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5,890 result(s) for "CHANG, QING"
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In-memory mechanical computing
Mechanical computing requires matter to adapt behavior according to retained knowledge, often through integrated sensing, actuation, and control of deformation. However, inefficient access to mechanical memory and signal propagation limit mechanical computing modules. To overcome this, we developed an in-memory mechanical computing architecture where computing occurs within the interaction network of mechanical memory units. Interactions embedded within data read-write interfaces provided function-complete and neuromorphic computing while reducing data traffic and simplifying data exchange. A reprogrammable mechanical binary neural network and a mechanical self-learning perceptron were demonstrated experimentally in 3D printed mechanical computers, as were all 16 logic gates and truth-table entries that are possible with two inputs and one output. The in-memory mechanical computing architecture enables the design and fabrication of intelligent mechanical systems. Here, Mei and Chen propose an in-memory mechanical computing architecture with simplified and reduced data exchange, where computing occurs within mechanical memory units, to facilitate the design of intelligent mechanical systems.
Advances in CRISPR/Cas-based Gene Therapy in Human Genetic Diseases
CRISPR/Cas genome editing is a simple, cost effective, and highly specific technique for introducing genetic variations. In mammalian cells, CRISPR/Cas can facilitate non-homologous end joining, homology- directed repair, and single-base exchanges. Cas9/Cas12a nuclease, dCas9 transcriptional regulators, base editors, PRIME editors and RNA editing tools are widely used in basic research. Currently, a variety of CRISPR/Cas-based therapeutics are being investigated in clinical trials. Among many new findings that have advanced the field, we highlight a few recent advances that are relevant to CRISPR/Cas-based gene therapies for monogenic human genetic diseases.
LncRNA PVT1 promotes proliferation and invasion through enhancing Smad3 expression by sponging miR-140-5p in cervical cancer
Background Cervical cancer is one of the most frequent malignancies among females worldwide. Increasing evidence have indicated the participation of long noncoding RNAs (lncRNAs) in the progression and metastasis of cervical cancer. Our present study was conducted to explore the effects of lncRNA plasmacytoma variant translocation 1 (PVT1) on the progression of cervical cancer and the underlying mechanisms. Materials and methods Expressions of PVT1, miR-140-5p and Smad3 in cervical cancer cell lines were detected by qRT-PCR and western blotting. Bioinformatics analysis and luciferase assays were used to elucidate the potential correlations between PVT1, miR-140-5p and Smad3. The roles of PVT1 on the progression of cervical cancer cells were determined by transfecting sh-RNA through series function assays such as colony formation assay, wound healing assay, transwell assay. Results PVT1 and Smad3 were upregulated, and miR-140-5p was downregulated in cervical cancer cells. PVT1 could bind directly with miR-140-5p, and Smad3 was a downstream target of miR-140-5p. Inhibition of PVT1 could enhance expression of miR-140-5p, inhibit the expression of Smad3, significantly inhibited the proliferation, migration, invasion in cervical cancer cells. While transfection of miR-140-5p inhibitor could partially reverse the above changes in cervical cancer cells. Conclusions The results revealed that PVT1 could promote the proliferation and metastasis via increasing the Smad3 expression by sponging miR-140-5p, which might be a promising prognostic and therapeutic target for cervical cancer.
Power Electronics-Enabled Autonomous Power Systems
Power systems worldwide are going through a paradigm shift from centralized generation to distributed generation. This book presents the SYNDEM (i.e., synchronized and democratized) grid architecture and its technical routes to harmonize the integration of renewable energy sources, electric vehicles, storage systems, and flexible loads, with the synchronization mechanism of synchronous machines, to enable autonomous operation of power systems, and to promote energy freedom. This is a game changer for the grid. It is the sort of breakthrough — like the touch screen in smart phones — that helps to push an industry from one era to the next, as reported by Keith Schneider, a New York Times correspondent since 1982. This book contains an introductory chapter and additional 24 chapters in five parts: Theoretical Framework, First-Generation VSM (virtual synchronous machines), Second-Generation VSM, Third-Generation VSM, and Case Studies. Most of the chapters include experimental results. As the first book of its kind for power electronics-enabled autonomous power systems, it • introduces a holistic architecture applicable to both large and small power systems, including aircraft power systems, ship power systems, microgrids, and supergrids • provides latest research to address the unprecedented challenges faced by power systems and to enhance grid stability, reliability, security, resiliency, and sustainability • demonstrates how future power systems achieve harmonious interaction, prevent local faults from cascading into wide-area blackouts, and operate autonomously with minimized cyber-attacks • highlights the significance of the SYNDEM concept for power systems and beyond Power Electronics-Enabled Autonomous Power Systems is an excellent book for researchers, engineers, and students involved in energy and power systems, electrical and control engineering, and power electronics. The SYNDEM theoretical framework chapter is also suitable for policy makers, legislators, entrepreneurs, commissioners of utility commissions, energy and environmental agency staff, utility personnel, investors, consultants, and attorneys.
Inhibition of the Notch1 Pathway Promotes the Effects of Nucleus Pulposus Cell-Derived Exosomes on the Differentiation of Mesenchymal Stem Cells into Nucleus Pulposus-Like Cells in Rats
Stem cell therapies for intervertebral disc degeneration have been demonstrated as a promising strategy. Previous studies have shown that human nucleus pulposus cell- (NPC-) derived exosomes can induce the differentiation of mesenchymal stem cells (MSCs) into NP-like cells in vitro. However, the mechanism of MSC differentiation into NP-like cells with the induction of NPC exosomes is still unclear. Here, we verified the induction effects of NPC exosomes on the differentiation of MSCs into NP-like cells. In addition, the Notch1 pathway was downregulated in this process. Then, DAPT and soluble Jagged1 (SJAG) were applied to inhibit or enhance the expression of the Notch1 pathway, respectively, resulting in the upregulation or downregulation of collagen II, aggrecan, and Sox9 in MSCs. Knocking down of Notch1 protein facilitated the effects of NPC exosomes on the differentiation of MSCs into NP-like cells. NPC exosomes were more effective than an indirect coculture system in terms of the differentiation of MSCs into NP-like cells. Inhibition of NPC exosome secretion with Rab27a siRNA prevented the induction effects of an indirect coculture system on the differentiation of MSCs into NP-like cells. Transwell migration assays revealed that NPC exosomes could promote the migration of MSCs. Taken together, the Notch1 pathway was negatively associated with the differentiation of MSCs into NP-like cells with the treatments of NPC exosomes. Inhibition of the Notch1 pathway facilitates NPC exosome-induced differentiation of MSCs into NP-like cells in vitro. NPC exosomes play a key role in the differentiation of MSCs into NP-like cells in an indirect coculture system of NPCs and MSCs.
Chitosan Wound Dressings Incorporating Exosomes Derived from MicroRNA‐126‐Overexpressing Synovium Mesenchymal Stem Cells Provide Sustained Release of Exosomes and Heal Full‐Thickness Skin Defects in a Diabetic Rat Model
There is a need to find better strategies to promote wound healing, especially of chronic wounds, which remain a challenge. We found that synovium mesenchymal stem cells (SMSCs) have the ability to strongly promote cell proliferation of fibroblasts; however, they are ineffective at promoting angiogenesis. Using gene overexpression technology, we overexpressed microRNA‐126‐3p (miR‐126‐3p) and transferred the angiogenic ability of endothelial progenitor cells to SMSCs, promoting angiogenesis. We tested a therapeutic strategy involving controlled‐release exosomes derived from miR‐126‐3p‐overexpressing SMSCs combined with chitosan. Our in vitro results showed that exosomes derived from miR‐126‐3p‐overexpressing SMSCs (SMSC‐126‐Exos) stimulated the proliferation of human dermal fibroblasts and human dermal microvascular endothelial cells (HMEC‐1) in a dose‐dependent manner. Furthermore, SMSC‐126‐Exos also promoted migration and tube formation of HMEC‐1. Testing this system in a diabetic rat model, we found that this approach resulted in accelerated re‐epithelialization, activated angiogenesis, and promotion of collagen maturity in vivo. These data provide the first evidence of the potential of SMSC‐126‐Exos in treating cutaneous wounds and indicate that modifying the cells—for example, by gene overexpression—and using the exosomes derived from these modified cells provides a potential drug delivery system and could have infinite possibilities for future therapy. Stem Cells Translational Medicine 2017;6:736–747
Glacier mass-balance estimates over High Mountain Asia from 2000 to 2021 based on ICESat-2 and NASADEM
High Mountain Asia (HMA) glaciers are critical water reserves for montane regions, which are readily influenced by climate change. The glacier mass balance during 2000–2021 over HMA was estimated by comparing the elevations from ICESat-2 and the NASADEM. Radar penetration depth could be one of the intrinsic error sources in estimating glacier mass balance by using NASADEM. Therefore, we doubled elevation differences between the X-band Shuttle Radar Topography Missions (SRTMs) and NASADEM to estimate the potential error. The spatial characteristics of the altitude-dependent penetration depth can be detected in most sub-regions of HMA. Relatively deep penetrations in the Himalaya (2.3–3.7 m) and Hissar Alay (4.3 m) regions and small penetrations in the south-eastern HMA (1.0 m) were observed. The HMA region experienced a significant mass loss at a rate of −0.18 ± 0.12 m w.e. a−1, in which the Hengduan Shan exhibited the highest mass loss of −0.62 ± 0.10 m w.e. a−1, the West Kun Lun experienced a substantial mass gain of 0.23 ± 0.13 m w.e. a−1, and the Karakoram showed a more or less balance. Our results are in agreement with previous studies that assessed the mass balance of HMA glaciers from different methods.
Crosstalk between gut microbiota and host immune system and its response to traumatic injury
Millions of microorganisms make up the complex microbial ecosystem found in the human gut. The immune system’s interaction with the gut microbiota is essential for preventing inflammation and maintaining intestinal homeostasis. Numerous metabolic products that can cross-talk between immune cells and the gut epithelium are metabolized by the gut microbiota. Traumatic injury elicits a great and multifaceted immune response in the minutes after the initial offense, containing simultaneous pro- and anti-inflammatory responses. The development of innovative therapies that improve patient outcomes depends on the gut microbiota and immunological responses to trauma. The altered makeup of gut microbes, or gut dysbiosis, can also dysregulate immunological responses, resulting in inflammation. Major human diseases may become more common as a result of chronic dysbiosis and the translocation of bacteria and the products of their metabolism beyond the mucosal barrier. In this review, we briefly summarize the interactions between the gut microbiota and the immune system and human disease and their therapeutic probiotic formulations. We also discuss the immune response to traumatic injury.