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يدور موضوع الكتاب حول \"الاستراتيجيات العسكرية في الصين القديمة\" هذا ‏العنوان يدخل في حقل الكتب العسكرية أو ما يعرف بـ (الأدب العسكري) وهو حسب ‏مؤلفه الصيني \"لي تشينغ بين\" أحد أعظم ميراث ثقافي للأمة الصينية، أدب غني ‏بالدلالات الثقافية والمزايا الفريدة التي تعرف إليها المؤلف بعد أن بحث في الأدب ‏العسكري القديم في بلاده بما في ذلك أحد أعظم أعماله وهي فن الحرب لما يفوق ‏الثلاثين عاما. لقد صرح أن هذا الأدب يتمتع بحكمة كبيرة، واستراتيجيات بالإضافة ‏إلى مفاتيح النجاح ويمكن أن يتم الرجوع إلى الكتب العسكرية القديمة لتقييم ‏الاستراتيجيات الفعالة من قبل العديد من الأشخاص، بمن فيهم القادة العسكريون، ‏السياسيون، الدبلوماسيون، رجال الأعمال، وحتى الناس العاديون. ولأن الكتب ‏العسكرية تلعب دور ناقل الثقافة، لذلك، يفترض المؤلف أنه من الأفضل لكل شخص ‏متعلم أن يقرأ هذا النوع من الكتب بغض النظر عن مهنته. ‏ كتاب \"الاستراتيجيات العسكرية في الصين القديمة\" هو نقطة في بحر العدد الهائل ‏من الكتب الصينية الكلاسيكية القديمة بالإضافة للأدب العسكري العميق، لقد اختار ‏المؤلف ما يزيد عن ثلاثمائة بند في ثمانين كتابا عسكريا قديما وأضاف الشروحات ‏الصينية والترجمات الإنجليزية المتوافقة في هذا الكتاب بهدف مساعدة القراء في فهم ‏ودراسة الأدب العسكري القديم. يتضمن هذا الكتاب ترجمة الأصل الإنجليزي ‏‎\"Military Strategies in ‎Ancient China\"‎‏ نقلته إلى العربية نهى حسن ويأتي باللغتين العربية والصينية مما ‏يسهم في تعلم اللغة الصينية للناطقين بالضاد.

Covalent organic frameworks have recently gained increasing attention in photocatalytic hydrogen generation from water. However, their structure-property-activity relationship, which should be beneficial for the structural design, is still far-away explored. Herein, we report the designed synthesis of four isostructural porphyrinic two-dimensional covalent organic frameworks (MPor-DETH-COF, M = H 2 , Co, Ni, Zn) and their photocatalytic activity in hydrogen generation. Our results clearly show that all four covalent organic frameworks adopt AA stacking structures, with high crystallinity and large surface area. Interestingly, the incorporation of different transition metals into the porphyrin rings can rationally tune the photocatalytic hydrogen evolution rate of corresponding covalent organic frameworks, with the order of CoPor-DETH-COF < H 2 Por-DETH-COF < NiPor-DETH-COF < ZnPor-DETH-COF. Based on the detailed experiments and calculations, this tunable performance can be mainly explained by their tailored charge-carrier dynamics via molecular engineering. This study not only represents a simple and effective way for efficient tuning of the photocatalytic hydrogen evolution activities of covalent organic frameworks at molecular level, but also provides valuable insight on the structure design of covalent organic frameworks for better photocatalysis. Covalent organic frameworks (COFs) present well-defined materials for constructing structure-property-activity relationships. Herein, authors explore isostructural porphyrinic two-dimensional COFs with tunable of photocatalytic H 2 production rates arising from tailored charge-carrier dynamics.

كتاب شجرة المظلات تأليف باي بينغ، تدور أحداث القصة الصينية حول الباندا الصغير جواجوا وأخته يايا لديهما مظلة حمراء متعلقان بها للغاية. يوما ما تمزقت فرمتها الأم، ولشدة تعلق المظلة بالصغيرين، فقد تحولت إلى شجرة تثمر مظلات حمراء، وتوزعها على عابري السبيل، وكان الصغيران يقصدانها كل يوم ويناملن تحت ظلها.

Regulatory T (Treg) cells are essential for maintaining immune homeostasis and tolerance, but the mechanisms regulating the stability and function of Treg cells have not been fully elucidated. Here we show SUMO-specific protease 3 (SENP3) is a pivotal regulator of Treg cells that functions by controlling the SUMOylation and nuclear localization of BACH2. Treg cell-specific deletion of Senp3 results in T cell activation, autoimmune symptoms and enhanced antitumor T cell responses. SENP3-mediated BACH2 deSUMOylation prevents the nuclear export of BACH2, thereby repressing the genes associated with CD4 + T effector cell differentiation and stabilizing Treg cell-specific gene signatures. Notably, SENP3 accumulation triggered by reactive oxygen species (ROS) is involved in Treg cell-mediated tumor immunosuppression. Our results not only establish the role of SENP3 in the maintenance of Treg cell stability and function via BACH2 deSUMOylation but also clarify the function of SENP3 in the regulation of ROS-induced immune tolerance. Regulatory T cells are crucial for the establishment and maintenance of peripheral immune tolerance, yet the mechanisms regulating their stability and function remain to be fully elucidated. Here the authors show SENP3 maintains Treg cell stability and function via BACH2 deSUMOylation.

Brain organoids have been used to recapitulate the processes of brain development and related diseases. However, the lack of vasculatures, which regulate neurogenesis and brain disorders, limits the utility of brain organoids. In this study, we induced vessel and brain organoids, respectively, and then fused two types of organoids together to obtain vascularized brain organoids. The fused brain organoids were engrafted with robust vascular network-like structures and exhibited increased number of neural progenitors, in line with the possibility that vessels regulate neural development. Fusion organoids also contained functional blood–brain barrier-like structures, as well as microglial cells, a specific population of immune cells in the brain. The incorporated microglia responded actively to immune stimuli to the fused brain organoids and showed ability of engulfing synapses. Thus, the fusion organoids established in this study allow modeling interactions between the neuronal and non-neuronal components in vitro, particularly the vasculature and microglia niche. Understanding how the organs form and how their cells behave is essential to finding the causes and treatment for developmental disorders, as well as understanding certain diseases. However, studying most organs in live animals or humans is technically difficult, expensive and invasive. To address this issue, scientists have developed models called ‘organoids’ that recapitulate the development of organs using stem cells in the lab. These models are easier to study and manipulate than the live organs. Brain organoids have been used to recapitulate brain formation as well as developmental, degenerative and psychiatric brain conditions such as microcephaly, autism and Alzheimer’s disease. However, these brain organoids lack the vasculature (the network of blood vessels) that supplies a live brain with nutrients and regulates its development, and which has important roles in brain disorders. Partly due to this lack of blood vessels, brain organoids also do not develop a blood brain barrier, the structure that prevents certain contents of the blood, including pathogens, toxins and even certain drugs from entering the brain. These characteristics limit the utility of existing brain organoids. To overcome these limitations, Sun, Ju et al. developed brain organoids and blood vessel organoids independently, and then fused them together to obtain vascularized brain organoids. These fusion organoids developed a robust network of blood vessels that was well integrated with the brain cells, and produced more neural cell precursors than brain organoids that had not been fused. This result is consistent with the idea that blood vessels can regulate brain development. Analyzing the fusion organoids revealed that they contain structures similar to the blood-brain barrier, as well as microglial cells (immune cells specific to the brain). When exposed to lipopolysaccharide – a component of the cell wall of certain bacteria – these cells responded by initiating an immune response in the fusion organoids. Notably, the microglial cells were also able to engulf connections between brain cells, a process necessary for the brain to develop the correct structures and work normally. Sun, Ju et al. have developed a new organoid system that will be of broad interest to researchers studying interactions between the brain and the circulatory system. The development of brain-blood-barrier-like structures in the fusion organoids could also facilitate the development of drugs that can cross this barrier, making it easier to treat certain conditions that affect the brain. Refining this model to allow the fusion organoids to grow for longer times in the lab, and adding blood flow to the system will be the next steps to establish this system.

Long-distance entanglement distribution is essential for both foundational tests of quantum physics and scalable quantum networks. Owing to channel loss, however, the previously achieved distance was limited to ~100 kilometers. Here we demonstrate satellite-based distribution of entangled photon pairs to two locations separated by 1203 kilometers on Earth, through two satellite-to-ground downlinks with a summed length varying from 1600 to 2400 kilometers. We observed a survival of two-photon entanglement and a violation of Bell inequality by 2.37 ± 0.09 under strict Einstein locality conditions. The obtained effective link efficiency is orders of magnitude higher than that of the direct bidirectional transmission of the two photons through telecommunication fibers.

The early afterglow of a gamma-ray burst (GRB) can provide critical information on the jet and progenitor of the GRB. The extreme brightness of GRB 221009A allows us to probe its early afterglow in unprecedented detail. In this Letter, we report comprehensive observation results of the early afterglow of GRB 221009A (from T 0+660 s to T 0+1860 s, where T 0 is the Insight-HXMT/HE trigger time) in X-ray/gamma-ray energy band (from 20 keV to 20 MeV) by Insight-HXMT High Energy X-ray Telescope, GECAM-C, and Fermi/Gamma-ray Burst Monitor. We find that the spectrum of the early afterglow in 20 keV–20 MeV can be well described by a cutoff power law with an extra power law that dominates the low- and high-energy bands, respectively. The cutoff power law E peak is ∼30 keV, and the power-law photon index is ∼1.8 throughout the early afterglow phase. By fitting the light curves in different energy bands, we find that a significant achromatic break (from keV to TeV) is required at T 0 + 1246−26+27 s (i.e., 1021 s since the afterglow starting time T AG = T 0+225 s), providing compelling evidence of a jet break. Interestingly, both the pre-break and post-break decay slopes vary with energy, and these two slopes become closer in the lower energy band, making the break less identifiable. Intriguingly, the spectrum of the early afterglow experienced a slight hardening before the break and a softening after the break. These results provide new insights into the physics of this remarkable GRB.

Cleavage of transfer (t)RNA and ribosomal (r)RNA are critical and conserved steps of translational control for cells to overcome varied environmental stresses. However, enzymes that are responsible for this event have not been fully identified in high eukaryotes. Here, we report a mammalian tRNA/rRNA-targeting endoribonuclease: SLFN13, a member of the Schlafen family. Structural study reveals a unique pseudo-dimeric U-pillow-shaped architecture of the SLFN13 N′-domain that may clamp base-paired RNAs. SLFN13 is able to digest tRNAs and rRNAs in vitro, and the endonucleolytic cleavage dissevers 11 nucleotides from the 3′-terminus of tRNA at the acceptor stem. The cytoplasmically localised SLFN13 inhibits protein synthesis in 293T cells. Moreover, SLFN13 restricts HIV replication in a nucleolytic activity-dependent manner. According to these observations, we term SLFN13 RNase S13. Our study provides insights into the modulation of translational machinery in high eukaryotes, and sheds light on the functional mechanisms of the Schlafen family. Translation inhibition is a strategy for organisms to overcome various environmental stresses including viral infections. Here the authors show that a tRNA/rRNA-targeting RNase Schlafen13 inhibits protein synthesis by directly digesting cytoplasmic tRNA and rRNA with the ability to restrict viral propagation.

Burdock ( ) is a popular vegetable in China and Japan that is consumed for its general health benefits. The principal active component of burdock is arctigenin, which shows a range of bioactivities and . Here, we investigated the potential anti-tumor effects of arctigenin using two human hepatocellular carcinoma (HCC) cell lines, HepG2 and Hep3B, and sought to elucidate its potential mechanisms of action. Our results showed that arctigenin treatment inhibited cell growth in both HepG2 and Hep3B cell lines (IC of 4.74 nM for HepG2 cells, and of 59.27 nM for Hep3B cells). In addition, migration, invasion, and colony formation by HepG2 cells were significantly inhibited by arctigenin. By contrast, treatment of Hep3B cells with arctigenin did not alter these parameters. Arctigenin also significantly reduced the levels of gankyrin mRNA and protein in HepG2 cells, but not in Hep3B cells. A luciferase assay indicated that arctigenin targeted the -450 to -400 region of the gankyrin promoter. This region is also the potential binding site for both C/EBPα and PPARα, as predicted and confirmed by an online software analysis and ChIP assay. Additionally, a co-immunoprecipitation (Co-IP) assay showed that binding between C/EBPα and PPARα was increased in the presence of arctigenin. However, arctigenin did not increase the expression of C/EBPα or PPARα protein. A binding screening assay and liquid chromatography-mass spectrometry (LC-MS) were performed to identify the mechanisms by which arctigenin regulates gankyrin expression. The results suggested that arctigenin could directly increase C/EBPα binding to the gankyrin promoter (-432 to -422 region), but did not affect PPARα binding. Expression of gankyrin, , and were analyzed in tumor tissues of patients using real-time PCR. Both and showed negative correlations with gankyrin. In tumor-bearing mice, arctigenin had a significant inhibitory effect on HCC growth. In conclusion, our results suggested that arctigenin could inhibit liver cancer growth by directly recruiting C/EBPα to the gankyrin promoter. PPARα subsequently bound to C/EBPα, and both had a negative regulatory effect on gankyrin expression. This study has identified a new mechanism of action of arctigenin against liver cancer growth.

Head and neck squamous cell carcinoma (HNSCC) causes much health and economic burden, and the therapeutic results must be improved. Glucose metabolism is an essential component of tumor metabolism and is instrumental in its development. Glucose transporter types (GLUTs) can uptake glucose from the extracellular matrix (ECM), regulating cellular metabolism in several cancers. However, the function of different GLUT proteins in HNSCC remains unclear. To clarify the role of GLUTs in HNSCC, several open-access online databases (Oncomine, GEPIA, Kaplan–Meier, cBioPortal, GeneMANIA, and TIMER) were used to evaluate the differential expression, clinical significance, genetic alteration, and relative immune cell infiltration. The expression of GLUTs was detected in clinical patient samples by immunohistochemistry. The mRNA level of SLC2A1/3 significantly increased in HNSCC, while SLC2A4 reduced. SLC2A3 was related to the advanced clinical stage and short overall survival (OS) in HNSCC. Also, higher SLC2A1/2 mRNA expression was related to shorter OS in HNSCC patients. The expression of GLUTs was related to diverse immune cells, including B cells, CD4 + T cells, CD8 + T cells, dendritic cells (DCs), macrophages, and Treg cells in HNSCC. Moreover, the high expression of GLUTs was demonstrated by immunohistochemistry in patient tissues. GLUTs might have a potential role in HNSCC's progression and development. Therefore, the current findings might offer a novel perception for selecting GLUT family prognostic markers and treatment for HNSCC patients.