristics, translation factors, clinical implications and microenvironment associations of different subtypes of tumor cells were analyzed. The interaction of subtype and fibroblasts were analyzed.
Results
We established a heterogeneity landscape of HCC malignant cells by integrated 52 single-cell RNA sequencing data and 5 spatial transcriptomics data. We identified three subtypes in tumor cells, including ARG1
+
metabolism subtype (Metab-subtype), TOP2A
+
proliferation phenotype (Prol-phenotype), and S100A6
+
pro-metastatic subtype (EMT-subtype). Enrichment analysis found that the three subtypes harbored different features, that is metabolism, proliferating, and epithelial-mesenchymal transition. Trajectory analysis revealed that both Metab-subtype and EMT-subtype originated from the Prol-phenotype. Translation factor analysis found that EMT-subtype showed exclusive activation of SMAD3 and TGF-β signaling pathway. HCC dominated by EMT-subtype cells harbored an unfavorable prognosis and a deserted microenvironment. We uncovered a positive loop between tumor cells and fibroblasts mediated by SPP1-CD44 and CCN2/TGF-β-TGFBR1 interaction pairs. Inhibiting CCN2 disrupted the loop, mitigated the transformation to EMT-subtype, and suppressed metastasis.
Conclusion
By establishing a heterogeneity landscape of malignant cells, we identified a three-subtype classification in HCC. Among them, S100A6
+
tumor cells play a crucial role in metastasis. Targeting the feedback loop between tumor cells and fibroblasts is a promising anti-metastatic strategy.
Journal Article
LncRNA CAIF inhibits autophagy and attenuates myocardial infarction by blocking p53-mediated myocardin transcription
Increasing evidence suggests that long noncoding RNAs (lncRNAs) play crucial roles in various biological processes. However, little is known about the effects of lncRNAs on autophagy. Here we report that a lncRNA, termed cardiac autophagy inhibitory factor (CAIF), suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53-mediated myocardin transcription. Myocardin expression is upregulated upon H
2
O
2
and ischemia/reperfusion, and knockdown of myocardin inhibits autophagy and attenuates myocardial infarction. p53 regulates cardiomyocytes autophagy and myocardial ischemia/reperfusion injury by regulating myocardin expression. CAIF directly binds to p53 protein and blocks p53-mediated myocardin transcription, which results in the decrease of myocardin expression. Collectively, our data reveal a novel CAIF-p53-myocardin axis as a critical regulator in cardiomyocyte autophagy, which will be potential therapeutic targets in treatment of defective autophagy-associated cardiovascular diseases.
Little is known about the role of long lncRNAs in autophagy. The authors identify lncCAIF, and show that it suppresses cardiac autophagy and attenuates myocardial infarction by targeting p53 -mediated transcription of myocardin.
Journal Article