Nantong, China

Nantong University
Nantong, China

Nantong University , colloquially known in Chinese as Tong da , was established in 1912. The university is located in Nantong, Jiangsu province, China. It occupies 4000 acres and have 800 thousand square meters used for school buildings. Nantong is comprehensive university constructed by Jiangsu Provincial Government and the state Ministry of Transport. It is composed of three parts, Nantong Medical College, Nantong Engineering College and Nantong Normal College and has four campuses: the new campus, Qixiu campus, Zhongxiu campus and Qidong campus. The enrollment is nearly 34 thousand full-time students, among whom 1550 are graduates and 300 are oversea students. The university has 84 undergraduate programs based on nine major disciplines, which are literature, science, engineering, medical science, education, economics, law, history and management. Wikipedia.

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News Article | May 23, 2017

DURHAM, N.C. -- Once hailed as a breakthrough in cancer treatment, immunotherapies are now raising concerns as doctors note new side effects like severe allergic reactions, acute-onset diabetes and heart damage. These drugs, which work by unleashing the immune system to fight cancer, are only effective in about a fifth of cases, prompting many patients to wonder if they are worth the risk. But a new study from Duke University researchers suggests there may be a quick and easy way to predict which cancer patients are likely to benefit from immunotherapy treatments. The researchers showed that a molecule called PD-L1, which is blocked by the popular immunotherapy drug nivolumab, acts not only on immune cells but also on the nerve cells that signal pain. That insight could lead to a simple test that measures subtle differences in pain sensitivity to gauge whether or not the body is responding to treatment. The findings, published May 22 in Nature Neuroscience, underscore the surreptitious nature of cancer, which uses a variety of tricks to evade detection by the body's natural defense mechanisms. "Cancer cells are smart. We already knew that they produced PD-L1 to suppress the immune system," said senior study author Ru-Rong Ji, Ph.D., professor of anesthesiology and neurobiology at Duke University School of Medicine. "But there's another defense system at play as well, and that is pain. We showed that this well-known molecule can mask pain, so that cancers can grow without setting off any alarms before metastasis." In its early stages, when cancer cells are just starting to grow and multiply in a given tissue or organ, the disease is not usually painful. But as the cancer becomes more aggressive and spreads throughout the body, these cells secrete thousands of pain-inducing chemicals, which either trigger pain-sensing nerve fibers or, in the case of molecules like nerve growth factor, generate entirely new ones. The pain can become so unbearable that some cancer patients die from opioid overdoses. Ji has been studying pain for over twenty years. Recently, his group noticed that mouse models of melanoma didn't show the typical signs of pain that he observed in mice with other kinds of cancer, which would flinch or lick their hind paws whenever they were in discomfort. Ji also knew that melanoma cells could produce a molecule called PD-L1, which latched onto a receptor called PD-1 on the surface of white blood cells, effectively putting the brakes on the immune response. Ji wondered whether there was a connection. So his team treated mice with nivolumab, a drug that prevents PD-L1 from binding to PD-1. Then they poked the animals' hind paws with a calibrated filament and measured how much force it took for them to withdraw their hind paws. They found that the mice responded to much lower forces than before treatment, indicating they had become more sensitive to pain. In addition, they also found that nivolumab caused spontaneous pain in mice with melanoma, which made them tend to their affected hindpaws like never before. Next, the researchers performed the opposite experiment. They injected PD-L1 -- the pain-masking factor in this equation -- into the hind paws or spinal cord of mouse models of three different kinds of pain -- inflammatory, neuropathic and bone cancer pain. In every case, the injections of PD-L1 had an analgesic effect, deadening the mice's sensitivity to pain. "The effect was surprisingly fast," said Ji. "We saw a reduction of pain in under half an hour." To figure out the mechanism behind this quick response, Ji's team examined the sensory neurons of the dorsal root ganglion (DRG), a collection of nerves and neurons near the top of the spinal cord. They isolated these cells from mouse DRGs as well as human DRGs from donors and cultured them in a dish, with or without PD-L1, and then recorded their electrical activity. The researchers found that PD-L1 impaired the ability of sodium channels to fire neurons (action potentials) in response to pain. Ji believes the finding could potentially lead to new treatments for pain, as well as new ways to predict the efficacy of already existing treatments based on PD-1 and PD-L1. "The response to cancer drugs can take a long time, weeks to months," he said. "The response to pain happens in minutes to hours." In the future, Ji would like to explore whether the mechanism uncovered in this study also applies to other immunotherapy treatments. He is also interested in working with clinicians to measure changes in patients' pain sensitivity after treatment, a first step toward developing a diagnostic test. The study was a collaboration between Duke University and two Chinese universities, Fudan University and Nantong University. Professor Yu-Qiu Zhang from Fudan University, the co-senior author of the paper, is a well-known expert in cancer pain. The lead author, Dr. Gang Chen, was an Assistant Professor at Duke and is now a Professor at Nantong. The research was supported by the National Institutes of Health (NS87988, DE17794, and DE22743), the National Science Fund of China (31420103903), and the National Research Foundation of Korea (2013R1A6A3A04065858) CITATION: "PD-L1 inhibits acute and chronic pain by suppressing nociceptive neuron activity via PD-1," Gang Chen, Yong Ho Kim, Hui Li, Hao Luo, Da-Lu Liu, Zhi-Jun Zhang, Mark Lay, Wonseok Chang, Yu-Qiu Zhang, and Ru-Rong Ji. Nature Neuroscience, May 22, 2017. DOI: doi:10.1038/nn.4571

Ji R.-R.,Duke University | Xu Z.-Z.,Duke University | Gao Y.-J.,Nantong University
Nature Reviews Drug Discovery | Year: 2014

Current analgesics predominately modulate pain transduction and transmission in neurons and have limited success in controlling disease progression. Accumulating evidence suggests that neuroinflammation, which is characterized by infiltration of immune cells, activation of glial cells and production of inflammatory mediators in the peripheral and central nervous system, has an important role in the induction and maintenance of chronic pain. This Review focuses on emerging targets-such as chemokines, proteases and the WNT pathway-that promote spinal cord neuroinflammation and chronic pain. It also highlights the anti-inflammatory and pro-resolution lipid mediators that act on immune cells, glial cells and neurons to resolve neuroinflammation, synaptic plasticity and pain. Targeting excessive neuroinflammation could offer new therapeutic opportunities for chronic pain and related neurological and psychiatric disorders. © 2014 Macmillan Publishers Limited.

Yu B.,Nantong University | Zhou S.,Nantong University | Yi S.,Nantong University | Gu X.,Nantong University
Progress in Neurobiology | Year: 2015

Non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), have attracted much attention since their regulatory roles in diverse cell processes were recognized. Emerging studies demonstrate that many ncRNAs are differentially expressed after injury to the nervous system, significantly affecting nerve regeneration. In this review, we compile the miRNAs and lncRNAs that have been reported to be dysregulated following a variety of central and peripheral nerve injuries, including acquired brain injury, spinal cord injury, and peripheral nerve injury. We also list investigations on how these miRNAs and lncRNAs exert the regulatory actions in neurodegenerative and neuroregenerative processes through different mechanisms involving their interaction with target coding genes. We believe that comprehension of the expression profiles and the possible functions of ncRNAs during the processes of nerve injury and regeneration will help understand the molecular mechanisms responsible for post-nerve-injury changes, and may contribute to the potential use of ncRNAs as a diagnostic marker and therapeutic target for nerve injury. © 2015 Elsevier Ltd.

Gu X.,Nantong University | Ding F.,Nantong University | Yang Y.,Nantong University | Liu J.,Nantong University
Progress in Neurobiology | Year: 2011

Surgical repair of severe peripheral nerve injuries represents not only a pressing medical need, but also a great clinical challenge. Autologous nerve grafting remains a golden standard for bridging an extended gap in transected nerves. The formidable limitations related to this approach, however, have evoked the development of tissue engineered nerve grafts as a promising alternative to autologous nerve grafts. A tissue engineered nerve graft is typically constructed through a combination of a neural scaffold and a variety of cellular and molecular components. The initial and basic structure of the neural scaffold that serves to provide mechanical guidance and optimal environment for nerve regeneration was a single hollow nerve guidance conduit. Later there have been several improvements to the basic structure, especially introduction of physical fillers into the lumen of a hollow nerve guidance conduit. Up to now, a diverse array of biomaterials, either of natural or of synthetic origin, together with well-defined fabrication techniques, has been employed to prepare neural scaffolds with different structures and properties. Meanwhile different types of support cells and/or growth factors have been incorporated into the neural scaffold, producing unique biochemical effects on nerve regeneration and function restoration. This review attempts to summarize different nerve grafts used for peripheral nerve repair, to highlight various basic components of tissue engineered nerve grafts in terms of their structures, features, and nerve regeneration-promoting actions, and finally to discuss current clinical applications and future perspectives of tissue engineered nerve grafts. © 2010 Elsevier Ltd.

Yang W.-C.,CAS Institute of Genetics and Developmental Biology | Shi D.-Q.,CAS Institute of Genetics and Developmental Biology | Chen Y.-H.,Nantong University
Annual Review of Plant Biology | Year: 2010

The multicellular female gametophyte, a unique feature of higher plants, provides us with an excellent experimental system to address fundamental questions in biology. During the past few years, we have gained significant insight into the mechanisms that control embryo sac polarity, gametophytic cell specification, and recognition between male and female gametophytic cells. An auxin gradient has been shown for the first time to function in the female gametophyte to regulate gametic cell fate, and key genes that control gametic cell fate have also been identified. This review provides an overview of these exciting discoveries with a focus on molecular and genetic data. Copyright © 2010 by Annual Reviews. All rights reserved.

Wu Y.F.,Nantong University | Tang J.B.,Nantong University
Journal of Hand Surgery: European Volume | Year: 2014

Over the last decade, both basic researchers and surgeons have sought to identify the most appropriate techniques to be applied in flexor tendon repairs. Recent developments in experimental tendon repairs and clinical outcomes of newer repair techniques have been reviewed in an attempt to comprehensively summarize the most critical mechanical factors affecting the performance of tendon repairs and the surgical factors influencing clinical outcomes. Among them, attention to annular pulleys, the purchase and tension of the core suture, and the direction and curvature of the path of tendon motion have been found to be determining factors in the results of tendon repair. © The Author(s) 2013.

Tang J.B.,Nantong University
Hand Clinics | Year: 2013

This article reviews recent reports of outcomes of flexor tendon repair and discusses the problems associated with such surgeries. Reports of no repair rupture in individual case series have emerged recently. Their results move toward the clinical goal of primary repair without repair rupture. The Strickland method remains the most common to record the outcomes. Outcomes should be provided by subzones of the tendon injuries, and the level of expertise of the surgeons expertise should be reported to allow comparisons of the results. © 2013.

Tang J.B.,Nantong University
Journal of Hand Surgery | Year: 2014

During primary or delayed primary repair of the flexor digitorum profundus tendon, surgeons often face difficulty in passing the retracted tendon or repaired tendon under the dense, fibrous A4 pulley. The A4 pulley is the narrowest part of the flexor sheath, proximal to the terminal tendon. Disrupted tendon ends (or surgically repaired tendons) are usually swelling, making passage of the tendons under this pulley difficult or even impossible. During tendon repair in the A4 pulley area, when the trauma is in the middle part of the middle phalanx and the A3 pulley is intact, the A4 pulley can be vented entirely to accommodate surgical repair and facilitate gliding of the repaired tendon after surgery. Venting the pulley does not disturb tendon function when the other major pulleys are intact and when the venting of the A4 pulley and adjacent sheath is limited to the middle half of the middle phalanx. Such venting is easily achieved through a palmar midline or lateral incision of the A4 pulley and its adjacent distal or/and proximal sheath, which helps ensure a more predictable recovery of digital flexion and extension. © 2014 ASSH Published by Elsevier, Inc. All rights reserved.

A tissue engineered nerve graft for repairing peripheral nerve injury consists of a nerve conduit and a extracellular matrix (ECM) that is secreted by autologous or allogeneic support cells and obtained by decellularization. A preparation method of the ECM-modified tissue engineered nerve grafts containing support cells, nerve conduit and constructing a ECM-modified tissue engineered nerve graft.

A tissue engineered nerve graft for repairing peripheral nerve injury consists of a nerve conduit and a extracellular matrix (ECM) that is secreted by autologous or allogeneic support cells and obtained by decellularization. A preparation method of the ECM-modified tissue engineered nerve grafts containing support cells, nerve conduit and constructing a ECM-modified tissue engineered nerve graft.

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