Hanzhong, China

Nanjing Medical University

www.njmu.edu.cn
Hanzhong, China

Nanjing Medical University is a university in Nanjing, Jiangsu Province, China. It was established in 1934 in Zhenjiang, but subsequently relocated to Nanjing in 1957. The university has two main campuses: Wutai and Jiangning, both of which have international student apartments.In 2014, Academic Ranking of World Universities ranked it between 401-500 in the world and 26-32 in China. It was one of the first universities to offer an English taught Bachelor of Medicine, Bachelor of Surgery program, as approved by the Ministry of Education of the People's Republic of China . Wikipedia.

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Microbiome leader Prof. Borody at China FMT Conference calls for Investment in Faecal Transplant Clinical Trials to Fight Serious Diseases A future where faecal transplants in China will cure conditions like autism, IBD, arthritis, Parkinson's disease and even MS was presented by global Faecal Microbiota Transplantation (FMT) leader Professor Thomas Borody (MD, PhD) in his keynote presentation on non Clostridium difficile conditions, to open the international China Microbiota Transplantation Conference in Nanjing (April 12-14, 2017). Professor Borody, the Founder and Medical Director of the Centre for Digestive Diseases (CDD) in Sydney, Australia said many diseases have a unique microbiome profile which can be progressively changed to a normal profile with FMT treatment. At the state-of-the-art CDD facility, Prof. Borody and his team have performed more than 12,000 FMTs. Prof. Borody is at the forefront of FMT research, being the first to report successful treatment of IBD in 1988. He invented, among other therapies, the freeze-dried oral FMT capsule system. He is also recognized as the first physician to successfully formulate the highly effective Triple Therapy that would become the gold standard for treating Helicobacter pylori infection, which can lead to peptic ulcers and stomach cancer, so common in China. In his keynote presentation, Prof. Borody also shared findings from recent ground-breaking clinical trials in IBD and autism, which he personally designed and remained involved in, as examples of the need for greater FMT clinical trial investment in serious diseases: -- The FOCUS Study - the first adequately powered randomized double blind controlled trial for ulcerative colitis -- The Autism Study - where cognitive improvement change was found after just 5 weeks of treatment He said more research funding was needed to bring FMT treatment into the mainstream medical world. "The healthy human flora or its components, appears to be the most complete probiotic treatment available today, capable of eradicating 'bad' bacteria and spores and supplying 'good' bacteria for recolonization of the damaged gut microbiome," said Prof. Borody. Prior to the conference Prof. Borody visited the FMT Bank in Nanjing with China's FMT leader Professor Faming Zhang, who was the first to perform FMT in China and has carried out over 1600 treatments to date. Prof. Borody has collaborated closely with Professor Faming Zhang, who is the Director of Intestinal Diseases Center at the 2nd Affiliated Hospital, Nanjing Medical University. Like the US and Australia, China is facing increasing challenges around the management of diseases, many with rising incidence including IBD, Parkinson's disease, MS, and many autoimmune conditions. About: What is Faecal Microbiota Transplantation The human bowel contains a complex population of bacteria known as the gut microbiota. These organisms and the chemicals they produce can affect the bowel and the body as a whole, and these effects can have both positive and negative impacts on a person's health. The human gut microbiota protects us from pathogenic or 'bad' bacteria. FMT involves the infusion of healthy human donor faecal bacteria via colonoscope or enema into a bowel that contains abnormal bacteria that are making the bowel 'sick'. This infusion process can be a single infusion or it can be repeated over a period of time, depending on the severity of the patient's condition. The use of healthy human flora appears to be the most complete probiotic treatment available today, capable of eradicating 'bad' bacteria and spores and supplying 'good' bacteria for recolonisation of the gut in certain conditions. The Centre for Digestive Diseases offers FMT primarily for the treatment of Clostridium difficile and treats selected patients with ulcerative colitis, irritable bowel sydrome, constipation and Crohn's disease. Other conditions are assessed on a case by case basis. About: Prof. Thomas Borody BSc (MED) (HONS), MBBS (HONS), MD, PhD, DSc, FRACP, FACG, FACP, AGAF Medical Director, Gastroenterologist (www.cdd.com.au) Prof. Thomas Borody is the founder and Medical Director of CDD. His keen interest in medical research led to the establishment of the Centre to provide both diagnostic procedures and effective treatments. Prof. Borody has published over 250 articles and abstracts. His knowledge and expertise has been sought after by patients from around the world. He is a reviewer for numerous medical journals and has developed novel therapies in gastrointestinal areas such as Inflammatory Bowel Disease, Irritable Bowel Syndrome, Parasite infestation, ulcer disease and resistant Helicobacter pylori and C. difficile. Prof. Borody continues to conduct research in order to improve current therapies and develop new treatments. Contact: Susan Fitzpatrick-Napier Digital Mantra Group SG +65 6809 3869 AU +61 2 8218 2144 USA +1 650 798 5238


Microbiome leader Prof. Borody at China FMT Conference calls for Investment in Faecal Transplant Clinical Trials to Fight Serious Diseases A future where faecal transplants in China will cure conditions like autism, IBD, arthritis, Parkinson's disease and even MS was presented by global Faecal Microbiota Transplantation (FMT) leader Professor Thomas Borody (MD, PhD) at the opening of the China Microbiota Transplantation Conference in Nanjing, in his keynote presentation on non Clostridium difficile conditions (April 12-14, 2017). Professor Borody, the founder and Medical Director of the Centre for Digestive Diseases (CDD) in Sydney, Australia said many diseases have a unique microbiome profile which can be progressively changed to a normal profile with FMT treatment (www.cdd.com.au). The conference, hosted by the Chinese Medical Doctor Association, attracted more than 700 attendees with 50 oral presentations from China, Australia, USA and Europe. FMT has its origins in China with earliest treatments dating back to the 4th century. Prof. Borody is at the forefront of FMT research being first to report successful treatment of IBD in 1988. He invented, among other therapies, the freeze-dried oral FMT capsule system. He is also globally recognized as the first physician to successfully formulate the highly effective Triple Therapy that become the gold standard for treating Helicobacter pylori infection, which can lead to peptic ulcers and stomach cancer, so common in China. Prof. Borody in his presentation also shared findings from recent ground-breaking clinical trials in IBD and autism that he personally designed and was involved as an example of the need for greater FMT clinical trial investment in serious diseases: -- The FOCUS Study -- the first adequately powered randomized double blind controlled trial for ulcerative colitis -- The Autism Study -- where cognitive improvement change was found after just 5 weeks of treatment At the CDD, Prof. Borody has had success using FMT in a broad range of conditions including IBS, IBD, autism and other neurological and autoimmune diseases. He said more research funding was needed to bring FMT treatment into the mainstream medical world. "We've seen profound remission in three MS patients that are out of wheelchairs," he said. Like the US and Australia China is facing increasing challenges around the management of diseases, many with rising incidence including IBD, Parkinson's disease, MS, and many autoimmune conditions. At the state-of-the-art CDD facility in Sydney Prof. Borody and his team have performed more than 12,000 FMTs. "The healthy human flora or its components, appears to be the most complete probiotic treatment available today, capable of eradicating 'bad' bacteria and spores and supplying 'good' bacteria for recolonization of the damaged gut microbiome," said Prof. Borody. Prior to the conference Prof. Borody visited the FMT Bank in Nanjing with China's FMT leader Professor Faming Zhang, who was the first to perform FMT in China and has carried out over 1600 treatments to date. Prof. Borody has collaborated closely with Professor Faming Zhang, the Director of Intestinal Diseases Center at the 2nd Affiliated Hospital, Nanjing Medical University. About: What is Faecal Microbiota Transplantation The human bowel contains a complex population of bacteria known as the gut microbiota. These organisms and the chemicals they produce can affect the bowel and the body as a whole, and these effects can have both positive and negative impacts on a person's health. The human gut microbiota protects us from pathogenic or 'bad' bacteria. FMT involves the infusion of healthy human donor faecal bacteria via colonoscope or enema into a bowel that contains abnormal bacteria that are making the bowel 'sick'. This infusion process can be a single infusion or it can be repeated over a period of time, depending on the severity of the patient's condition. The use of healthy human flora appears to be the most complete probiotic treatment available today, capable of eradicating 'bad' bacteria and spores and supplying 'good' bacteria for recolonisation of the gut in certain conditions. The Centre for Digestive Diseases offers FMT primarily for the treatment of Clostridium difficile and treats selected patients with ulcerative colitis, irritable bowel sydrome, constipation and Crohn's disease. Other conditions are assessed on a case by case basis. About: Prof. Thomas Borody BSc (MED) (HONS), MBBS (HONS), MD, PhD, DSc, FRACP, FACG, FACP, AGAF Medical Director, Gastroenterologist (www.cdd.com.au) Prof. Thomas Borody is the founder and Medical Director of CDD. His keen interest in medical research led to the establishment of the Centre to provide both diagnostic procedures and effective treatments. Prof. Borody has published over 250 articles and abstracts. His knowledge and expertise has been sought after by patients from around the world. He is a reviewer for numerous medical journals and has developed novel therapies in gastrointestinal areas such as Inflammatory Bowel Disease, Irritable Bowel Syndrome, Parasite infestation, ulcer disease and resistant Helicobacter pylori and C. difficile. Prof. Borody continues to conduct research in order to improve current therapies and develop new treatments. Contact: Susan Fitzpatrick-Napier Digital Mantra Group SG +65 6809 3869 AU +61 2 8218 2144 USA +1 650 798 5238 Home | About us | Services | Partners | Events | Login | Contact us | Privacy Policy | Terms of Use | RSS


Jin X.,Nanjing Medical University
European Journal of Neuroscience | Year: 2016

Neural stem cells (NSCs) give rise to neurons during development. NSCs persist and neurogenesis continues in restricted regions of postnatal and adult brains. Adult-born neurons integrate into existing neural circuits by synaptic connections and participate in the regulation of brain function. Thus, understanding NSCs and neurogenesis may be crucial in the development of new strategies for brain repair. Here, we introduce the lineage of NSCs from embryonic to adult stages and summarize recent studies on maturation and integration of adult-born neurons. We also discuss the regulation and potential functions of adult neurogenesis in physiological and pathological conditions. © 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd


Sun B.,Nanjing Medical University | Karin M.,University of California at San Diego
Trends in Pharmacological Sciences | Year: 2014

Inflammation has been implicated in the initiation and progression of gastrointestinal (GI) cancers. Inflammation also plays important roles in subverting immune tolerance, escape from immune surveillance, and conferring resistance to chemotherapeutic agents. Targeting key regulators and mediators of inflammation represents an attractive strategy for GI cancer prevention and treatment. However, the targeting of inflammation in GI cancer is not straightforward and sometimes inflammation may contribute to tumor regression. We discuss the origins and effects of inflammation in GI cancer and how to target it successfully. © 2014 Elsevier Ltd.


Sun L.,Nanjing Medical University
Journal of the National Cancer Institute | Year: 2013

Epithelial-to-mesenchymal transition (EMT) plays a pivotal role in lung cancer metastasis. The class III deacetylase sirtuin 1 (SIRT1) possesses both pro- and anticarcinogenic properties. The role of SIRT1 in lung cancer EMT is largely undefined. The effect of SIRT1 on migration of lung cancer cells was evaluated by wound healing assay in vitro and metastasis assay in nude mice in vivo. Protein expression in human lung cancers and cultured lung cancer cells was assessed by western blotting and immunohistochemistry. Interaction between protein and DNA was measured by chromatin immunoprecipitation assay. SIRT1 promoter activity was determined by reporter assay. SIRT1 activation antagonized migration of lung cancer cells by suppressing EMT in vitro. Activation of SIRT1 by resveratrol also statistically significantly hampered (by 68.33%; P < .001, two-sided test) lung cancer cell metastasis in vivo. Hypoxia repressed SIRT1 transcription through promoting the competition between Sp1 and HIC1 on the SIRT1 proximal promoter in a SUMOylation-dependent manner. Disruption of SUMOylation by targeting either Ubc9 or PIASy restored SIRT1 expression in and favored an epithelial-like phenotype of cancer cells, thereby preventing metastasis. Decreased SIRT1 combined with elevated PIASy expression was implicated in more-invasive types of lung cancers in humans. We have identified a novel pathway that links SIRT1 down-regulation to hypoxia-induced EMT in lung cancer cells and may shed light on the development of novel antitumor therapeutics.


Triggering receptor expressed on myeloid cells 2 (TREM2) gene is a recently identified susceptibility gene for Alzheimer's disease (AD), as its low-frequency variants increase the risk of this disease with an odds ratio similar to that of an APOE e{open}4 allele. To date, the expression and biologic functions of TREM2 under AD context remain largely unknown. Using APPswe/PS1dE9 mice, a transgenic model of AD, we showed that TREM2 was upregulated in microglia during disease progression. For the first time, we provided in vitro and in vivo evidence that this upregulation was attributed to the increased amyloid-β (Aβ)1-42 levels in the brain. By knockdown and overexpression of TREM2 in cultured primary microglia, we revealed that TREM2 modulated microglial functions under AD context, as it facilitated Aβ1-42 phagocytosis and inhibited Aβ1-42-triggered proinflammatory responses. Meanwhile, this modulation was dependent on DAP12, the adapter protein of TREM2. More importantly, overexpression of TREM2 in the brain of APPswe/PS1dE9 mice markedly ameliorated AD-related neuropathology including Aβ deposition, neuroinflammation, and neuronal and synaptic losses, which was accompanied by an improvement in spatial cognitive functions. Taken together, our data suggest that the upregulation of TREM2 serves as a compensatory response to Aβ1-42 and subsequently protects against AD progression by modulation of microglia functions. These findings provide insights into the role of TREM2 in AD pathogenesis, and highlight TREM2 as a potential therapeutic target for this disease.Neuropsychopharmacology advance online publication, 20 August 2014; doi:10.1038/npp.2014.164.


Hereditary retinal dystrophies (HRDs) are a group of monogenic diseases characterized by an irreversible loss of photoreceptors. HRDs exhibit significant genetic and clinical heterogeneities challenging traditional techniques for determining disease-causal mutations. This study aims to develop an efficient molecular diagnostic platform for HRDs, and to determine the genetic basis for 25 randomly collected Chinese families with a variety of HRDs. We designed a high throughput sequence capture microarray targeting 179 genes associated with HRDs and 10 candidate genes. We combined sequence capture with next-generation sequencing (NGS) to screen for mutations in the cohort of Chinese families. Variants detected by NGS were filtered, validated, and prioritized by pathogenicity analysis. Genotypes and phenotypes were correlated. We identified four recurrent single mutations, two compound mutations, and eight novel putative causative mutations, including five putative pathogenic alleles (e.g., premature stop codons and frame shifts) and three novel missense variants that are very likely pathogenic. These findings provided specific genetic diagnoses in 14 of 25 families (56%). Among these, identification of a mutation in VCAN in a family with a complicated phenotype helped to finalize the clinical diagnosis as Wagner syndrome. In another five families, 11 potential novel pathogenic variants were identified. A substantial number of potential new genes and new mutations associated with HRDs remain to be discovered. Identification of the novel HRDs-causing mutations in our study not only provides a better understanding of genotype-phenotype relationships in these diseases, but also demonstrates that the approach described herein is an effective method for large scale mutation detection among diverse and complicated HRDs cases.


What is the profile of miRNAs in seminal plasma of patients with non-obstructive azoospermia (NOA)? miR-141, miR-429 and miR-7-1-3p are significantly increased in seminal plasma of patients with NOA compared with fertile controls. There is currently an urgent need to develop a noninvasive diagnostic test for NOA. Altered microRNA (miRNA) profiles have been proposed as potential biomarkers for the diagnosis of disease states. A total of 200 subjects (n = 100 for NOA, n = 100 for fertile control) were recruited to participate in this study. Recruitment took place from May 2008 to June 2010. We employed a strategy consisting of initial screening by TaqMan Low Density Array then further validation with a TaqMan quantitative RT-PCR assay. Validation of the profiling results was conducted in two independent phases. In addition, the expression of the three validated seminal plasma miRNAs (sp-miRNAs) was examined in testicular tissues of patients with NOA and of fertile controls. Methylation status and functional analyses were also performed for the identified sp-miRNAs. miR-141, miR-429 and miR-7-1-3p were significantly increased in seminal plasma of patients with NOA compared with fertile controls. As sensitive and specific biomarkers, the profiling of these three identified sp-miRNAs provides a novel noninvasive, semen-based test for NOA diagnosis. The methylation status of these sp-miRNAs was inversely associated with their expression patterns. Additionally, we found that Cbl and Tgfβ2 were down-regulated by miR-141, while Rb1 and Pik3r3 were down-regulated by miR-7-1-3p. miRNA expression profile was investigated in seminal plasma samples from only a small number of NOA patients. In future investigations, a larger sample size should be adopted and the functional role of the three sp-miRNAs should be further characterized in animal models. Given that sp-miRNAs show reproducible and stable expression levels, they are potentially novel noninvasive biomarkers for the diagnosis of NOA. We propose that the three sp-miRNAs described above may participate in a methylation-miRNA-gene network related to NOA development. This work provides a foundation for interpretation of miRNA changes associated with pathogenesis of NOA and extends the current understanding of human NOA pathogenesis.


Patent
Nanjing Medical University | Date: 2016-03-23

Provided is a polypeptide having anti-tumor activity. The amino acid sequence of the polypeptide is FPGSDRF, X-FPGSDRF, FPGSDRF-Z, or X-FPGSDRF-Z, S being a phosphorylated serine residue, X and Z each being an amino acid residue or an amino acid sequence, X being selected from one of F, (R)9, (R)9-F, 6-aminocaproic acid, 6-aminocaproic acid-F, 6-aminocaproic acid-(R)9, and 6-aminocaproic acid-(R)9-F, and Z being selected from one of A, (G) n-RGD, and A-(G)n-RGD. The polypeptide has no toxicity for normal histocytes. However, when being used with chemicals (such as arsenic trioxide), the polypeptide can increase toxicity for tumor cells. Also provided are uses of the polypeptide for preparing anti-tumor drugs.


An anti-tumor polypeptide, having an amino acid sequence represented by FPGSDRF (SEQ ID NO. 15), X-FPGSDRF, FPGSDRF-Z, or X-FPGSDRF-Z, in which the various capital letters denote amino acids: F: phenylalanine; P: proline; G: glycine; S: serine; D: aspartic acid; R: arginine; S is a phosphorylated serine residue, X and Z are an amino acid residue or an amino acid sequence, respectively, X is one selected from the group consisting of F, (R)_(9), (R)_(9)-F, 6-aminocaproic acid, 6-aminocaproic acid-F, 6-aminocaproic acid-(R)_(9), and 6-aminocaproic acid-(R)_(9)-F, Z is one selected from the group consisting of A, (G)_(n)-RGD, and A-(G)_(n)-RGD; and n is an integer greater than or equal to 0.

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