Xijing Hospital

Fengcheng, China

Xijing Hospital

Fengcheng, China

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Since its inception, MMAAP foundation has awarded over 40 Fellowship and Project grants to support the work of exceptional physician scientists and investigators with the vision, drive and dedication to find new and innovative ways towards advancements in the targeted medical fields. These outstanding award recipients represent more than 20 prestigious Chinese medical institutions including Peking Union Medical College Hospital, Xijing Hospital, the Fourth Military Medical University, Peking University Institute of Hematology, West China Hospital, Sichuan University, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, and others. "The visionary leadership of MMAAP Foundation Chairman and Founder, Howard P. Milstein, has brought together and funded exchanges between outstanding researchers, medical talent, and institutions in these regions," said Sean X. Leng, MD, PhD, President of MMAAP Foundation. "The 2017 recipients are among the most talented investigators in their fields and our support of their work is vital to both furthering medical research and strengthening relations between the U.S. and China." Grant applications were evaluated through a two-step peer review process according to the National Institute of Health standard. Panels of Chinese and U.S. experts in their respective fields jointly reviewed all proposals, and finalists were submitted for approval by MMAAP Foundation. The U.S. panels in Geriatrics, Skin Disease, Hematology, Reproductive Medicine, and Translational Medicine include members of the American Geriatrics Society, Medical Advisory Committee of American Skin Association, New York Blood Center, Jones Foundation for Reproductive Medicine, as well as members of other leading U.S. institutions in each field. The mission of Milstein Medical Asian American Partnership Foundation (MMAAP Foundation) is to improve world health by developing mutually beneficial partnerships between the U.S. and China, as well as greater Asia. Working with some of the premier health organizations in the world, MMAAP Foundation brings together and funds exchanges among the best research, medical talent, and institutions in the regions. This strategy is a high priority for MMAAP Foundation's founder Howard P. Milstein. MMAAP Foundation is a 501(c) (3) non-profit organization. For more than 50 years, the Milstein family has been actively involved in health-related and medical philanthropy. MMAAP Foundation builds upon this distinguished history in five areas: Senior Healthcare, Skin Disease and Melanoma, Reproductive Biology, Blood Research, and Translational Medicine. MMAAP Foundation works in close collaboration with other medical organizations supported by the Milstein family, including American Skin Association, Milstein Melanoma Research Program at The Rockefeller University, Howard and Georgeanna Jones Foundation for Reproductive Medicine, New York Blood Center, and the Program for Translational Chemical Biology at New York-Presbyterian Hospital/Weill Cornell Medical Center. For more information, please visit MMAAP Foundation's website at www.mmaapf.org. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/milstein-medical-asian-american-partnership-foundation-announces-2017-fellowship-and-project-awards-300447740.html

News Article | October 23, 2015
Site: www.nature.com

In this Letter, author Yong-Bin Yan was incorrectly associated with affiliation number 5 (Department of Ophthalmology, Xijing Hospital) instead of affiliation number 4 (State Key Laboratory of Membrane Biology, School of Life Sciences, Tsinghua University, Beijing 100084, China). Also, an additional affiliation has been added to author Kang Zhang (number 15; Institute of Molecular Medicine, Peking University, Beijing 100871, China), and affiliation number 3 has changed from ‘Department of Ophthalmology and Biomaterials and Tissue Engineering Center’ to ‘Shiley Eye Institute and Biomaterials and Tissue Engineering Center’. These have all been corrected in the online versions of the paper.

Yin X.,PLA Fourth Military Medical University | Yin Y.,PLA Fourth Military Medical University | Cao F.-L.,The 222th Hospital of CPLA | Chen Y.-F.,PLA Fourth Military Medical University | And 4 more authors.
PLoS ONE | Year: 2012

Background: Spinal cord injury (SCI), including immediate mechanical injury and secondary injury, is associated with the inflammatory response, apoptosis and oxidative stress in response to traumatic injury. Tanshinone IIA (TIIA) is one of the major extracts obtained from Salvia miltiorrhiza BUNGE, which has anti-inflammatory and anti-apoptotic effects on many diseases. However, little is known about the effects of TIIA treatment on SCI. Therefore, the aim of the present study is to evaluate the pharmacological action of TIIA on secondary damage and the underlying mechanisms of experimental SCI in rats. Methodology/Principal Findings: SCI was generated using a weight drop device on the dorsal spinal cord via a two-level T9-T11 laminectomy. SCI in rats resulted in severe trauma, characterized by locomotor disturbance, edema, neutrophil infiltration, the production of astrocytes and inflammatory mediators, apoptosis and oxidative stress. TIIA treatment (20 mg/kg, i.p.) after SCI induced significant effects: (1) improved motor function (Basso, Beattie and Bresnahan scores), (2) reduced the degree of tissue injury (histological score), neutrophil infiltration (myeloperoxidase activity) and the expression of astrocytes, (3) inhibited the activation of SCI-related pathways, such as NF-κB and MAPK signaling pathways, (4) decreased the production of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and iNOS, (5) reduced apoptosis (TUNEL staining, and Bcl-2 and caspase-3 expression) and (6) reversed the redox state imbalance. Conclusions/Significance: The results clearly show that TIIA has a prominent protective effect against SCI through inhibiting the inflammatory response and apoptosis in the spinal cord tissue after SCI. © 2012 Yin et al.

Yang M.,Xijing Hospital | Yan M.,Xijing Hospital | Zhang R.,PLA Fourth Military Medical University | Li J.,Xijing Hospital | Luo Z.,Xijing Hospital
Cancer Science | Year: 2011

It has been proven that "side population (SP)" cells that exclude Hoechst 33342 dye are enriched with cancer stem cells in several tumors. In the present study we aimed to isolate and characterize SP cells from human primary osteosarcoma. Side population cells were detected in osteosarcoma samples. In vitro, SP cells regenerated both SP and non-SP and the clonogenicity of SP cells was higher than that of non-SP cells, just like stem cells. In vivo, SP cells exhibited heightened tumorigenicity and only the SP fraction had the capacity to self- renew both in vitro and in vivo. Furthermore, SP cells exhibited increased multidrug resistance and the RNA expression of ATP-binding cassette protein transporters was increased in the SP group. In addition, "stemness" genes Oct-4 and Nanog were also upregulated in the SP group. However, the expression of other putative stem cell markers (CD44, CD117 and CD133) had no significant difference between SP and non-SP for each individual marker. These findings suggest that SP cells derived from osteosarcoma are enriched with tumorigenic cells with stem-like properties and might be an ideal target for clinical therapy. © 2011 Japanese Cancer Association.

Wang R.-A.,Xijing Hospital | Wang R.-A.,PLA Fourth Military Medical University
Cancer and Metastasis Reviews | Year: 2014

Gene mutation’s role in initiating carcinogenesis has been controversial, but it is consensually accepted that both carcinogenesis and cancer metastasis are gene-regulated processes. MTA1, a metastasis-associated protein, has been extensively researched, especially regarding its role in cancer metastasis. In this review, I try to elucidate MTA1’s role in both carcinogenesis and metastasis from a different angle. I propose that MTA1 is a stress response protein that is upregulated in various stress-related situations such as heat shock, hypoxia, and ironic radiation. Cancer cells are mostly living in a stressful environment of hypoxia, lack of nutrition, and immune reaction attacks. To cope with all these stresses, MTA1 expression is upregulated, plays a role of master regulator of gene expression, and helps cancer cells to survive and migrate out of their original dwelling. © 2014, The Author(s).

Shi C.,PLA Fourth Military Medical University | Shi J.,Xijing Hospital | Xu Z.,PLA Fourth Military Medical University
Scandinavian Journal of Infectious Diseases | Year: 2011

The mechanisms of latency and the causes of reactivation of Mycobacterium tuberculosis remain poorly understood; an important reason for this gap in knowledge is the absence of a standardized animal model of latent tuberculosis infection (LTBI). A complete LTBI model should incorporate 2 aspects of LTBI: a persistent infection model with a low bacterial load and a latent infection model that is modified from the Cornell model. Many parameters must be carefully considered to establish an LTBI model, including the inoculating dose, the route of infection, the time interval between infection and the initiation of antibiotic therapy, and the genetic background of the host animal. The responsiveness of this mouse model of LTBI can be assessed through the integrated use of indices, including Karnofsky performance status, bacterial load in spleen and lungs, induced levels of interferon-gamma and tumour necrosis factor-alpha, expression of interleukin (IL)-10 and IL-4 in tissues, specific antigen load in organs, time required for hormone-induced TB relapse, expression level of dormancy genes, and CD4 T-cell count. © 2011 Informa Healthcare.

Ye R.,Nanjing University | Zhao G.,Xijing Hospital | Liu X.,Nanjing University
Expert Review of Neurotherapeutics | Year: 2013

Numerous studies have identified pathophysiological mechanisms of acute ischemic stroke and have provided proof-of-principle evidence that strategies designed to impede the ischemic cascade, namely neuroprotection, can protect the ischemic brain. However, the translation of these therapeutic agents to the clinic has not been successful. Ginsenoside Rd, a dammarane-type steroid glycoside extracted from ginseng plants, has exhibited an encouraging neuroprotective efficacy in both laboratory and clinical studies. This article attempts to provide a synopsis of the physiochemical profile, pharmacokinetics, pharmacodynamics, clinical efficacy, safety and putative therapeutic mechanisms of Rd. Finally, the authors discuss the validity of Rd as a neuroprotective agent for acute ischemic stroke. © 2013 Expert Reviews Ltd.

Yi X.,Xijing Hospital | Zhang G.,Xijing Hospital | Yuan J.,Xijing Hospital
Transplantation Proceedings | Year: 2013

Objective: Donor preconditioning by fenoldopam is demonstrated to improve graft function in recipients. Involvement of hypoxia-inducible factor-1alpha (HIF-1α) and heme oxygenase-1 (HO-1) in renoprotection after fenoldopam pretreatment was investigated. Methods: Donor Sprague-Dawley (SD) rats were intravenously treated with fenoldopam (5 μg/kg · min), Sch23390 (10 μg/kg · min), or fenoldopam + Sch23390 for 1 hour. Kidneys experiencing 24 hours of cold preservation were transplanted into syngeneic SD recipients. Ten days after transplantion, serum concentrations of creatinine (sCR), blood urea nitrogen (BUN), interleukin (IL)-8, and tumor necrosis factor (TNF)-α in recipient were determined. Grafts were procured for histopathological examination, apoptosis analysis, and measurements of malondialdehyde and total superoxide dismutase activities; meanwhile, both protein level and mRNA level of HIF-1α and HO-1 were assessed. Results: Fenoldopam preconditioning significantly decreased the serum concentrations of sCR, BUN, IL-8, and TNF-α in recipients. Low apoptosis rate and reduced oxidative stress were found in these grafts. Increased HIF-1α activation and HO-1 expression were observed in fenoldopam pretreatment group. Sch23390 partly inhibited the effects of fenoldopam in the combination group. Conclusion: Donor preconditioning by fenoldopam exerts renoprotection in grafts, at least in part, through HIF-1α activation and HO-1 expression. This provides a preference for further studies. © 2013 Elsevier Inc.

Zhang X.Y.,Xijing Hospital
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2011

This study was aimed to investigate the effect of curcumin in combination with bortezomib on the proliferation and apoptosis of human MM cell line H929 in vitro, and to explore its mechanisms. MTT assay was applied to detect the inhibitory effects of curcumin and bortezomib either alone or combined at different concentrations on H929 cells, and flow cytometry was employed to assay the apoptosis rate. In addition, RT-PCR was used to analyze the mRNA expression of gene BCL-2, BAX, cyclin D1. Immunofluorescence technique was performed to study the location changes of NF-κB P65 in different groups. The results showed that both curcumin and bortezomib inhibited the proliferation of MM cell line H929 in dose-dependent manner, and combination of these two drugs displayed synergistical effect. A much higher apoptosis rate was determined by flow cytometry in combinative groups than that in single or control group. And RT-PCR showed, as compared with curcumin or bortezomib group, there was mRNA expression decrease of BCL-2, cyclin D1 but increase of BAX in combined group. The expression of NF-κB P65 in nucleus was downregulated in either the curcumin or bortezomib group, however, distribution of NF-κB P65 in cytoplasm was observed in combined group. It is concluded that the combination of curcumin and bortezomib is much more effective for the inhibiting proliferation and promoting apoptosis of H929 cell line, which may function by inhibiting the transcription of NF-κB and apoptosis-related genes.

To observe the influence of electroacupuncture (EA) of "Chize" (LU 5, He-sea acupoint) and "Shangjuxu" (ST 37, lower He-sea acupoint) on mesenteric microcirculation, vasoactive intestinal peptide (VIP) levels in the lung, colon and hypothalamus tissues in rats with chronic obstructive pulmonary disease (COPD), so as to investigate its mechanism underlying improvement of lung derived intestinal disorders in clinical practice. Thirty-two male Wistar rats were randomly divided into normal control, model, EA-Chize (LU 5, EA-LU 5) and EA-Shangjuxu (ST 37, EA-ST 37) groups, with 8 rats being in each group. COPD model was established by intratracheal infusion of Lipopolysaccharide (LPS, 1 mg/mL, 0.2 mL/rat) and forced inhaling smoke, once daily for 28 days. EA was applied to bilateral LU 5 and ST 37 for 20 min, once every other day for 12 sessions. The state of mesenteric microcirculation was observed under microscope and divided into grade 0 (stagnation of blood flow), I (slow flowing and silt-like state), II (faster flowing with slight or obvious grainy feeling) and III (fast flowing without grainy feeling). The contents of VIP in the lung, colon and hypothalamus were detected using radioimmunoassay (RIA). Following modeling, the microvascular calibers were increased slightly in the model, EA-LU 5 and EA-ST 37 groups. Compared with the normal group, the blood flow velocity was increased significantly in model group (P < 0.05). In comparison with the model group, the blood flow velocity was reduced significantly in EA-LU 5 and EA-ST 37 groups (P < 0.01). There were no significant differences between EA-LU 5 and EA-ST 37 groups in blood flow velocity, among the four groups in VIP contents of the lung tissue (P > 0.05). The content of VIP in the colon was markedly higher in the model group than in the normal group, and that in the hypothalamus was obviously lower in the EA-LU 5 group than in the model group (all P < 0.05). EA stimulation of "Chize" (LU 5) can notably reduce hypothalamic VIP content and slow down blood flow velocity of the mesenteric microvessels in COPD rats.

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