Liu M.-G.,PLA Fourth Military Medical University |
Liu M.-G.,Seoul National University |
Liu M.-G.,Kings College |
Chen J.,PLA Fourth Military Medical University |
And 2 more authors.
Progress in Neurobiology
Affective disorders and cognitive deficits are common comorbidities of chronic pain in the clinical setting, which severely affect the quality of life of pain patients and impose a great difficulty upon clinical pain therapy. Despite large numbers of human studies examining this issue, there are surprisingly few reports investigating the comorbidities of chronic pain in animal models. This review summarizes and integrates previous reports of animal studies on pain and comorbidity, covering pain-evoked anxiety, depression, attentional deficits, cognitive impairment and locomotor dysfunction in rodents. Moreover, pain-induced alterations in synaptic plasticity are also discussed in terms of long-term potentiation and long-term depression, synaptic transmission, neuronal excitability and structural correlates in 'pain matrix'. Finally, we conclude this review by pointing out some unresolved problems and future research directions. © 2014 Elsevier Ltd. Source
Xu X.,CAS Institute of Biophysics |
Duan S.,CAS Institute of Biophysics |
Yi F.,Salk Institute for Biological Studies |
Ocampo A.,Salk Institute for Biological Studies |
And 5 more authors.
Due to their fundamental role in energy production, mitochondria have been traditionally known as the powerhouse of the cell. Recent discoveries have suggested crucial roles of mitochondria in the maintenance of pluripotency, differentiation, and reprogramming of induced pluripotent stem cells (iPSCs). While glycolytic energy production is observed at pluripotent states, an increase in mitochondrial oxidative phosphorylation is necessary for cell differentiation. Consequently, a transition from somatic mitochondrial oxidative metabolism to glycolysis seems to be required for successful reprogramming. Future research aiming to dissect the roles of mitochondria in the establishment and homeostasis of pluripotency, as well as combining cell reprogramming with gene editing technologies, may unearth novel insights into our understanding of mitochondrial diseases and aging. © 2013 Elsevier Inc. Source
Du L.,CAS Institute of Chemistry |
Li J.,CAS Institute of Biophysics |
Chen C.,CAS Institute of Biophysics |
Chen C.,Beijing Institute for Brain Disorders |
Liu Y.,CAS Institute of Chemistry
Free Radical Research
Antioxidants are believed to have great potential for the treatment of diseases that are induced by oxidative stress. However, their pharmaceutical application is severely limited by their poor bioavailability and low biocompatibility. To solve this problem, the antioxidants can be encapsulated or covalently linked with nanomaterials to form nanoantioxidants. In this review, we aim to summarize the use of nanocarriers for antioxidant delivery and discuss their enhancement of antioxidant activity. We also suggest future research directions toward bringing nanoantioxidants into the realm of clinical applications. © 2014 Informa UK, Ltd. Source
Zhao Y.,Shanghai University |
Liu X.-Z.,Shanghai University |
Tian W.-W.,Shanghai University |
Guan Y.-F.,Shanghai University |
And 3 more authors.
CNS Neuroscience and Therapeutics
Aim: Visfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and exists in intracellular and extracellular compartments. The intracellular form of visfatin is proved to be nicotinamide phosphoribosyltransferase (NAMPT) and exhibits neuroprotection through maintaining intracellular NAD+ pool. However, whether extracellular form of visfatin has NAMPT activity and the effect of extracellular visfatin in cerebral ischemia are unknown. Methods and Results: Plasma concentrations of visfatin, NAD+, and ATP were increased in mice upon cerebral ischemia. Cultured glia, but not neuron, was able to secrete visfatin. Oxygen-glucose deprivation (OGD) stress increased the secretion of visfatin from glia. Extracellular recombinant mouse wild-type visfatin, but not mouse H247A-mutant enzymatic-dead visfatin, had NAMPT enzymatic function in vitro. Treatment of wild-type visfatin, but not H247A-mutant enzymatic-dead visfatin, significantly attenuated detrimental effect of OGD on the cell viability and apoptosis in both cultured mouse neuron and glia. Treatment of neutralizing antibody, abolished the protective effect of extracellular visfatin on cell viability, but failed to block the antiapoptotic effect of extracellular visfatin. At last, we observed that plasma visfatin concentrations decreased in 6-month-old but not 3-month-old SHR-SP compared with that in age-matched Wistar-Kyoto rats. Inhibition of NAMPT enzymatic function of visfatin (by FK866) accelerated the occurrence of stroke in SHR-SP. Conclusions: Extracellular visfatin has NAMPT enzymatic activity and maybe be neuroprotective just as intracellular visfatin in cerebral ischemic injury. © 2014 John Wiley & Sons Ltd. Source
Wang L.,CAS Institute of Biophysics |
Wu J.,Salk Institute for Biological Studies |
Fang W.,Beijing Hospital of the Ministry of Health |
Liu G.-H.,CAS Institute of Biophysics |
And 3 more authors.
The CRISPR/Cas system has proven to be a powerful gene editing tool both in vitro and in vivo. A recent flurry of studies of in vivo gene editing using the CRISPR/Cas system bring bright prospects in creating animal models and targeted gene therapy of human genetic diseases. © 2015 IBCB, SIBS, CAS All rights reserved. Source