Yan Dong

Peking University, Beijing, Beijing Shi, China

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Publications (6)16.67 Total impact

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    ABSTRACT: Infectious diseases, mostly caused by bacteria and viruses but also a result of fungal and parasitic infection, have been one of the most important public health concerns throughout human history. The first step in combating these pathogens is to get a timely and accurate diagnosis at an affordable cost. Many kinds of diagnostics have been developed, such as pathogen culture, biochemical tests and serological tests, to help detect and fight against the causative agents of diseases. However, these diagnostic tests are generally unsatisfactory because they are not particularly sensitive and specific and are unable to deliver speedy results. Nucleic acid-based diagnostics, detecting pathogens through the identification of their genomic sequences, have shown promise to overcome the above limitations and become more widely adopted in clinical tests. Here we review some of the most popular nucleic acid-based diagnostics and focus on their adaptability and applicability to routine clinical usage. We also compare and contrast the characteristics of different types of nucleic acid-based diagnostics.
    Frontiers of medicine. 06/2012; 6(2):173-86.
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    ABSTRACT: We observed nuclear swelling in glutamate (Glu)-treated astrocytes that was concomitant with but independent of astrocytic cell swelling. We confirmed Glu-induced nuclear swelling with nuclei isolated from astrocytes. Ammonia is metabolically related to Glu and could induce a nuclear swelling in intact astrocytes but shrinkage in isolated nuclei. Other compounds such as glutamine, aspartate, taurine, glycine, and ATP did not cause any nuclear swelling in isolated nuclei of astrocytes. Surprisingly, Glu and ammonia did not induce nuclear swelling in microglia, C6, HEK 293, or Hep G2 cell lines in cultures and their isolated nuclei. The Glu- and ammonia-induced nuclear size changes appear to be a specific response of astrocytes to these two closely related metabolic compounds.
    Journal of Neuroscience Research 05/2011; 89(12):2041-51. · 2.97 Impact Factor
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    ABSTRACT: The expression of the N-methyl-D-aspartate receptor (NMDA-R) in astrocytes is controversial. The receptor is commonly considered neuron-specific. We showed that astrocytes in primary cultures differentially expressed mRNA of NMDA-R subunits, NR1, NR2A and NR2B, in development, ischemia and post-ischemia. One-week-old cultures expressed detectable NR1 mRNA, which fell significantly at 2 weeks and became barely detectable at 4 weeks. NR2A and NR2B mRNA were both significantly up-regulated from 1 to 2 weeks. In 4 weeks, 2 h of ischemia caused a significant up-regulation of NR1 and NR2B mRNA; while 6 h caused down-regulation of NR2A mRNA. Under 3 h of post-ischemia, only NR1 mRNA was increased. Ischemia induced the expression of major NMDA-R effecter, nitric oxide synthase 1, which was unaffected by AMPA-R antagonist CNQX, but dose-dependently inhibited by NMDA-R specific antagonist MK-801. These findings reflected that astrocyte could express inducible functional NMDA receptors without the presence of neurons.
    Neurochemical Research 12/2010; 35(12):2124-34. · 2.13 Impact Factor
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    ABSTRACT: A number of intrinsic factors are present intracellularly and could be turned on to protect cells from stress and injury, including cerebral ischemia. The degree of protection of these factors is dependent on the time of induction, their concentration, as well as the duration and extent of injury. This review summarizes recent studies on some of the protective factors with specific emphasis on two recently discovered intrinsic protective proteins: 14-3-3gamma protein and neuroglobin. Both of them were originally discovered in neurons, later identified in astrocytes under ischemic conditions, and demonstrated to have protective effect on nerve cells from apoptosis. Understanding the mode of induction and role of protection of these intrinsic protective proteins would be beneficial for the future development of pharmacotherapy in extending the therapeutic time window, which would lead to better stroke management for patients.
    Molecular Neurobiology 06/2010; 41(2-3):218-31. · 5.47 Impact Factor
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    ABSTRACT: Ischemia occurs in the brain as the result of stroke and other related injuries and few therapies are effective. If more is understood then potential treatments could be investigated. It was previously reported that 14-3-3gamma could be up-regulated by ischemia in astrocyte to protect cells from ischemia-induced apoptosis. In this study, we attempted to uncover the mechanism responsible for this 14-3-3gamma up-regulation in primary culture of astrocytes under ischemic-like conditions. It was found that in vitro ischemia may activate PI3K/Akt and MAPK signaling pathways. Astrocyte cultures were treated with LY294002 (PI3K inhibitor), U0126 (ERK inhibitor), SB203580 (p38 inhibitor) and SP600125 (JNK inhibitor). Only SP600125 could inhibit the ischemia-induced 14-3-3gamma up-regulation in astrocytes. At the same time, we observed an ischemia-induced nuclear translocation of p-c-Jun, a major downstream component of JNK. Inhibition of AP-1 with curcumin also inhibited 14-3-3gamma up-regulation indicating that ischemia-induced up-regulation of 14-3-3gamma in astrocyte involves activation of the JNK/p-c-Jun/AP-1 pathway.
    Journal of Neurochemistry 05/2009; 109 Suppl 1:182-8. · 3.97 Impact Factor
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    ABSTRACT: The unexpected finding of astrocytes to release glutamate as gliotransmitter challenges the traditional concepts on astrocyte being "passive" in CNS communications. Glutamate is the major excitatory transmitter in transferring information between neurons, but is now also known to activate astrocyte through transporters and receptors. Together with the sensitive swelling response, astrocytes could respond directly to glutamate and neuronal activity. Other new functions of astrocytes include modulation of synaptic plasticity and cerebral blood flow (CBF). The classic glutamate deplenishment through glutamine synthesis and CO(2) production does not account for the total glutamate internalized into astrocytes. This leads us to speculate there are many hidden functions of glutamate in neurons and astrocytes waiting to be discovered. In this review, we attempted to reexamine some of these new and older functions of glutamate and to reevaluate the roles of glutamate intoning these two cell types.
    Neurochemical Research 07/2008; 33(12):2480-6. · 2.13 Impact Factor