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Liver transplantation is the ultimate method for treating end-stage liver disease. With the increasing prevalence of obesity, the number of patients with non-alcoholic fatty liver, a common cause of chronic liver disease, is on the rise and may become the main cause of liver transplantation in the future. With the increasing gap between the number of donor livers and patients waiting for liver transplantation and the increasing prevalence of non-alcoholic fatty liver, the proportion of steatosis livers among non-standard donor organs is also increasing. Ischemia-reperfusion injury has historically been the focus of attention in the liver transplantation process, and severe ischemia-reperfusion injury leads to adverse outcomes of liver transplantation. Studies have shown that the production of reactive oxygen species and subsequent oxidative stress play a key role in the pathogenesis of hepatic ischemia and reperfusion injury and non-alcoholic fatty liver. Furthermore, the sensitivity of fatty liver transplantation to ischemia-reperfusion injury has been suggested to be related to the production of reactive oxygen species (ROS) and oxidative stress. In ischemia-reperfusion injury, Kupffer cell and macrophage activation along with mitochondrial damage and the xanthine/xanthine oxidase system promote marked reactive oxygen species production and the inflammatory response and apoptosis, resulting in liver tissue injury. The increased levels of ROS and lipid peroxidation products, vicious circle of ROS and oxidative stress along with mitochondrial dysfunction promoted the progress of non-alcoholic fatty liver. In contrast to the non-fatty liver, a non-alcoholic fatty liver produces more reactive oxygen species and suffers more serious oxidative stress when subjected to ischemia-reperfusion injury. We herein review the effects of reactive oxygen species on ischemia-reperfusion injury and non-alcoholic fatty liver injury as well as highlight several treatment approaches.

Sorafenib is the first-line treatment of advanced hepatocellular carcinoma (HCC). However, there is a lack of validated biomarkers to predict sorafenib sensitivity. In this study we investigated the role of ACSL4, a positive-activating enzyme of ferroptosis, in sorafenib-induced cell death and HCC patient outcome. We showed that ACSL4 protein expression was negatively associated with IC 50 values of sorafenib in a panel of HCC cell lines ( R  = −0.952, P  < 0.001). Knockdown of ACSL4 expression by specific siRNA/sgRNA significantly attenuated sorafenib-induced lipid peroxidation and ferroptosis in Huh7 cells, and also rescued sorafenib-induced inhibition of xenograft tumor growth in vivo. We selected 29 HCC patients with surgery as primary treatment and sorafenib as postoperative adjunct therapy from a hospital-based cohort. A high proportion (66.7%) of HCC patients who had complete or partial responses to sorafenib treatment (according to the revised RECIST guideline) had higher ACSL4 expression in the pretreated HCC tissues, compared with those who had stable or progressed tumor growth (23.5%, P  = 0.029). Since ACSL4 expression was independent of sorafenib treatment, it could serve as a useful predictive biomarker. Taken together, this study demonstrates that ACSL4 is essential for sorafenib-induced ferroptosis and useful for predicting sorafenib sensitivity in HCC. This study may have important translational impacts in precise treatment of HCC.

Recently, carbon dioxide capture and conversion, along with hydrogen from renewable resources, provide an alternative approach to synthesis of useful fuels and chemicals. People are increasingly interested in developing innovative carbon dioxide hydrogenation catalysts, and the pace of progress in this area is accelerating. Accordingly, this perspective presents current state of the art and outlook in synthesis of light olefins, dimethyl ether, liquid fuels, and alcohols through two leading hydrogenation mechanisms: methanol reaction and Fischer-Tropsch based carbon dioxide hydrogenation. The future research directions for developing new heterogeneous catalysts with transformational technologies, including 3D printing and artificial intelligence, are provided. Carbon dioxide (CO 2 ) capture and conversion provide an alternative approach to synthesis of useful fuels and chemicals. Here, Ye et al. give a comprehensive perspective on the current state of the art and outlook of CO 2 catalytic hydrogenation to the synthesis of light olefins, dimethyl ether, liquid fuels, and alcohols.

Accumulating evidence suggests that circular RNAs have the abilities to regulate gene expression during the progression of sepsis‐associated acute kidney injury. Circular RNA VMA21 (circVMA21), a recent identified circular RNA, could reduce apoptosis to alleviate intervertebral disc degeneration in rats and protect WI‐38 cells from lipopolysaccharide‐induced injury. However, the role of circVMA21 in sepsis‐associated acute kidney injury (sepsis‐associated AKI) is unknown. In this study, we first demonstrated that circVMA21 alleviated sepsis‐associated AKI by reducing apoptosis and inflammation in rats and HK‐2 cells. Additionally, to explore the molecule mechanism underlying the amelioration, after the bioinformatics analysis, we confirmed that miR‐9‐3p directly bound to circVMA21 by luciferase and RNA immunoprecipitation assay, and the effector protein of miR‐9‐3p was SMG1. Furthermore, the oxidative stress caused by sepsis‐associated AKI was down‐regulated by circVMA21. In conclusion, circVMA21 plays an important role in the regulating sepsis‐associated AKI via adjusting miR‐9‐39/SMG1/inflammation axis and oxidative stress.

Hashimoto’s thyroiditis (HT) is the most common autoimmune disease characterized by lymphocytic infiltration and thyrocyte destruction. Dissection of the interaction between the thyroidal stromal microenvironment and the infiltrating immune cells might lead to a better understanding of HT pathogenesis. Here we show, using single-cell RNA-sequencing, that three thyroidal stromal cell subsets, ACKR1 + endothelial cells and CCL21 + myofibroblasts and CCL21 + fibroblasts, contribute to the thyroidal tissue microenvironment in HT. These cell types occupy distinct histological locations within the thyroid gland. Our experiments suggest that they might facilitate lymphocyte trafficking from the blood to thyroid tissues, and T cell zone CCL21 + fibroblasts may also promote the formation of tertiary lymphoid organs characteristic to HT. Our study also demonstrates the presence of inflammatory macrophages and dendritic cells expressing high levels of IL-1β in the thyroid, which may contribute to thyrocyte destruction in HT patients. Our findings thus provide a deeper insight into the cellular interactions that might prompt the pathogenesis of HT. Hashimoto’s Thyroiditis is an autoimmune disease with a complex pathomechanism. Authors here show by single cell RNA sequencing that the thyroidal microenvironment in the disease is characterised by three stromal cell subtypes that are potentially responsible for the recruitment of infiltrating inflammatory immune cells, such as macrophages and dendritic cells.

We investigated the electron-pairing mechanism in an iron-based superconductor, iron selenide (FeSe), using scanning tunneling microscopy and spectroscopy. Tunneling conductance spectra of stoichiometric FeSe crystalline films in their superconducting state revealed evidence for a gap function with nodal lines. Electron pairing with twofold symmetry was demonstrated by direct imaging of quasiparticle excitations in the vicinity of magnetic vortex cores, Fe adatoms, and Se vacancies. The twofold pairing symmetry was further supported by the observation of striped electronic nanostructures in the slightly Se-doped samples. The anisotropy can be explained in terms of the orbital-dependent reconstruction of electronic structure in FeSe.

Intravenous immunoglobulin (IVIG) treatment is commonly used to treat Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) with controversial therapeutic effect. We conducted a comprehensive meta-analysis through combining the published eligible studies to evaluate the effectiveness of IVIG on SJS and TEN treatment. A total of 26 studies were selected from public available databases. The combination of IVIG and corticosteroid markedly reduced the recovery time (by 1.63 days, 95% CI: 0.83-2.43, P < 0.001), compared with solo corticosteroid group. The favorable effects were greater in Asian (2.19, 95% CI: 1.41-2.97, P < 0.001), TEN (2.56, 95% CI: 0.35-4.77, P = 0.023) and high-dose IVIG treated individuals (1.78, 95% CI: 0.42-3.14, P = 0.010). The hospitalization length reduced by 3.19 days (95% CI: 0.08-6.30, P = 0.045), though the outcome was proven to be unstable. We found heterogeneities, which sources were probably regional factors. Besides, IVIG was inclined to decrease SJS/TEN mortality (SMR: 0.84, 95% CI: 0.66-1.08, P = 0.178). This impact was possibly more profound when patients were treated with high dose IVIG (SMR: 0.74, 95% CI: 0.50-1.08, P = 0.116), or when patients were diagnosed as TEN (SMR: 0.68, 95% CI: 0.45-1.01, P = 0.058). Our current meta-analysis suggests that IVIG combined with corticosteroid could reduce recovery time for SJS and TEN. This effect is greater among Asian patients. Whereas, its impact on reducing mortality is not significant.

Circular RNAs (circRNAs) are a group of non‐coding RNAs implicated in the pathogenesis of cancer progression, which exert their functions via regulation of microRNAs (miRNAs) and genes. The present study uses gain‐ and loss‐of‐function approaches to evaluate the functions of hsa_circRNA_002178 in angiogenesis along with energy metabolism and underlying downstream signals. The expression pattern of hsa_circRNA_002178 in clinical breast cancer tissues and its association with prognosis were characterized at first. Next, the energy metabolism and angiogenesis as well as cell viability were evaluated when the expression of hsa_circRNA_002178 in breast cancer cells was knocked down by siRNA. The interaction between hsa_circRNA_002178 and its downstream miR‐328‐3p was identified, followed by the analysis of their functions in regulation of breast cancer cellular behaviours. The target gene of miR‐328‐3p was predicted and verified, followed by identifying its role in the breast cancer progression. Higher expression of hsa_circRNA_002178 shared an association with worse prognosis in breast cancer. The inhibition of hsa_circRNA_002178 resulted in reductions in cell viability, energy metabolism and tube formation ability. Hsa_circRNA_002178 could competitively bind to miR‐328‐3p and down‐regulated its expression. Restoration of miR‐328‐3p eliminated the tumour‐promoting effects of hsa_circRNA_002178. COL1A1, as a target of miR‐328‐3p, could be up‐regulated by overexpression of hsa_circRNA_002178. In vivo experiments further confirmed the inhibition of tumour growth and inflammation by silencing hsa_circRNA_002178 or up‐regulating miR‐328‐3p. Taken together, hsa_circRNA_002178 is highlighted as a promising target for breast cancer due to the anti‐tumour effects achieved by silencing hsa_circRNA_002178.

In the field of welding robotics, visual sensors, which are mainly composed of a camera and a laser, have proven to be promising devices because of their high precision, good stability, and high safety factor. In real welding environments, there are various kinds of weld joints due to the diversity of the workpieces. The location algorithms for different weld joint types are different, and the welding parameters applied in welding are also different. It is very inefficient to manually change the image processing algorithm and welding parameters according to the weld joint type before each welding task. Therefore, it will greatly improve the efficiency and automation of the welding system if a visual sensor can automatically identify the weld joint before welding. However, there are few studies regarding these problems and the accuracy and applicability of existing methods are not strong. Therefore, a weld joint identification method for visual sensor based on image features and support vector machine (SVM) is proposed in this paper. The deformation of laser around a weld joint is taken as recognition information. Two kinds of features are extracted as feature vectors to enrich the identification information. Subsequently, based on the extracted feature vectors, the optimal SVM model for weld joint type identification is established. A comparative study of proposed and conventional strategies for weld joint identification is carried out via a contrast experiment and a robustness testing experiment. The experimental results show that the identification accuracy rate achieves 98.4%. The validity and robustness of the proposed method are verified.

Human tubulin beta class IVa (TUBB4A) is a member of the β-tubulin family. In most normal tissues, expression of TUBB4A is little to none, but it is highly expressed in human prostate cancer. Here we show that high expression levels of TUBB4A are associated with aggressive prostate cancers and poor patient survival, especially for African-American men. Additionally, in prostate cancer cells, TUBB4A knockout (KO) reduces cell growth and migration but induces DNA damage through increased γH2AX and 53BP1. Furthermore, during constricted cell migration, TUBB4A interacts with MYH9 to protect the nucleus, but either TUBB4A KO or MYH9 knockdown leads to severe DNA damage and reduces the NF-κB signaling response. Also, TUBB4A KO retards tumor growth and metastasis. Functional analysis reveals that TUBB4A/GSK3β binds to the N-terminal of MYH9, and that TUBB4A KO reduces MYH9-mediated GSK3β ubiquitination and degradation, leading to decreased activation of β-catenin signaling and its relevant epithelial-mesenchymal transition. Likewise, prostate-specific deletion of Tubb4a reduces spontaneous tumor growth and metastasis via inhibition of NF-κB, cyclin D1, and c-MYC signaling activation. Our results suggest an oncogenic role of TUBB4A and provide a potentially actionable therapeutic target for prostate cancers with TUBB4A overexpression. The β-tubulin family protein TUBB4A is highly expressed in cancer but it’s molecular role is unclear. Here, the authors show that TUBB4A is required to protect the nucleus from genomic instability during migration and that it’s over expression promotes cancer progression.