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| 1 | Caspase-1 inhibitor Ac-YVAD-CHO attenuates quinolinic acid-induced increases in p53 and apoptosis in rat striatum显示文摘Aim: To study the effects of the caspase-1 inhibitor Ac-YVAD-CHO on quinolinic acid (QA)-induced apoptosis. Methods: Rats were pre-treated with intrastriatal infusion of Ac-YVAD-CHO (2-8 ug) before intrastriatal injection of QA (60 nmol). Striatal total proteins, genomic DNA, and nuclear proteins were isolated. The effects of Ac-YVAD-CHO on QA-induced caspase-1 activity, internucleosomal DNA fragmentation, IkB-α degradation, NF-kB, and AP-1 activation, and increases in p53 protein levels were measured with enzyme assays, agarose gel electrophoresis, electrophoresis mobility shift assays, and Western blot analysis. Results: Pre-treatment with Ac-YVAD-CHO inhibited QA-induced intemucleosomal DNA fragmentation. Ac-YVAD-CHO inhibited QA-induced increases in caspase-1 activity and p53 protein levels, but had no effect on QA-induced IkB-α degradation, NF-kB or AP-1 activation. Conclusion: Caspase-1 is involved in QA-induced p53 upregulation but not IkB-α degradation. Inhibition of caspase-1 attenuates QA-induced apoptosis in rat striatum. | YiCAO Zhen-lunGU FangLIN RongHAN Zheng-hongQIN | 2005 | Acta Pharmacologica Sinica2005，26，2： | 2 |
| 2 | The role of chloroplasts and microsomal fractions in polar lipid synthesis acetate by cell-free preparation from spinach (Spinacia oleracea) leaves显示文摘 | Ronghan P G Holland R Slack C R | 1980 | Biochem J1980，188，： | 1 |
| 3 | Anion charge and lattice volume dependent lithium ion migration in compounds with fcc anion sublattices显示文摘Proper design principles are essential for the efficient development of superionic conductors.However,the existing design principles are mainly proposed from the perspective of crystal structures.In this work,the face-centered cubic(fcc)anion sublattices were creatively constructed to study the effects of anion charge and lattice volume on the stability of lithium ion occupation and lithium ion migration by the density functional theory calculations.Both the large negative anion charges and large lattice volumes would increase the relative stabilities of lithium-anion tetrahedron,making lithium ions prefer to occupy the tetrahedral sites. | Zhenming Xu Xin Chen Ronghan Chen Xin Li Hong Zhu | 2020 | npj Computational Materials2020，，1： | 1 |
| 4 | Investigation on quality of cubic GaN/GaAs(100) by double-crystal X-ray diffraction显示文摘 | Dapeng Xu Rutian Wang Hui Yang Lianxi Zheng Jianbin Li Lihong Duan Ronghan Wu | 1999 | Science in China Series A: Mathematics1999，，5： | 1 |
| 5 | Combined anterior scle- ra staphylectomy and vitrectomy with anterior sclera staphyloma and vitreous hemorrhage occurring 38 years after cataract surgery显示文摘 | Qinxiang Zheng Ronghan Wu Wensheng Li | 2011 | Case Reports in Ophthalmological Medicine2011，，34： | 1 |
| 6 | Chain reaction models for vehicle queuing on single-lane road section显示文摘 | YAO Ronghan JIA Jing | 2012 | Journal of Jilin University(Engineering and Technology Edition)2012，42，4： | 1 |
| 7 | Hyaluronic acid-curcumin conjugate suppresses the fibrotic functions of myofibroblasts from contractive joint by the PTGER2 demethylation显示文摘Joint contracture is a fibrotic complication induced by joint immobilization and trauma,which is characterized as excessive myofibroblast proliferation in joint capsule.The treatments of joint contracture are unsatisfied and patients are suffered from joint dysfunction.Our previous study has shown that curcumin can inhibit myofibroblast proliferation in vitro,but the major challenge is the low aqueous solubility and biological activity of curcumin.In this study,hyaluronic acid-curcumin(HA-Cur)conjugate was synthesized to suppress myofibroblasts in joint contracture.Cells were isolated from the joint capsules of joint contracture patients and induced to active myofibroblasts by transforming growth factor-b(TGF-b).The anti-fibrotic function and mechanisms of HA-Cur were investigated by immunohistochemistry,reverse transcription-quantitative polymerase chain reaction(PCR),methylation-specific PCR,western blot,transwell migration assay and proliferation assay.Results showed that 30 lM HA-Cur significantly attenuated the fibrotic functions of myofibroblast in joint contracture in vitro by regulating the methylation of prostaglandin E receptor 2(PTGER2)and inhibiting TGF-b signaling.This may provide a mechanism for the treatment of joint contracture,and provide a molecular target PTGER2 for therapy during the pathogenesis of joint contracture. | Dongjie Yu Ze Zhuang Jianhua Ren Xuefeng Hu Zhe Wang Jieyu Zhang Yuansen Luo Kun Wang Ronghan He Yunbing Wang | 2019 | Regenerative Biomaterials2019，6，5： | 1 |
| 8 | Study on restraining frost growth at initial stage by hydrophobic coating and hygroscopic coating 显示文摘 | Cai Liang Wang Ronghan Hou Puxiu Zhang Xiaosong | 2011 | Energy and Buildings2011，43，： | 1 |
| 9 | Mineralization of calcium phosphate controlled by biomimetic selfassembled peptide monolayers via surface electrostatic potentials显示文摘The functions of acidic-rich domains in non-collagenous protein during biomineralization are thought to induce nucleation and control the growth of hydroxyapatite.The tripeptide Asp-Ser-Ser(DSS)repeats are the most common acidic-rich repeated unit in non-collagenous protein of dentin phosphoprotein,the functions of which have aroused extensive interests.In this study,biomimetic peptides(DSS)n(n=2 or 3)were designed and fabricated into self-assembled monolayers(SAMs)on Au(111)surface as biomimetic organic templates to regulate hydroxyapatite(HAp)mineralization in 1.5 simulated body fluid(1.5 SBF)at 37°C.The early mineralization processes and minerals deposited on the SAMs were characterized by X-ray diffraction,scanning electron microscope,and Fourier transform infrared spectroscopy analyses.The SAM-DSS9/DSS9G showed the highest capacity to induce HAp nucleation and growth,followed by SAM-DSS6/DSS6G,SAM-COOH,and SAMOH.The SAM-(DSS)n had more negative zeta potentials than SAM-COOH surface,indicating that DSS repeats contributed to the biomineralization,which not only provided strong affinity with Ca2+ions through direct electrostatic bonds,but more importantly influence surface electrostatic potentials of the assembled organic template for nucleation. | Shuo Wang Yongdong Yang Ronghan Wang Xiangdong Kong Xiumei Wang | 2020 | Bioactive Materials2020，5，2： | 0 |
| 10 | Glycogen synthase kinase 3 controls T-cell exhaustion by regulating NFAT activation显示文摘Cellular immunity mediated by CD8+T cells plays an indispensable role in bacterial and viral clearance and cancers.However,persistent antigen stimulation of CD8+T cells leads to an exhausted or dysfunctional cellular state characterized by the loss of effector function and high expression of inhibitory receptors during chronic viral infection and in tumors.Numerous studies have shown that glycogen synthase kinase 3(GSK3)controls the function and development of immune cells,but whether GSK3 affects CD8+T cells is not clearly elucidated.Here,we demonstrate that mice with deletion of Gsk3αand Gsk3βin activated CD8+T cells(DKO)exhibited decreased CTL differentiation and effector function during acute and chronic viral infection.In addition,DKO mice failed to control tumor growth due to the upregulated expression of inhibitory receptors and augmented T-cell exhaustion in tumor-infiltrating CD8+T cells.Strikingly,anti-PD-1 immunotherapy substantially restored tumor rejection in DKO mice.Mechanistically,GSK3 regulates T-cell exhaustion by suppressing TCR-induced nuclear import of NFAT,thereby in turn dampening NFAT-mediated exhaustion-related gene expression,including TOX/TOX2 and PD-1.Thus,we uncovered the molecular mechanisms underlying GSK3 regulation of CTL differentiation and T-cell exhaustion in anti-tumor immune responses. | Yubing Fu Jinjia Wang Chenfeng Liu Kunyu Liao Xianjun Gao Ronghan Tang Binbin Fan Yazhen Hong Nengming Xiao Changchun Xiao Wen-Hsien Liu | 2023 | Cellular & Molecular Immunology2023，20，10： | 0 |
| 11 | Hsa_circ_0002137 stabled by LIN28B promotes osteosarcoma cell growth through the hsa-miR-1246/BCL2 axis显示文摘Circular RNAs(circRNAs)are a novel class of non-coding RNA that have recently shown to have huge capabilities in the regulation of gene expression at the posttranscriptional level.Growing evidence has indicated that circRNAs could serve as competing endogenous RNAs(ceRNAs)to sponge microRNAs(miRNAs)and suppress functions of targeted miRNAs.Osteosarcoma(OS)is the most common malignant primary bone cancer.Hsa_circ_0002137 is upregulated in OS.However,the role of hsa_circ_0002137 in OS remains unclear.Using miRNA pull-down assay,we showed that cir_0002137 sponged hsa-miR-1246,and BCL2 apoptosis regulator(BCL2)mRNA was a potential target of hsa-miR-1246 in human osteosarcoma(HOS)cells.Further,we found that hsa_cir_0002137 could enhance the expression of BCL2 hsa-miR-1246 and promote HOS cell growth through sponging hsa-miR-1246.Moreover,RNA binding protein immunoprecip itation(RIP)assay revealed that lin-28 homolog B(LIN28B)protein associated with hsa_circ_0002137,and LIN28B could increase hsa_circ_0002137 stability and thus accelerate OS cell growth.Our work was the first to study the functions of hsa_circ_0002137,has-miR-1246 and LIN28B in OS,and these results may provide novel therapeutic targets for OS treatment. | FEI ZHANG JIANZHONG LAI RONGHAN HE YI SHI KUN XU SHIHAI JIANG TANGZHAO LIANG WANYU ZHAO WEIDA REN LEI ZHU SONG JIN KUN WANG | 2022 | BIOCELL2022，46，3： | 0 |
| 12 | High energy density in ultra-thick and flexible electrodes enabled by designed conductive agent/binder composite显示文摘Thick electrodes can increase incorporation of active electrode materials by diminishing the proportion of inactive constituents,improving the overall energy density of batteries.However,thick electrodes fabricated using the conventional slurry casting approach frequently exhibit an exacerbated accumulation of carbon additives and binders on their surfaces,invariably leading to compromised electrochemical properties.In this study,we introduce a designed conductive agent/binder composite synthesized from carbon nanotube and polytetrafluoroethylene.This agent/binder composite facilitates production of dry-process-prepared ultra-thick electrodes endowed with a three-dimensional and uniformly distributed percolative architecture,ensuring superior electronic conductivity and remarkable mechanical resilience.Using this approach,ultra-thick LiCoO_(2)(LCO) electrodes demonstrated superior cycling performance and rate capabilities,registering an impressive loading capacity of up to 101.4 mg/cm^(2),signifying a 242% increase in battery energy density.In another analytical endeavor,time-of-flight secondary ion mass spectroscopy was used to clarify the distribution of cathode electrolyte interphase(CEI) in cycled LCO electrodes.The results provide unprecedented evidence explaining the intricate correlation between CEI generation and carbon distribution,highlighting the intrinsic advantages of the proposed dry-process approach in fine-tu ning the CEI,with excellent cycling performance in batteries equipped with ultra-thick electrodes. | Xiaoyu Shen Hailong Yu Liubin Ben Wenwu Zhao Qiyu Wang Guanjun Cen Ronghan Qiao Yida Wu Xuejie Huang | 2024 | Journal of Energy Chemistry2024，90，3： | 0 |
| 13 | Extraction of mode attenuation coefficient from low frequency reverberation signal显示文摘A method of extracting normal mode attenuation coefficient from low frequency reverberation signal has been proposed.Pseudo-inverse normal mode filtering method is implemented to get single mode reverberation field firstly.Based on the assumption of separability of modal back-scattering matrix,effective back-scattering matrix element can be calculated using single mode average reverberation intensity.Finally,mode attenuation coefficient is extracted by comparing effective back-scattering matrix elements at different ranges.The extracted mode attenuation coefficients are used to predict sound transmission loss at the same experiment area. Results show that the predicted transmission loss agrees well with the measured data.This method avoids the difficult of treating the coupling between bottom scattering attenuation and normal mode propagation attenuation.Research on extraction of mode attenuation coefficient from low frequency reverberation signal is useful for both geoacoustic inversion and rapid underwater environment assessment. | ZHANG Ronghan LI Qi | 2013 | Chinese Journal of Acoustics2013，32，3： | 0 |
| 14 | L-type calcium channel blockers enhance 5-HTP-induced antinociception in mice显示文摘AIM: To investigate the involvement of L-type Ca2+ channels in antinociceptive action induced by the 5-HT precursor,5-hydroxytryptophan (5-HTP). METHODS: Female Kunming mice were treated with either 5-HTP (20-80 mg/kg,ip) alone, or the combination of 5-HTP and fluoxetine (2-8 mg/kg, ip), pargyline (15-60 mg/kg, ip), nimodipine (2.5-10 mg/kg, ip), nifedipine (2.5-10 mg/kg, ip), verapamil (2.5-10 mg/kg, ip), CaCl2 (5-20 mmol/L, icv), or EGTA(0.5-3 mmol/L, icv) prior to the hot-plate test (55 C, hind-paw licking latency). In addition, locomotor activity inmice treated with 5-HTP alone was measured using an ambulometer with five activity boxes. RESULTS: Ipinjection of 5-HTP alone had no influence on the spontaneous locomotor activity, whereas dose-dependently in-creased the latency to licking hind-paw in the hot-plate test in mice. The inhibitory effects of 5-HTP on nociceptiveresponse were significantly enhanced by fluoxetine in the mouse hot-plate test. At a sub-effective dose, pargylinecould cause a leftward shift in the dose-response curve of 5-HTP-induced antinociception. Co-administration with5-HTP and nimodipine, nifedipine, or verapamil obviously potentiated the antinociceptive effects elicited by 5-HTP.Interestingly, 5-HTP-induced antinociception was antagonized by CaCl2 and enhanced by EGTA injected icv in themouse hot-plate test. CONCLUSION: These findings suggest that systemic administration of 5-HTP may yield theantinociceptive effects, which are related to Ca2+ influx from extracellular fluid through L-type Ca2+ channels. | Jian-huiLIANG Jun-xuLI Xu-huaWANG BiCHEN YingLU PanZHANG RongHAN Xiang-fengYE | 2004 | Acta Pharmacologica Sinica2004，25，5： | 0 |
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