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"Yu, Chun"
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قصة نجاح مجموعة تينسنت للبرمجيات : إمبراطورية تينسنت ما هوا تينغ
يتناول الكتاب الحديث عن (ما هو تينغ) الرجل الذي يحب الجميع أن يكرهه وأحد عمالقة صناعة الإنترنت الستة في الصين، عشر سنوات هي المدة التي احتاجها (ما هو تينغ) ليجعل من مؤسسة تينسنت نموذجا لصناعة الإنترنت في الصين بل والعالم، (تينسنت) قصة مؤسسة بدأت على يد مطور برامج رسائل لتصبح صاحبة أعلى قيمة سوقية لشركات الإنترنت في الصين، (كيو كيو) برنامج المحادثة الذي كان سببا في نجاح (ما هو تينغ) في حياته العملية وكان أيضا سببا في عثوره على شريكة حياته، فقد كان نجاح (ما هو تينغ) مبنيا على تقليد الآخرين، فكان التلميذ الذي تفوق على أساتذته، لقد بدأ من حيث انتهى الآخرون ليصنع أشهر برنامج محادثة في الصين والذي تجاوزت شهرته البرنامج الأصلي ICQ، إنها قصة كفاح وصعود رجل حلم وكافح من أجل تحقيق حلمه، رجل يسميه الصينيون بيل جيتس الصين، رجل بدءا من لا شيء وأصبح يملك كل شيء.
Book
Spatiotemporal manipulation of ciliary glutamylation reveals its roles in intraciliary trafficking and Hedgehog signaling
Tubulin post-translational modifications (PTMs) occur spatiotemporally throughout cells and are suggested to be involved in a wide range of cellular activities. However, the complexity and dynamic distribution of tubulin PTMs within cells have hindered the understanding of their physiological roles in specific subcellular compartments. Here, we develop a method to rapidly deplete tubulin glutamylation inside the primary cilia, a microtubule-based sensory organelle protruding on the cell surface, by targeting an engineered deglutamylase to the cilia in minutes. This rapid deglutamylation quickly leads to altered ciliary functions such as kinesin-2-mediated anterograde intraflagellar transport and Hedgehog signaling, along with no apparent crosstalk to other PTMs such as acetylation and detyrosination. Our study offers a feasible approach to spatiotemporally manipulate tubulin PTMs in living cells. Future expansion of the repertoire of actuators that regulate PTMs may facilitate a comprehensive understanding of how diverse tubulin PTMs encode ciliary as well as cellular functions.
Tubulin post-translational modifications (PTMs) occur spatiotemporally throughout cells, therefore assessing the physiological roles in specific subcellular compartments has been challenging. Here the authors develop a method to rapidly deplete tubulin glutamylation inside the primary cilia by targeting an engineered deglutamylase to the axoneme.
Journal Article
Fault-tolerant cooperative control of unmanned aerial vehicles
\"This book focuses on the fault-tolerant cooperative control (FTCC) of multiple unmanned aerial vehicles (multi-UAVs). It provides systematic and comprehensive descriptions of FTCC issues in multi-UAVs concerning faults, external disturbances, strongly unknown nonlinearities, and input saturation. Further, it addresses FTCC design from longitudinal motions to attitude motions, and outer-loop position motions of multi-UAVs. The books detailed control schemes can be used to enhance the flight safety of multi-UAVs. As such, the book offers readers an in-depth understanding of UAV safety in cooperative/formation flight and corresponding design methods. The FTCC methods presented here can also provide guidelines for engineers to improve the safety of aerospace engineering systems. The book offers a valuable asset for scientists and researchers, aerospace engineers, control engineers, lecturers and teachers, and graduates and undergraduates in the system and control community, especially those working in the field of UAV cooperation and multi-agent systems.\"-- Back cover.
Book
Increased Interleukin-17 and Glucocorticoid Receptor-β Expression in Interstitial Lung Diseases and Corticosteroid Insensitivity
Treatment responsiveness to corticosteroids is excellent for cryptogenic organizing pneumonia (COP) and sarcoidosis, but suboptimal for idiopathic pulmonary fibrosis (IPF)/usual interstitial pneumonia (UIP). We hypothesise that the differential expression of IL-17 contributes to variable corticosteroid sensitivity in different interstitial lung diseases.
To determine the associations among expression of IL-17, glucocorticoid receptor-β and responsiveness to corticosteroid treatment in interstitial lung diseases.
Immunohistochemical (IHC) staining was performed on formalin-fixed paraffin-embedded (FFPE) lung tissues obtained by bronchoscopic, CT-guided or surgical biopsies, and quantified by both cell counting (% positive cells) by individuals and by software IHC Profiler plugin of ImageJ (opacity density score). We studied the effect of IL-17 on corticosteroid sensitivity in human fibroblast MRC5 cell line.
Compared with specimens from patients with COP (n =13) and sarcoidosis (n =13), those from IPF patients (n = 21) had greater GR-β and IL-17 expression and neutrophil infiltration. Radiographic progression after oral corticosteroid treatment was positively correlated with the expression in IL-17 and GR-β/GR-α ratio in all patients (COP, sarcoidosis and IPF) and also within the IPF subgroup only. IL-17 expression level was positively associated with GR-β and GR-β/GR-α ratio. In MRC5 cells, exogenous IL-17 increased the production of collagen I and up-regulated GR-β expression and dexamethasone's suppressive effect on collagen I production was impaired by IL-17, and silencing IL-17 receptor A gene attenuated the effect of IL-17.
Up-regulation of GR-β/GR-α ratio by IL-17 could be associated with the relative corticosteroid-insensitivity of IPF.
Journal Article
إمبراطورية تينسنت ما هو تينغ : قصة نجاح مجموعة تينسنت للبرمجيات (وي تشات-كيو كيو)
يتناول الكتاب الحديث عن (ما هو تينغ) الرجل الذي يحب الجميع أن يكرهه وأحد عمالقة صناعة الإنترنت الستة في الصين، عشر سنوات هي المدة التي احتاجها (ما هو تينغ) ليجعل من مؤسسة تينسنت نموذجا لصناعة الإنترنت في الصين بل والعالم، (تينسنت) قصة مؤسسة بدأت على يد مطور برامج رسائل لتصبح صاحبة أعلى قيمة سوقية لشركات الإنترنت فى الصين، (كيو كيو) برنامج المحادثة الذي كان سببا في نجاح (ما هو تينغ) في حياته العملية وكان أيضا سببا في عثوره على شريكة حياته، فقد كان نجاح (ما هو تينغ) مبنيا على تقليد الآخرين، فكان التلميذ الذي تفوق على أساتذته، لقد بدأ من حيث انتهى الآخرون ليصنع أشهر برنامج محادثة في الصين والذي تجاوزت شهرته البرنامج الأصلي ICQ، إنها قصة كفاح وصعود رجل حلم وكافح من أجل تحقيق حلمه، رجل يسميه الصينيون بيل جيتس الصين، رجل بدءا من لا شيء وأصبح يملك كل شيء.
BOOK
The emerging roles and functions of circular RNAs and their generation
Circular RNAs (circRNAs) are closed long non-coding RNAs, in which the 5’ and 3’ termini are covalently linked by back-splicing of exons from a single pre-mRNA. Emerging evidence indicates that circRNAs are broadly expressed in mammalian cells and show cell type- or tissue-specific expression patterns. Importantly, circRNAs have been shown to participate in regulating various biological processes. Functionally, circRNAs can influence cellular physiology through various molecular mechanisms, such as serving as a decoy for microRNAs or RNA-binding proteins to modulate gene expression or translation of regulatory proteins. The biogenesis of circRNAs is known to be tightly regulated by
cis-
(intronic complementary sequences) and/or trans-factors (splicing factors) that constitute a cell- and context-dependent regulatory layer in the control of gene expression. However, our understanding of the regulation and function of circRNAs is still limited. In this review, we summarize the current progress in elucidating the functional roles, mechanisms and biogenesis of circRNAs. We also discuss the relationship between regulation and formation of circRNAs.
Journal Article
Ferroptosis Signature Shapes the Immune Profiles to Enhance the Response to Immune Checkpoint Inhibitors in Head and Neck Cancer
As a type of immunogenic cell death, ferroptosis participates in the creation of immunoactive tumor microenvironments. However, knowledge of spatial location of tumor cells with ferroptosis signature in tumor environments and the role of ferroptotic stress in inducing the expression of immune‐related molecules in cancer cells is limited. Here the spatial association of the transcriptomic signatures is demonstrated for ferroptosis and inflammation/immune activation located in the invasive front of head and neck squamous cell carcinoma (HNSCC). The association between ferroptosis signature and inflammation/immune activation is more prominent in HPV‐negative HNSCC compared to HPV‐positive ones. Ferroptotic stress induces PD‐L1 expression through reactive oxygen species (ROS)‐elicited NF‐κB signaling pathway and calcium influx. Priming murine HNSCC with the ferroptosis inducer sensitizes tumors to anti‐PD‐L1 antibody treatment. A positive correlation between the ferroptosis signature and the active immune cell profile is shown in the HNSCC samples. This study reveals a subgroup of ferroptotic HNSCC with immune‐active signatures and indicates the potential of priming HNSCC with ferroptosis inducers to increase the antitumor efficacy of immune checkpoint inhibitors. Ferroptosis stress elicits PD‐L1 expression in head and neck cancer cells and modulates tumor microenvironments to an immune‐active state, highlighting the potential of priming tumors with ferroptosis inducers to potentiate the antitumor efficacy of immunotherapy.
Journal Article
High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy
Mitochondrial dysfunction and impaired Ca
2+
handling are involved in the development of diabetic cardiomyopathy (DCM). Dynamic relative protein 1 (Drp1) regulates mitochondrial fission by changing its level of phosphorylation, and the Orai1 (Ca
2+
release-activated calcium channel protein 1) calcium channel is important for the increase in Ca
2+
entry into cardiomyocytes. We aimed to explore the mechanism of Drp1 and Orai1 in cardiomyocyte hypertrophy caused by high glucose (HG). We found that Zucker diabetic fat rats induced by administration of a high-fat diet develop cardiac hypertrophy and impaired cardiac function, accompanied by the activation of mitochondrial dynamics and calcium handling pathway-related proteins. Moreover, HG induces cardiomyocyte hypertrophy, accompanied by abnormal mitochondrial morphology and function, and increased Orai1-mediated Ca
2+
influx. Mechanistically, the Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1) prevents cardiomyocyte hypertrophy induced by HG by reducing phosphorylation of Drp1 at serine 616 (S616) and increasing phosphorylation at S637. Inhibition of Orai1 with single guide RNA (sgOrai1) or an inhibitor (BTP2) not only suppressed Drp1 activity and calmodulin-binding catalytic subunit A (CnA) and phosphorylated-extracellular signal-regulated kinase (p-ERK1/2) expression but also alleviated mitochondrial dysfunction and cardiomyocyte hypertrophy caused by HG. In addition, the CnA inhibitor cyclosporin A and p-ERK1/2 inhibitor U0126 improved HG-induced cardiomyocyte hypertrophy by promoting and inhibiting phosphorylation of Drp1 at S637 and S616, respectively. In summary, we identified Drp1 as a downstream target of Orai1-mediated Ca
2+
entry, via activation by p-ERK1/2-mediated phosphorylation at S616 or CnA-mediated dephosphorylation at S637 in DCM. Thus, the Orai1–Drp1 axis is a novel target for treating DCM.
Journal Article