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      • Ultrathin Trilayer Assemblies as Long-Lived Barriers against Water and Ion Penetration in Flexible Bioelectronic Systems

        Song, Enming,Li, Rui,Jin, Xin,Du, Haina,Huang, Yuming,Zhang, Jize,Xia, Yu,Fang, Hui,Lee, Yoon Kyeung,Yu, Ki Jun,Chang, Jan-Kai,Mei, Yongfeng,Alam, Muhammad A.,Huang, Yonggang,Rogers, John A. American Chemical Society 2018 ACS NANO Vol.12 No.10

        <P>Biomedical implants that incorporate active electronics and offer the ability to operate in a safe, stable fashion for long periods of time must incorporate defect-free layers as barriers to biofluid penetration. This paper reports an engineered material approach to this challenge that combines ultrathin, physically transferred films of silicon dioxide (t-SiO<SUB>2</SUB>) thermally grown on silicon wafers, with layers of hafnium oxide (HfO<SUB>2</SUB>) formed by atomic layer deposition and coatings of parylene (Parylene C) created by chemical vapor deposition, as a dual-sided encapsulation structure for flexible bioelectronic systems. Accelerated aging tests on passive/active components in platforms that incorporate active, silicon-based transistors suggest that this trilayer construct can serve as a robust, long-lived, defect-free barrier to phosphate-buffered saline (PBS) solution at a physiological pH of 7.4. Reactive diffusion modeling and systematic immersion experiments highlight fundamental aspects of water diffusion and hydrolysis behaviors, with results that suggest lifetimes of many decades at physiological conditions. A combination of ion-diffusion tests under continuous electrical bias, measurements of elemental concentration profiles, and temperature-dependent simulations reveals that this encapsulation strategy can also block transport of ions that would otherwise degrade the performance of the underlying electronics. These findings suggest broad utility of this trilayer assembly as a reliable encapsulation strategy for the most demanding applications in chronic biomedical implants and high-performance flexible bioelectronic systems.</P> [FIG OMISSION]</BR>

      • Abiraterone for Treatment of Metastatic Castration-resistant Prostate Cancer: a Systematic Review and Meta-analysis

        Zhou, Zhi-Rui,Liu, Shi-Xin,Zhang, Tian-Song,Xia, Jun,Li, Bo Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.3

        Introduction: Although most prostate cancers initially respond to castration with luteinizing hormonereleasing analogues or bilateral orchiectomy, progression eventually occurs. Based on the exciting results of several randomized controlled trials (RCTs), it seems that patients with metastatic castration-resistant prostate cancer (mCRPC) might benefit more from treatment withabiraterone. Therefore we conducted a systematic review to evaluate the efficacy and toxicity of abiraterone in the treatment of mCRPC. Methods: Literature was searched from Embase, PubMed, Web of Science, and Cochrane Library up to July, 2013. Quality of the study was evaluated according to the Cochrane's risk of bias of randomized controlled trial (RCT) tool, then the Grading of Recommendations Assessment, Development and Evaluation (GRADE) System was used to rate the level of evidence. Stata 12.0 was used for statistical analysis. Summary data from RCTs comparing abiraterone plus prednisone versus placebo plus prednisone for mCRPC were meta-analyzed. Pooled hazard ratios (HRs) for overall survival (OS), radiographic progression-free survival (RPFS) and time to PSA progression (TTPP); Pooled risk ratios (RR) for PSA response rate, objective response rate and adverse event were calculated. Results: Ten trials were included in the systematic review; Data of 2,283 patients (1,343 abiraterone; 940 placebo) from two phase 3 trials: COU-AA-301 and COU-AA-302 were meta-analyzed. Compared with placebo, abiraterone significantly prolonged OS (HR, 0.74; 95% confidence interval [CI], 0.66 to 0.84), RPFS (HR, 0.59; 95% CI, 0.48 to 0.74) and time to PSA progression (HR, 0.55; 95% CI, 0.43 to 0.70); it also significantly increased PSA response rate (RR, 3.63; 95% CI, 1.72 to 7.65) and objective response rate (RR, 3.05; 95% CI, 1.51 to 6.15). This meta-analysis suggested that the adverse events caused by abiraterone are acceptable and can be controlled. Conclutios: Abiraterone significantly prolonged OS, RPFS and time to progression patients with mCRPC, regardless of prior chemotherapy or whether chemotherapy-na$\ddot{i}$ve, and no unexpected toxicity was evident. Abiraterone can serve as a new standard therapy for mCRPC.

      • KCI등재

        Wear-life analysis of deep groove ball bearings based on Archard wear theory

        Guangwei Yu,Wei Xia,Zhuoyuan Song,Rui Wu,Siling Wang,Yuan Yao 대한기계학회 2018 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.32 No.7

        A quasi-dynamic method is proposed to evaluate the characteristics of ball bearings, which include pressure distribution over the contact area between the ball and the raceway, sliding velocity distribution, and lubrication parameters. The extent of permissible wear is confirmed based on the Archard wear equation. A mathematical model for wear-life analysis is then presented for 6000 deep groove ball bearings with axial loads. The effects of axial loads, rotating speed, and structural parameters on wear characteristics of bearings are analyzed. A number of conclusions are drawn. Based on the proposed mathematical model, the wear life of a bearing decreases with increased axial load. The wear life of the bearing decreases as the rotational speed of the inner ring increases. The wear life of the bearing exhibits nearly linear increment as the groove curvature of the inner ring increases and decreases as the groove curvature of the outer ring increases.

      • Mini-Array of Multiple Tumor-associated Antigens (TAAs) in the Immunodiagnosis of Esophageal Cancer

        Qin, Jie-Jie,Wang, Xiao-Rui,Wang, Peng,Ren, Peng-Fei,Shi, Jian-Xiang,Zhang, Hong-Fei,Xia, Jun-Fen,Wang, Kai-Juan,Song, Chun-Hua,Dai, Li-Ping,Zhang, Jian-Ying Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.6

        Sera of cancer patients may contain antibodies that react with a unique group of autologous cellular antigens called tumor-associated antigens (TAAs). The present study aimed to determine whether a mini-array of multiple TAAs would enhance antibody detection and be a useful approach in esophageal cancer detection and diagnosis. Our mini-array of multiple TAAs consisted of eleven antigens, p53, pl6, Impl, CyclinB1, C-myc, RalA, p62, Survivin, Koc, CyclinD1 and CyclinE full-length recombinant proteins. Enzyme-linked immunosorbent assays (ELISA) were used to detect autoantibodies against eleven selected TAAs in 174 sera from patients with esophageal cancer, as well as 242 sera from normal individuals. In addition, positive results of ELISA were confirmed by Western blotting. In a parallel screening trial, with the successive addition of antigen to a final total of eleven TAAs, there was a stepwise increase in positive antibody reactions. The eleven TAAs were the best parallel combination, and the sensitivity and specificity in diagnosing esophageal cancer was 75.3% and 81.0%, respectively. The positive and negative predictive values were 74.0% and 82.0%, respectively, indicating that the parallel assay of eleven TAAs raised the diagnostic precision significantly. In addition, the levels of antibodies to seven antigens, comprising p53, Impl, C-myc, RalA, p62, Survivin, and CyclinD1, were significantly different in various stages of esophageal cancer, which showed that autoantibodies may be involved in the pathogenesis and progression of esophageal cancer. All in all, this study further supports our previous hypothesis that a combination of antibodies might acquire higher sensitivity for the diagnosis of certain types of cancer. A customized mini-array of multiple carefully-selected TAAs is able to enhance autoantibody detection in the immunodiagnosis of esophageal cancer and autoantibodies to TAAs might be reference indicators of clinical stage.

      • KCI등재

        The complete mitochondrial genome of the Common Red Apollo, Parnassius epaphus (Lepidoptera: Papilionidae: Parnassiinae)

        Yun-liangWang,Yan-hong Chen,Chen-chen Xia,Xue-qin Xia,Rui-song Tao,Jia-sheng Hao 한국응용곤충학회 2015 Journal of Asia-Pacific Entomology Vol.18 No.2

        The complete mitochondrial genome of Parnassius epaphus (Lepidoptera: Papilionidae: Parnassiinae) was 15, 458 bp in length, harboring typical 13 protein-coding genes (PCGs), 22 transferRNA genes (tRNAs), two ribosomal RNA genes (rRNAs) and a non-coding control region (AT-rich region), with an 81.4% A + T content. The gene orientation and arrangement are the same as those of other sequenced lepidopterans. All PCGs startwith the typical ATN codon, with the exception of the COI gene that utilizes CGA as its initial codon. In addition, all PCGs terminate at the common stop codon TAA or TAG, except for the COII genewhich uses single T as its stop codon. All tRNAs possess the typical clover-leaf structure, except for tRNAser(AGN), inwhich the dihydrouridine (DHU) arm forms a simple loop. The predicted lrRNA and srRNA secondary structures harbor six domainswith 49 helices and three domains with 33 helices, respectively. In total, P. epaphus mitogenome harbors 12 intergenic spacers. The 122 bp longest one located between tRNAser(AGN) and tRNAGlu is characterized by the multiple duplications of TTTTTCTTTTT and TTTATCTATTTCTTTmotifs, and this sequence is the largest intergenic spacer among all butterflies detected to date. The 496 bp AT-rich region is located between srRNA and tRNAMet, containing some conserved structural characteristic of lepidopterans, such as the motif ATAGA followed by an 18-bp poly-T stretch, a microsatellite-like (AT)9 element preceded by the ATTTA motif. Moreover, two tRNA-like sequences (tRNATrp-like, tRNALeu(UUR)-like) and two sequence stretches potential to form stem-loop structures are also found in the AT-rich region.

      • KCI등재

        TSHR Variant Screening and Phenotype Analysis in 367 Chinese Patients With Congenital Hypothyroidism

        Zhang Hai-Yang,Wu Feng-Yao,Li Xue-Song,Tu Ping-Hui,Zhang Cao-Xu,Yang Rui-Meng,Cui Ren-Jie,Wu Chen-Yang,Fang Ya,Yang Liu,Song Huai-Dong,Zhao Shuang-Xia 대한진단검사의학회 2024 Annals of Laboratory Medicine Vol.44 No.4

        Background: Genetic defects in the human thyroid-stimulating hormone (TSH) receptor (TSHR) gene can cause congenital hypothyroidism (CH). However, the biological functions and comprehensive genotype–phenotype relationships for most TSHR variants associated with CH remain unexplored. We aimed to identify TSHR variants in Chinese patients with CH, analyze the functions of the variants, and explore the relationships between TSHR genotypes and clinical phenotypes. Methods: In total, 367 patients with CH were recruited for TSHR variant screening using whole-exome sequencing. The effects of the variants were evaluated by in-silico programs such as SIFT and polyphen2. Furthermore, these variants were transfected into 293T cells to detect their Gs/cyclic AMP and Gq/11 signaling activity. Results: Among the 367 patients with CH, 17 TSHR variants, including three novel variants, were identified in 45 patients, and 18 patients carried biallelic TSHR variants. In vitro experiments showed that 10 variants were associated with Gs/cyclic AMP and Gq/11 signaling pathway impairment to varying degrees. Patients with TSHR biallelic variants had lower serum TSH levels and higher free triiodothyronine and thyroxine levels at diagnosis than those with DUOX2 biallelic variants. Conclusions: We found a high frequency of TSHR variants in Chinese patients with CH (12.3%), and 4.9% of cases were caused by TSHR biallelic variants. Ten variants were identified as loss-of-function variants. The data suggest that the clinical phenotype of CH patients caused by TSHR biallelic variants is relatively mild. Our study expands the TSHR variant spectrum and provides further evidence for the elucidation of the genetic etiology of CH.

      • SCOPUSSCIE

        Cannabidiol Promotes Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells in the Inflammatory Microenvironment via the CB2-dependent p38 MAPK Signaling Pathway

        Lin Li,Jin Feng,Lei Sun,Yao-wei Xuan,Li Wen,Yun-xia Li,Shuo Yang,Biao Zhu,Xiao-yu Tian,Shuang Li,Li-sheng Zhao,Rui-jie Dang,Ting Jiao,Hai-song Zhang,Ning Wen Korean Society for Stem Cell Research 2022 International journal of stem cells Vol.15 No.4

        Background and Objectives: Chronic inflammation of bone tissue often results in bone defects and hazards to tissue repair and regeneration. Cannabidiol (CBD) is a natural cannabinoid with multiple biological activities, including anti-inflammatory and osteogenic potential. This study aimed to investigate the efficacy and mechanisms of CBD in the promotion of bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation in the inflammatory microenvironment. Methods and Results: BMSCs isolated from C57BL/6 mice, expressed stem cell characteristic surface markers and presented multidirectional differentiation potential. The CCK-8 assay was applied to evaluate the effects of CBD on BMSCs' vitality, and demonstrating the safety of CBD on BMSCs. Then, BMSCs were stimulated with lipopolysaccharide (LPS) to induce inflammatory microenvironment. We found that CBD intervention down-regulated mRNA expression levels of inflammatory cytokines and promoted cells proliferation in LPS-treated BMSCs, also reversed the protein and mRNA levels downregulation of osteogenic markers caused by LPS treatment. Moreover, CBD intervention activated the cannabinoid receptor 2 (CB2) and the p38 mitogen-activated protein kinase (MAPK) signaling pathway. While AM630, a selective CB2 inhibitor, reduced phosphorylated (p)-p38 levels. In addition, AM630 and SB530689, a selective p38 MAPK inhibitor, attenuated the enhancement of osteogenic markers expression levels by CBD in inflammatory microenvironment, respectively. Conclusions: CBD promoted osteogenic differentiation of BMSCs via the CB2/p38 MAPK signaling pathway in the inflammatory microenvironment.

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