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| 1 | MicroRNA-145 targets vascular endothelial growth factor and inhibits invasion and metastasis of osteosarcoma cells显示文摘MicroRNAs 是在 tumorigenesis 起一个深刻作用的重要基因管理者。MicroRNA-145 (miR-145 ) ,在 microRNAs 的家庭的一个重要成员,作为肿瘤 suppressor 在肿瘤和幕的几种类型是下面表示的。角色和在 osteosarcoma carcinogenesis 的 miR-145 的可能的小径仍然是未知的。在这研究,我们发现 miR-145 在 osteosarcoma 纸巾是显著地下面表示的,并且 miR-145 的在表示上能禁止 osteosarcoma 房间的侵略和 angiopoiesis。而且,结果证明那脉管的 endothelial 生长因素(VEGF ) 表情在在 miR-145 transfection 以后的 osteosarcoma 房间是下面调整的。根据这些结果,我们执行了酶试金并且验证了那 miR-145 能在翻译水平由的下面调整 VEGF 对 VEGF 3 untranslated 区域(3UTR ) 部分有约束力。因此, miR-145 能禁止 osteosarcoma 房间的侵略和转移,这能被结束。机制之一明确地是由由到 VEGF mRNA 的 3UTR 的绑定的 miR-145 的 VEGF 表示的下面规定。这些新奇调查结果可以为 osteosarcoma 的有效基因治疗有广泛的含意。 | Qiang Wu Xiaojuan Xing Yulong Wei Zengwu Shao | 2012 | Acta Biochimica et Biophysica Sinica2012，44，5： | 18 |
| 2 | Traumatic brain injury stimulates sympathetic tone-mediated bone marrow myelopoiesis to favor fracture healing显示文摘Traumatic brain injury(TBI)accelerates fracture healing,but the underlying mechanism remains largely unknown.Accumulating evidence indicates that the central nervous system(CNS)plays a pivotal role in regulating immune system and skeletal homeostasis.However,the impact of CNS injury on hematopoiesis commitment was overlooked.Here,we found that the dramatically elevated sympathetic tone accompanied with TBI-accelerated fracture healing;chemical sympathectomy blocks TBIinduced fracture healing.TBI-induced hypersensitivity of adrenergic signaling promotes the proliferation of bone marrow hematopoietic stem cells(HSCs)and swiftly skews HSCs toward anti-inflammation myeloid cells within 14 days,which favor fracture healing.Knockout ofβ3-orβ2-adrenergic receptor(AR)eliminate TBI-mediated anti-inflammation macrophage expansion and TBIaccelerated fracture healing.RNA sequencing of bone marrow cells revealed that Adrb2 and Adrb3 maintain proliferation and commitment of immune cells.Importantly,flow cytometry confirmed that deletion ofβ2-AR inhibits M2 polarization of macrophages at 7th day and 14th day;and TBI-induced HSCs proliferation was impaired inβ3-AR knockout mice.Moreover,β3-andβ2-AR agonists synergistically promote infiltration of M2 macrophages in callus and accelerate bone healing process.Thus,we conclude that TBI accelerates bone formation during early stage of fracture healing process by shaping the anti-inflammation environment in the bone marrow.These results implicate that the adrenergic signals could serve as potential targets for fracture management. | Weijian Liu Wei Chen Mao Xie Chao Chen Zengwu Shao Yiran Zhang Haiyue Zhao Qingcheng Song Hongzhi Hu Xin Xing Xianyi Cai Xiangtian Deng Xinyan Li Peng Wang Guohui Liu Liming Xiong Xiao Lv Yingze Zhang | 2023 | Signal Transduction and Targeted Therapy2023，8，8： | 1 |
| 3 | Chitosan derived carbon membranes as protective layers on zinc anodes for aqueous zinc batteries显示文摘Aqueous zinc batteries with low cost and inherent safety are considered to be the most promising energy storage devices.However,they suffer from poor cycling stability and low coulombic efficiencies caused by the adverse zinc dendrites on the anodes during the discharging/charging processes.Chitosan is a kind of natural amino polysaccharide,which is rich in nitrogen and carbon.When sintered at high temperatures,carbon membranes have been achieved with excellent conductivity and graphitization degree,which could enhance the ability to induce zinc ion uniform deposition to some extent.In this work,a type of carbon membrane using chitosan as raw materials has been fabricated by sintering,and then assembled as the protect layers in aqueous zinc batteries.The results show that the samples could retain smoother surfaces when adopting the sintering temperature of 800℃,and the assembled batteries are able to achieve about 700 h at a current density of 0.25m A·cm^(-2),which is far longer than those of the similar batteries without any carbon membranes. | Haichao Li Zengwu Wei Yu Xia Junshan Han Xing Li | 2023 | International Journal of Minerals,Metallurgy and Materials2023，30，4： | 0 |
| 4 | Three-dimensional-printed titanium prostheses with bone trabeculae enable mechanical-biological reconstruction after resection of bone tumours显示文摘Reconstruction after resection has always been an urgent problem in the treatment of bone tumours.There are many methods that can be used to reconstruct bone defects;however,there are also many complications,and it is difficult to develop a safe and effective reconstruction plan for the treatment of bone tumours.With the rapid development of digital orthopaedics,three-dimensional printing technology can solve this problem.The three-dimensional printing of personalised prostheses has many advantages.It can be used to print complex structures that are difficult to fabricate using traditional processes and overcome the problems of stress shielding and low biological activity of conventional prostheses.In this study,12 patients with bone tumours were selected as research subjects,and based on individualised reverse-engineering design technology,a three-dimensional model of each prosthesis was designed and installed using medical image data.Ti6Al4V was used as the raw material to prepare the prostheses,which were used to repair bone defects after surgical resection.The operation time was 266.43±21.08 minutes(range 180-390 minutes),and intraoperative blood loss was 857.26±84.28 mL(range 800-2500 mL).One patient had delayed wound healing after surgery,but all patients survived without local tumour recurrence,and no tumour metastasis was found.No aseptic loosening or structural fracture of the prosthesis,and no non-mechanical prosthesis failure caused by infection,tumour recurrence,or progression was observed.The Musculo-Skeletal Tumour Society(MSTS)score of limb function was 22.53±2.09(range 16-26),and ten of the 12 patients scored≥20 and were able to function normally.The results showed that three-dimensional printed prostheses with an individualised design can achieve satisfactory short-term clinical efficacy in the reconstruction of large bone defects after bone tumour resection. | Feifei Pu Wei Wu Doudou Jing Yihan Yu Yizhong Peng Jianxiang Liu Qiang Wu Baichuan Wang Zhicai Zhang Zengwu Shao | 2022 | Biomaterials Translational2022，3，2： | 0 |
| 5 | The Quantitative Instability of Non-linearity System and the Particularity of Information显示文摘The present paper tries to discuss the quantity instability in the non-linearity dynamics equations without the limit of the stability in the dynamics equations. The result shows that the quantity instability of non-linearity can be deducted to the turning transformation in the curvature space. “The dynamics of varying acceleration' is not the issue of inertia system in science of the time. The particularity as information cannot limit the quantity instability with the quantity stability in inertia system. The particular information does have the significant meaning related to the turning transformation in evolution, in which each problem of non-linearity or matter evolution can go out of the inertia system by means of “kill three birds with one stone'. | OuYang Shoucheng Wei Ming Yuan Dongsheng Wang Zengwu | 2005 | 工程科学(英文版)2005，3，4： | 0 |
| 6 | Corrigendum to'Cellular senescence-driven transcriptional reprogramming of the MAFB/NOTCH3 axis activates the PI3K/AKT pathway and promotes osteosarcoma progression'[Genes&Diseases 11(2024)952-963]显示文摘The authors regret that some data errors were made in'Cellular senescence-driven transcriptional reprogramming of the MAFB/NOTCH3 axis activates the PI3K/AKT pathway and promotes osteosarcoma progression'at Figure 5F for the colony formation of MNNG/HOS cells with si-NOTCH3 and 5G for the tranwell assay of U2OS cells with si-NOCTH3.Correction and supplementation to Figure 5.The author used confusing experimental data and did not notice these errors when submitting the original manuscript.Here,the authors made the latest corrections to the data of the batch of U2OS cells and MNNG/HOS cells transfected with si-NoTCH3.The authors confirm that this correction will not alter the conclusions in the original manuscript. | Zhenhao Zhang Doudou Jing Baijun Xuan Zhicai Zhang Wei Wu Zengwu Shao | 2024 | Genes & Diseases2024，11，3： | 0 |
| 7 | Cellular senescence-driven transcriptional reprogramming of the MAFB/NOTCH3 axis activates the PI3K/AKT pathway and promotes osteosarcoma progression显示文摘Osteosarcoma is the most common primary malignancy of bones and primarily occurs in adolescents and young adults.However,a second smaller peak of osteosarcoma incidence was reported in the elderly aged more than 60.Elderly patients with osteosarcoma exhibit different characteristics compared to young patients,which usually results in a poor prognosis.The mechanism underlying osteosarcoma development in elderly patients is intriguing and of significant value in clinical applications.Senescent cells can accelerate tumor progression by metabolic reprogramming.Recent research has shown that methylmalonic acid(MMA)was significantly up-regulated in the serum of older individuals and played a central role in the development of aggressive characteristics.We found that the significant accumulation of MMA in elderly patients imparted proliferative potential to osteosarcoma cells.The expression of MAFB was excessively up-regulated in osteosarcoma specimens and was further enhanced in response to MMA accumulation as the patient aged.Specifically,we first confirmed a novel molecular mechanism between cellular senescence and cancer,in which the MMA-driven transcriptional reprogramming of the MAFB-NOTCH3 axis accelerated osteosarcoma progression via the activation of PI3K-AKT pathways.Moreover,the down-regulation of the MAFB-NOTCH3 axis increased the sensitivity and effect of AKT inhibitors in osteosarcoma through significant inhibition of AKT phosphorylation.In conclusion,we confirmed that MAFB is a novel age-dependent biomarker for osteosarcoma,and targeting the MAFB-NOTCH3 axis in combination with AKT inhibition can serve as a novel therapeutic strategy for elderly patients with osteosarcoma in experimental and clinical trials. | Zhenhao Zhang Doudou Jing Baijun Xuan Zhicai Zhang Wei Wu Zengwu Shao | 2024 | Genes & Diseases2024，11，2： | 0 |
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