An ultrastable sodium-ion battery anode enabled by carbon-coated porous NaTi2(PO4)3 olive-like nanospheres.

NaTi2(PO4)3 (NTP) is a promising anode material for sodium-ion batteries (SIBs). It has drawn wide attention because of its stable three-dimensional NASICON-type structure, proper redox potential, and large accommodation space for Na+. However, the inherent low electronic conductivity of the phosphate framework reduces its charge transfer kinetics, thus limiting its exploitation. Therefore, this paper proposes a material with carbon-coated porous NTP olive-like nanospheres (p-NTP@C) to tackle the issues above. Based on experimental data and theoretical calculations, the porous structure of the material is found to be able to provide more active sites and shorten the Na+ diffusion distance. In addition, the carbon coating can effectively improve the electron and Na+ diffusion kinetics. As the anode material for SIBs, the p-NTP@C olive-like nanospheres exhibit a high reversible capacity (127.3 mAh g-1 at 0.1 C) and ultrastable cycling performance (84.8% capacity retention after 10,000 cycles at 5 C). Furthermore, the sodium-ion full cells, composed of p-NTP@C anode and Na3V2(PO4)2F3@carbon cathode, also deliver excellent performance (75.7% capacity retention after 1000 cycles at 1 C). In brief, this nanostructure design provides a viable approach for the future development of long-life and highly stable NASICON-type anode materials.

Lycopene inhibits proliferation and promotes apoptosis of renal cancer 786-O cells through the SIRT1/NF-κB axis / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨番茄红素通过沉默信息调节因子1（SIRT1）/核因子-κB（NF-κB）轴对肾癌786-O细胞增殖、凋亡的影响。方法：常规培养人正常肾细胞HK-2和人肾癌细胞786-O，实验分为对照组（0.1% DMSO）、顺铂组（40 μg/mL）、番茄红素低质量浓度（2.5 μg/mL）组、番茄红素高质量浓度（5 μg/mL）组、番茄红素（5 μg/mL）+EX527（SIRT1抑制剂）（3 µmol/L）组。CCK-8法、克隆形成实验检测各组HK-2、786-O细胞的增殖能力，流式细胞术检测各组786-O细胞的凋亡，RH123、DCFH-DA染色分别检测各组786-O细胞的线粒体膜电位（MMP）、活性氧（ROS）水平，WB法检测各组786-O细胞中凋亡相关蛋白BAX、Bcl-2、C-casp3和SIRT1/NF-κB轴相关蛋白SIRT1、p-NF-κB蛋白的表达。786-O细胞移植瘤实验检测番茄红素低（5 mg/kg）、高质量浓度（20 mg/Kg）、顺铂（2 mg/kg）、番茄红素（20 mg/kg）+EX527（10 mg/kg）对移植瘤生长的影响，TUNEL法检测各组移植瘤组织中的细胞凋亡。结果：番茄红素呈剂量依赖性地抑制786-O细胞的增殖活性，番茄红素、顺铂均明显抑制786-O细胞的克隆形成能力且促进其凋亡，细胞中MMP损伤率升高而ROS水平降低，凋亡相关蛋白BAX、C-casp3表达均显著升高（均P<0.05）而Bcl-2表达下调（P<0.05），SIRT1表达显著升高（P<0.05）而p-NF-κB的表达显著降低（P<0.05），上述作用均可被EX527逆转；番茄红素、顺铂抑制786-O细胞移植瘤的生长且促进其细胞凋亡，其作用也能被EX527逆转。结论：番茄红素通过上调SIRT1、抑制NF-κB通路的激活进而抑制786-O细胞增殖且诱导其凋亡。

A cohort of five cases with asymmetric conjoined twining and literature review.

PURPOSE: Asymmetric conjoined twining (ACT) is a form of conjoined twining which is a rare malformation of monochorionic monoamniotic twin pregnancy. Most publications were single case reports. We reported a cohort of five cases with ACT from a single tertiary medical center and reviewed the case reports of ACT over the last decade to enrich the clinical research of this disease and summarized the clinical features of the disease. METHODS: We reviewed five cases of ACT admitted in Tianjin Children's Hospital from 17 March, 2008, through 7 March 2017. The cohort was analysed from general information, imaging manifestations, separation surgery, histopathological findings, outcome and follow-up. We searched the English literatures on case reports of ACT over the past decade from the PubMed database and presented details about the clinical characteristics, treatment, and prognosis of all cases. RESULTS: There were four males and one female in our cohort. Among the five cases, two parasites were located in epigastrium, two in rachis, and one in retroperitoneum (fetus in fetu, FIF). All of the parasites were separated successfully by operation in five cases and were confirmed to be ACT by histopathology reports. Four patients made an uneventful recovery except for one case of wound infection. All of them were doing well in follow-up. In the literature review, we found 41 cases of exoparasitic heteropagus twining (EHT) and 63 cases of FIF. CONCLUSIONS: ACT is very rare and usually diagnosed by prenatal ultrasonography (US). Computed tomography (CT) and magnetic resonance imaging (MRI) examinations are essential imaging examinations before separation surgery to delineate the anatomical relationship between the autosite and the parasite. In general, the separation surgery of ACT is less complicated and the prognosis is better compared with the symmetric conjoined twining (SCT).

Targeting adaptor protein SLP76 of RAGE as a therapeutic approach for lethal sepsis.

Accumulating evidence shows that RAGE has an important function in the pathogenesis of sepsis. However, the mechanisms by which RAGE transduces signals to downstream kinase cascades during septic shock are not clear. Here, we identify SLP76 as a binding partner for the cytosolic tail of RAGE both in vitro and in vivo and demonstrate that SLP76 binds RAGE through its sterile α motif (SAM) to mediate downstream signaling. Genetic deficiency of RAGE or SLP76 reduces AGE-induced phosphorylation of p38 MAPK, ERK1/2 and IKKα/ß, as well as cytokine release. Delivery of the SAM domain into macrophages via the TAT cell-penetrating peptide blocks proinflammatory cytokine production. Furthermore, administration of TAT-SAM attenuates inflammatory cytokine release and tissue damage in mice subjected to cecal ligation and puncture (CLP) and protects these mice from the lethality of sepsis. These findings reveal an important function for SLP76 in RAGE-mediated pro-inflammatory signaling and shed light on the development of SLP76-targeted therapeutics for sepsis.

Nonvolatile and Reversible Ferroelectric Control of Electronic Properties of Bi2Te3 Topological Insulator Thin Films Grown on Pb(Mg1/3Nb2/3)O3-PbTiO3 Single Crystals.

Single-phase (00 l)-oriented Bi2Te3 topological insulator thin films have been deposited on (111)-oriented ferroelectric 0.71Pb(Mg1/3Nb2/3)O3-0.29PbTiO3 (PMN-PT) single-crystal substrates. Taking advantage of the nonvolatile polarization charges induced by the polarization direction switching of PMN-PT substrates at room temperature, the carrier density, Fermi level, magnetoconductance, conductance channel, phase coherence length, and quantum corrections to the conductance can be in situ modulated in a reversible and nonvolatile manner. Specifically, upon the polarization switching from the positively poled Pr+ state (i.e., polarization direction points to the film) to the negatively poled Pr- (i.e., polarization direction points to the bottom electrode) state, both the electron carrier density and the Fermi wave vector decrease significantly, reflecting a shift of the Fermi level toward the Dirac point. The polarization switching from Pr+ to Pr- also results in significant increase of the conductance channel α from -0.15 to -0.3 and a decrease of the phase coherence length from 200 to 80 nm at T = 2 K as well as a reduction of the electron-electron interaction. All these results demonstrate that electric-voltage control of physical properties using PMN-PT as both substrates and gating materials provides a simple and a straightforward approach to realize reversible and nonvolatile tuning of electronic properties of topological thin films and may be further extended to study carrier density-related quantum transport properties of other quantum matter.

Tumor Suppressor Folliculin Regulates mTORC1 through Primary Cilia.

Folliculin (FLCN) is the tumor suppressor associated with Birt-Hogg-Dubé (BHD) syndrome that predisposes patients to incident of hamartomas and cysts in multiple organs. Its inactivation causes deregulation in the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. However, the underlying mechanism is poorly defined. In this study, we show that FLCN is a ciliary protein that functions through primary cilia to regulate mTORC1. In response to flow stress, FLCN associates with LKB1 and recruits the kinase to primary cilia for activation of AMPK resided at basal bodies, which causes mTORC1 down-regulation. In cells depleted of FLCN, LKB1 fails to accumulate in primary cilia and AMPK at the basal bodies remains inactive, thus nullifying the inhibitory effect of flow stress on mTORC1 activity. Our results demonstrate that FLCN is part of a flow sensory mechanism that regulates mTORC1 through primary cilia.

Angiotensin II facilitates fibrogenic effect of TGF-ß1 through enhancing the down-regulation of BAMBI caused by LPS: a new pro-fibrotic mechanism of angiotensin II.

Angiotensin II has progressively been considered to play an important role in the development of liver fibrosis, although the mechanism isn't fully understood. The aim of this study was to investigate a possible pro-fibrotic mechanism, by which angiotensin II would enhance the pro-fibrotic effect of transforming growth factor beta 1 (TGF-ß1) through up-regulation of toll-like receptor 4 (TLR4) and enhancing down-regulation of TGF-ß1 inhibitory pseudo-receptor-BAMBI caused by LPS in hepatic stellate cells (HSCs). Firstly, the synergistic effects of angiotensin II, TGF-ß1 and LPS on collagen 1α production were confirmed in vitro by ELISA, in which angiotensin II, LPS and TGF-ß1 were treated sequentially, and in vivo by immunofluorescence, in the experiments single or multiple intra-peritoneally implanted osmotic mini-pumps administrating angiotensin II or LPS combined with intra-peritoneal injections of TGF-ß1 were used. We also found that only LPS and TGF-ß1 weren't enough to induce obvious fibrogenesis without angiotensin II. Secondly, to identify the reason of why angiotensin II is so important, the minute level of TLR4 in activated HSCs - T6 and primary quiescent HSCs of rat, up-regulation of TLR4 by angiotensin II and blockage by different angiotensin II receptor type 1 (AT1) blockers in HSCs were assayed by western blotting in vitro and immunofluorescence in vivo. Finally, BAMBI expression level, which is regulated by LPS-TLR4 pathway, was detected by qRT-PCR and results showed angiotensin II enhanced the down-regulation of BAMBI mRNA caused by LPS in vitro and in vivo, and TLR4 neutralization antibody blocked this interactive effect. These data demonstrated that angiotensin II enhances LPS-TLR4 pathway signaling and further down-regulates expression of BAMBI through up-regulation of TLR4, which results in facilitation of pro-fibrotic activity of TGF-ß1. Angiotensin II, LPS and TGF-ß1 act synergistically during hepatic fibrogenesis, showing crosstalks between angiotensin II-AT1, LPS-TLR4 and TGF-ß1-BAMBI signal pathways in rat HSCs.

Regulation of mammalian target of rapamycin complex 1 by Bcl-2 and Bcl-XL proteins.

Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell growth and metabolism. Its activity is controlled by various types of signals, including growth factors, nutrients, and stresses. In this study, we show that changes in expression levels of two antiapoptotic proteins, Bcl-2 and Bcl-XL, also affect mTORC1 signaling activity. In cells overexpressing Bcl-XL, mTORC1 activity is increased and becomes less sensitive to growth factor or nutrient conditions. In contrast, reduction in expression levels of the two antiapoptotic proteins inhibits mTORC1 signaling activity. Our results suggest that the effect of Bcl-2 and Bcl-XL on mTORC1 is mediated by FKBP38, an inhibitor of mTORC1. The two proteins compete with mTORC1 for FKBP38 binding and hence alter mTORC1 activity. This study reveals a novel cross-talk between Bcl-2/XL and mTORC1 signaling, which is likely to contribute to cancer development.

[Screening of atherosclerosis related polypeptide from phage display peptide library].

OBJECTIVE: To screen atherosclerosis (AS) related polypeptide from phage display 12-peptide library, and verify the binding activity of selected positive phages and synthetic protein fragment. METHODS: We collected plasma from AS patients as target for biopanning against phage-displayed 12-peptide library. After 3 rounds of screening, 10 positive phages were picked up and the binding activity was proved by ELISA. Single-stranded DNA of the phages were purified and sequenced, and a similar polypeptide was synthesized to test the binding activity to AS patients plasma. RESULTS: Selected phages significantly bound to AS patients' plasma. Five of ten phages had GPRPPSAPNMPL sequence. Corresponding synthetic polypeptide also showed a high binding activity to AS patient plasma. CONCLUSION: AS-related polypeptide can be obtained by phage display, which facilitates the research into the immune mechanism of AS.