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Cellular structures consist of foams, honeycombs, and lattices. Lattices have many outstanding properties over foams and honeycombs, such as lightweight, high strength, absorbing energy, and reducing vibration, which has been extensively studied and concerned. Because of excellent properties, lattice structures have been widely used in aviation, bio-engineering, automation, and other industrial fields. In particular, the application of additive manufacturing (AM) technology used for fabricating lattice structures has pushed the development of designing lattice structures to a new stage and made a breakthrough progress. By searching a large number of research literature, the primary work of this paper reviews the lattice structures. First, based on the introductions about lattices of literature, the definition and classification of lattice structures are concluded. Lattice structures are divided into two general categories in this paper: uniform and non-uniform. Second, the performance and application of lattice structures are introduced in detail. In addition, the fabricating methods of lattice structures, i.e., traditional processing and additive manufacturing, are evaluated. Third, for uniform lattice structures, the main concern during design is to develop highly functional unit cells, which in this paper is summarized as three different methods, i.e., geometric unit cell based, mathematical algorithm generated, and topology optimization. Forth, non-uniform lattice structures are reviewed from two aspects of gradient and topology optimization. These methods include Voronoi-tessellation, size gradient method (SGM), size matching and scaling (SMS), and homogenization, optimization, and construction (HOC). Finally, the future development of lattice structures is prospected from different aspects.

Diabetic nephropathy (DN) is characterized by sterile inflammation with continuous injury and loss of renal inherent parenchyma cells. Podocyte is an essential early injury target in DN. The injury and loss of podocytes are closely associated with proteinuria, the early symptom of renal injury in DN. However, the exact mechanism for podocyte injury and death in DN remains ambiguous. In this study we investigated whether pyroptosis, a newly discovered cell death pathway was involved in DN. Diabetic mice were generated by high-fat diet/STZ injections. We showed that the expression levels of caspase-11 and cleavage of gasdermin D (GSDMD-N) in podocytes were significantly elevated, accompanied by reduced expression of podocyte makers nephrin and podocin, loss and fusion in podocyte foot processes, increased inflammatory cytokines NF-κB, IL-1β, and IL-18, macrophage infiltration, glomerular matrix expansion and increased urinary albumin to creatinine ratio (UACR). All these changes in diabetic mice were blunted by knockout of caspase-11 or GSDMD. Cultured human and mouse podocytes were treated with high glucose (30 mM), which significantly increased the expression levels of caspase-11 or caspase-4 (the homolog of caspase-11 in human), GSDMD-N, NF-κB, IL-1β, and IL-18, and decreased the expression of nephrin and podocin. Either caspase-4 or GSDMD knockdown by siRNA significantly blunted these changes. In summary, our results demonstrate that caspase-11/4 and GSDMD-mediated pyroptosis is activated and involved in podocyte loss under hyperglycemia condition and the development of DN.

Percutaneous Coronary Intervention (PCI) is currently the most conventional and effective method for clinically treating cardiovascular diseases such as atherosclerosis. Stent implantation, as one of the ways of PCI in the treatment of coronary artery diseases, has become a hot spot in scientific research with more and more patients suffering from cardiovascular diseases. However, vascular stent implanted into vessels of patients often causes complications such as In-Stent Restenosis (ISR). The vascular stent is one of the sophisticated medical devices, a reasonable structure of stent can effectively reduce the complications. In this paper, we introduce the evolution, performance evaluation standards, delivery and deployment, and manufacturing methods of vascular stents. Based on a large number of literature pieces, this paper focuses on designing structures of vascular stents in terms of “bridge (or link)” type, representative volume unit (RVE)/representative unit cell (RUC), and patient-specific stent. Finally, this paper gives an outlook on the future development of designing vascular stents.

PurposeAmblyopia is a leading cause of vision impairment among children and young adults. Individual studies showed significant variations in the prevalence of amblyopia in different regions and age groups. This study is to estimate the global prevalence of amblyopia by pooling its prevalence from the previous studies and to project the number of people affected through 2040.MethodsWe performed a systematic review and meta-analysis on the prevalence of amblyopia using data published before 20 October 2018. We estimated the prevalence rate of amblyopia and its 95% CI globally and by subgroups (eg, region and age). The prevalence data were applied to United Nations World Population Prospects to derive the projected number with amblyopia through 2040.ResultsA meta-analysis of 60 studies (1 859 327 subjects) showed that the pooled prevalence rate of amblyopia was 1.44% (95% CI 1.17% to 1.78%). Prevalences in Europe (2.90%) and North America (2.41%) were higher than in Asia (1.09%) and Africa (0.72%). The highest prevalence was found in subjects over 20 years old (3.29%). There was no difference in the prevalence between genders. We estimated 99.2 (95% CI 71.7 to 146.1) million people with amblyopia in 2019 worldwide, increasing to 175.2 (95% CI 81.3 to 307.8) million by 2030 and 221.9 (95% CI 83.7 to 429.2) million by 2040.ConclusionsThe amblyopia is becoming a significant vision problem worldwide. It is of great importance to design and implement amblyopia screening, treatment and related public health strategies.

Acute renal injury (AKI) causes a long-term risk for progressing into chronic kidney disease (CKD) and interstitial fibrosis. Yes-associated protein (YAP), a key transcriptional cofactor in Hippo signaling pathway, shuttles between the cytoplasm and nucleus, which is required for the renal tubular epithelial cells repair in the acute phase of AKI. In this study we investigated the role of YAP during ischemia-reperfusion (IR)-induced AKI to CKD. Mice were subjected to left kidney IR followed by removal of the right kidney on the day before tissue harvests. Mouse shRNA expression adenovirus (Ad-shYAP or Ad-shKLF4) and mouse KLF4 expression adenovirus (Ad-KLF4) were delivered to mice by intrarenal injection on D7 after IR. We showed that the expression and nucleus distribution of YAP were persistently increased until the end of experiment (D21 after IR). The sustained activation of YAP in post-acute phase of AKI was accompanied by renal dysfunction and interstitial fibrosis. Knockdown of YAP significantly attenuated IR-induced renal dysfunction and decreased the expression of fibrogenic factors TGF-β and CTGF in the kidney. We showed that the expression of the transcription factor KLF4, lined on the upstream of YAP, was also persistently increased. Knockdown on KLF4 attenuated YAP increase and nuclear translocation as well as renal functional deterioration and interstitial fibrosis in IR mice, whereas KLF4 overexpression caused opposite effects. KLF4 increased the expression of ITCH, and ITCH facilitated YAP nuclear translocation via degrading LATS1. Furthermore, we demonstrated in primary cultured renal tubular cells that KLF4 bound to the promoter region of YAP and positively regulates YAP expression. In biopsy sample from CKD patients, we also observed increased expression and nuclear distribution of YAP. In conclusion, the activation of YAP in the post-acute phase of AKI is implicated in renal functional deterioration and fibrosis although it exhibits beneficial effect in acute phase. Reprogramming factor KLF4 is responsible for the persistent activation of YAP. Blocking the activation of KLF4-YAP pathway might be a way to prevent the transition of AKI into CKD. About 28.5% of the acute kidney injury (AKI) patients cannot recover completely. AKI has become an important risk factor for chronic kidney disease (CKD). It has been reported that the activation of YAP facilitates the recovery of AKI, however, this experiment demonstrated that the activation of YAP may last to the post-acute phase of AKI. The persistent activation of YAP is implicated with renal deterioration and fibrosis. Reprogramming factor KLF4 was responsible for the persistent activation of YAP. Shutting down the KLF4-related persistent activation of YAP after acute phase of AKI might be a way to prevent the transition of AKI into CKD.

Rh(I)-catalyzed cycloisomerizations of bicyclo[1.1.0]butanes provide a fruitful approach to cyclopropane-fused heterocycles. Products and stereochemical outcome are highly dependent on catalyst. The triphenylphosphine (PPh 3 ) ligand provides pyrrolidines, placing substituents anti to the cyclopropyl group. The 1,2-bis(diphenylphosphino)ethane (dppe) ligand yields azepanes with substituents syn to the cyclopropyl group. In this work, quantum mechanical DFT calculations pinpoint a reversal of regio- and diastereoselectivity, suggesting a concerted (double) C−C bond cleavage and rhodium carbenoid formation, driven by strain-release. The ligand-influenced cleavage step determines the regioselectivity of carbometalation and product formation, and suggests new applications of bicyclobutanes. Ligands alter the regioselectivity of Rh(I)- catalyzed cycloisomerizations of bicyclobutanes. Here, mechanistic studies performed by the authors pinpoint a concerted C−C bond cleavage and carbenoid formation responsible for the divergence.

Backgrounds Many literature reviews summarized relationships between screen time and child health, but they only included a few studies conducted in Chinese children and adolescents. The potential influence of screen time may vary by social context. The current systematic review and meta-analysis aimed to evaluate relationships between screen time and health issues among Chinese school-aged children and adolescents. Methods Peer-reviewed articles written in Chinese and English were retrieved from CNKI, Wanfang, PubMed, Embase, and Web of Science from inception to June 2020. The Downs & Black checklist was applied to assess study quality. Meta analyses used random effect models and mixed effects model to calculate pooled adjusted odds ratios and 95% confidence intervals. Heterogeneity, sensitivity, and publication bias were assessed using Q and I 2 statistics, “one-study removed” analysis, the funnel plot, trim and fill analysis, and classical fail-safe N, respectively. Results In total, we identified 252 articles reporting 268 studies with unique samples. These studies investigated relationships between screen time and health issues of adiposity, myopia, psycho-behavioral problems, poor academic performance, cardiometabolic disease risks, sleep disorder, poor physical fitness, musculoskeletal injury, sub-health, and miscellaneous issues of height and pubertal growth, injury, sick leave, and respiratory symptoms. Proportions of studies reporting positive relationships with screen time were lowest in adiposity (50.6%) and higher in myopia (59.2%) and psycho-behavioral problems (81.8%). Other health issues were examined in 10 or less studies, all of which had more than half showing positive relationships. The pooled odds ratio from 19 studies comparing health risks with the screen time cutoff of 2 hours per day was 1.40 (95% CI: 1.31 to 1.50, I 2  = 85.9%). The pooled effect size was 1.29 (95% CI: 1.20 to 1.39) after trimming 7 studies for publication bias adjustments. Conclusions Findings exclusively generated from Chinese school-aged children and adolescents resonate those mainly from western countries. Evidence suggests that higher levels of screen time are related with greater risks of various health issues, although the relationships appear to be weak and intertwined with other confounding factors. Future studies need to investigate health-specific dose effects and mechanisms of screen time.

High-quality two-dimensional atomic layered p–n heterostructures are essential for high-performance integrated optoelectronics. The studies to date have been largely limited to exfoliated and restacked flakes, and the controlled growth of such heterostructures remains a significant challenge. Here we report the direct van der Waals epitaxial growth of large-scale WSe 2 /SnS 2 vertical bilayer p–n junctions on SiO 2 /Si substrates, with the lateral sizes reaching up to millimeter scale. Multi-electrode field-effect transistors have been integrated on a single heterostructure bilayer. Electrical transport measurements indicate that the field-effect transistors of the junction show an ultra-low off-state leakage current of 10 −14 A and a highest on–off ratio of up to 10 7 . Optoelectronic characterizations show prominent photoresponse, with a fast response time of 500 μs, faster than all the directly grown vertical 2D heterostructures. The direct growth of high-quality van der Waals junctions marks an important step toward high-performance integrated optoelectronic devices and systems. Growth of large area and defect-free two-dimensional semiconductor layers for high-performance p–n junction applications has been a great challenge. Yang et al. prepare millimeter-scaled WSe 2 /SnS 2 vertical heterojunctions by two-step van der Waals epitaxy, which show excellent optoelectronic properties.

Myasthenia gravis (MG) is an acquired neurological autoimmune disorder characterized by dysfunctional transmission at the neuromuscular junction, with its etiology associated with genetic and environmental factors. Anti-inflammatory regulatory T cells (Tregs) and pro-inflammatory T helper 17 (Th17) cells functionally antagonize each other, and the immune imbalance between them contributes to the pathogenesis of MG. Among the numerous factors influencing the balance of Th17/Treg cells, the gut microbiota have received attention from scholars. Gut microbial dysbiosis and altered microbial metabolites have been seen in patients with MG. Therefore, correcting Th17/Treg imbalances may be a novel therapeutic approach to MG by modifying the gut microbiota. In this review, we initially review the association between Treg/Th17 and the occurrence of MG and subsequently focus on recent findings on alterations of gut microbiota and microbial metabolites in patients with MG. We also explore the effects of gut microbiota on Th17/Treg balance in patients with MG, which may provide a new direction for the prevention and treatment of this disease.

Immune evasion contributes to cancer growth and progression. Cancer cells have the ability to activate different immune checkpoint pathways that harbor immunosuppressive functions. The programmed death protein 1 (PD-1) and programmed cell death ligands (PD-Ls) are considered to be the major immune checkpoint molecules. The interaction of PD-1 and PD-L1 negatively regulates adaptive immune response mainly by inhibiting the activity of effector T cells while enhancing the function of immunosuppressive regulatory T cells (Tregs), largely contributing to the maintenance of immune homeostasis that prevents dysregulated immunity and harmful immune responses. However, cancer cells exploit the PD-1/PD-L1 axis to cause immune escape in cancer development and progression. Blockade of PD-1/PD-L1 by neutralizing antibodies restores T cells activity and enhances anti-tumor immunity, achieving remarkable success in cancer therapy. Therefore, the regulatory mechanisms of PD-1/PD-L1 in cancers have attracted an increasing attention. This article aims to provide a comprehensive review of the roles of the PD-1/PD-L1 signaling in human autoimmune diseases and cancers. We summarize all aspects of regulatory mechanisms underlying the expression and activity of PD-1 and PD-L1 in cancers, including genetic, epigenetic, post-transcriptional and post-translational regulatory mechanisms. In addition, we further summarize the progress in clinical research on the antitumor effects of targeting PD-1/PD-L1 antibodies alone and in combination with other therapeutic approaches, providing new strategies for finding new tumor markers and developing combined therapeutic approaches.