GSPT1 Functions as a Tumor Promoter in Human Liver Cancer

Objective This study analyzed the role of G1 to S phase transition 1 protein(GSPT1)in promoting progression of liver cancer cells.Methods A bioinformatics database was used to analyze the expression levels of GSPT1 in liver cancer tissues and the prognosis of patients.Subsequently,Western blotting and quantitative PCR were used to verify the expression levels of GSPT1 between normal hepatocytes and hepatoma cells.We used a CRISPR/Cas9 system to construct knockouts of GSPT1 in HepG2 and HCCLM9 liver cancer cells.The effect of GSPT1 on liver cancer cell migration and invasion was analyzed using flow cytometry,migration,and tumor formation assays.Results The Cancer Genome Atlas Liver Hepatocellular Carcinoma dataset indicated that GSPT1 expression was upregulated in liver cancer cell lines,and patients with liver cancer had poor prognosis.Knockout of GSPT1 in cells significantly inhibited tumor proliferation,cell migration,and growth in vivo.Conclusion In this study,we found that GSPT1 promotes the migration and invasion of liver cancer cells.

MicroRNA-153对脑膜瘤细胞放疗敏感性的影响

目的探讨micro RNA-153对(mi R-153)对脑膜瘤细胞放疗敏感性的影响及其作用机制。方法采用实时荧光定量聚合酶链反应检测放疗前后脑膜瘤SF3061细胞系中mi R-153的表达变化,用脂质体转染技术将mi R-153 mimics及对照转染至SF3061细胞中,采用MTT法、流式细胞术及克隆形成实验检测放射处理后细胞的放疗敏感性变化。使用Target Scan预测及双荧光素酶报告基因实验验证mi R-153与视网膜母细胞瘤蛋白结合锌指1(RIZ1)的靶向作用,基因敲除RIZ1验证其对脑膜瘤细胞放疗敏感性的影响。结果脑膜瘤细胞经过放疗处理后mi R-153的表达水平降低;mi R-153 mimics提高放疗后细胞的增殖抑制率和凋亡率,降低细胞克隆形成率;Target Scan预测及双荧光素酶报告基因实验证实RIZ1是mi R-153的靶标;转染si-RIZ1增加脑膜瘤细胞的放疗敏感性。结论 mi R-153通过靶向干扰RIZ1的表达,增加脑膜瘤细胞的放疗敏感性。

含胰岛素心肌保护液的心肌保护作用

目的研究含胰岛素心肌保护液对心内直视手术的心肌保护效果。方法体外循环心脏手术患者68例,随机分为A、B两组,每组34例,A组采用含胰岛素心肌保护液进行灌注,B组采用含血心肌保护液灌注。观察两组患者自动复跳率、血管活性药物的使用情况、心肌酶的变化和心肌超微结果的变化。结果 A组患者自动复跳率较高,心脏手术过程中停跳液只需灌注1次。两组手术前后心肌酶的变化和心肌细胞超微结构无差异。结论含胰岛素心肌保护液配制简单,心脏手术过程中灌注次数较少,心肌保护效果较好,缩短了手术时间。

Overexpression of eRF3a Promotes Cell Proliferation and Migration in Liver Cancer

Objective:The eukaryotic release factor 3a(eRF3a),a member of the eukaryotic peptide chain release factor family,is overexpressed in several types of cancer.This study aims to investigate the biological role and mechanism of eRF3a in the progression of liver cancer.

An Investigation of Wideband Rectennas for Wireless Energy Harvesting

This paper is focused on a wireless energy harvesting system using a rectifying antenna (rectenna). The proposed device consists of a wideband cross-dipole antenna, a microwave low-pass filter and a doubling rectifying circuit using Shottcky diodes as rectifying elements. Previously, a few of wideband rectennas have been investigated at 1.7 to 2.5 GHz. The originality of this paper is on the new wideband rectenna design which can harvest the ambient radio frequency (RF) power at 1.7 to 2.5 GHz. In this system, a new wideband cross dipole is designed and used to achieve the required bandwidth and duel-polarization. In addition, the voltage doubling rectifying circuit is optimized to achieve the best performance at power density levels 2 which are typical in urban environments. The characteristics of the proposed rectenna over the desired frequency range are investigated, and the integrated rectenna is simulated, made and tested for low input power densities from 5 to 200 μW/cm2. The simulation and measurement results of the rectenna are compared and a good agreement is achieved. The results demonstrate that the maximum rectenna conversion efficiency is nearly 57% around 1.7 GHz and over 20% over the wideband of interest for the incident power density of 120 μW/cm2. It is noted that the impedance matching is one of the main factors affecting the rectenna energy conversion efficiency. This new wideband rectenna has great potential to harvest wireless energy in GSM/3G/4G and ISM 2.4 GHz bands.

3,6-dichlorobenzo[b]thiophene-2-carboxylic acid alleviates ulcerative colitis by suppressing mammalian target of rapamycin complex 1 activation and regulating intestinal microbiota

BACKGROUND 3,6-dichlorobenzo[b]thiophene-2-carboxylic acid(BT2)is a benzothiophene carboxylate derivative that can suppress the catabolism of branched-chain amino acid(BCAA)-associated mammalian target of rapamycin complex 1(mTORC1)activation.Previous studies have demonstrated the therapeutic effects of BT2 on arthritis,liver cancer,and kidney injury.However,the effects of BT2 on ulcerative colitis(UC)are unknown.AIM To investigate the anti-UC effects of BT2 and the underlying mechanism.METHODS Mouse UC models were created through the administration of 3.5%dextran sodium sulfate(DSS)for 7 d.The mice in the treated groups were administered salazosulfapyridine(300 mg/kg)or BT2(20 mg/kg)orally from day 1 to day 7.At the end of the study,all of the mice were sacrificed,and colon tissues were removed for hematoxylin and eosin staining,immunoblot analyses,and immunohistochemical assays.Cytokine levels were measured by flow cytometry.The contents of BCAAs including valine,leucine,and isoleucine,in mouse serum were detected by liquid chromatography-tandem mass spectrometry,and the abundance of intestinal flora was analyzed by 16S ribosomal DNA sequencing.RESULTS Our results revealed that BT2 significantly ameliorated the inflammatory symptoms and pathological damage induced by DSS in mice.BT2 also reduced the production of the proinflammatory cytokines interleukin 6(IL-6),IL-9,and IL-2 and increased the anti-inflammatory cytokine IL-10 level.In addition,BT2 notably improved BCAA catabolism and suppressed mTORC1 activation and cyclooxygenase-2 expression in the colon tissues of UC mice.Furthermore,highthroughput sequencing revealed that BT2 restored the gut microbial abundance and diversity in mice with colitis.Compared with the DSS group,BT2 treatment increased the ratio of Firmicutes to Bacteroidetes and decreased the abundance of Enterobacteriaceae and Escherichia-Shigella.CONCLUSION Our results indicated that BT2 significantly ameliorated DSS-induced UC and that the latent mechanism involved the suppression of BCAA-associated mTORC1 activation and modulation of the intestinal flora.

Ultrahigh lithiation dynamics of Li_(4)Ti_(5)O_(12)as an anode material with open diffusion channels induced by chemical presodiation

Spinel lithium titanate(Li_(4)Ti_(5)O_(12),LTO),with the merits of safety operation voltage,stable crystal structure,and minor lattice volume changes,becomes an optimal anode material for high-power Li-ion batteries.However,the inherent wide bandgap and low lithiation reactivity of Li_(4)Ti_(5)O_(12)bring about poor conductivity and lithiation dynamics,limiting its further applications.Herein,we design and prepare unique Li_(4)Ti_(5)O_(12)anode materials with extremely low dopant content of Na^(+)utilizing the amorphous precursors.The resultant Li_(4)Na_(0.008-)Ti_(5)O_(12.004)sample(denoted as NLTO-0.008)presents superior rate performances and cycle ability,with a reversible capacity of 149.4 mAh·g^(-1)at the current rate of10.0C.NLTO-0.008 retains the charge capacity of151.3 mAh·g^(-1)with a capacity loss of 0.5%after 1000cycles at the current rate of 1.0C(charge)/10.0C(discharge).The kinetic studies furtherly demonstrate that the lithiation reaction energy and diffusion energy barrier decrease by 28.8%and 30%,respectively.Crystal structure analysis indicates that Na^(+)occupies the 16d Li site and forms distorted LiO_(4)tetrahedron and TiO_(6)octahedron.This lattice distortion forms open diffusion channels,thus enhancing the Li^(+)diffusion dynamics and decreasing the lithiation reaction energy barrier for Li_(4)Ti_(5)O_(12).Therefore,the pre-sodiation strategy may arouse great interest in understanding and developing intercalation-type transitionmetal-based electrode materials in high-power lithium-ion batteries.

Generation of A Stable GFP-reporter Zika Virus System for High-throughput Screening of Zika Virus Inhibitors

Zika virus(ZIKV) is associated with severe birth defects and Guillain-Barre′ syndrome and no approved vaccines or specific therapies to combat ZIKV infection are currently available. To accelerate anti-ZIKV therapeutics research, we developed a stable ZIKV GFP-reporter virus system with considerably improved GFP visibility and stability. In this system a BHK-21 cell line expressing DC-SIGNR was established to facilitate the proliferation of GFP-reporter ZIKV. Using this reporter virus system, we established a high-throughput screening assay and screened a selected plant-sourced compounds library for their ability to block ZIKV infection. More than 31 out of 974 tested compounds effectively decreased ZIKV reporter infection. Four selected compounds, homoharringtonine(HHT), bruceine D(BD), dihydroartemisinin(DHA) and digitonin(DGT), were further validated to inhibit wild-type ZIKV infection in cells of BHK-21 and human cell line A549.The FDA-approved chronic myeloid leukemia treatment drug HHT and BD were identified as broad-spectrum flavivirus inhibitors. DHA, another FDA-approved antimalarial drug effectively inhibited ZIKV infection in BHK-21 cells. HHT, BD and DHA inhibited ZIKV infection at a post-entry stage. Digitonin was found to have inhibitory activity in the early stage of viral infection. Our research provides an efficient high-throughput screening assay for ZIKV inhibitors. The active compounds identified in this study represent potential therapies for the treatment of ZIKV infection.