求《盗墓笔记》和《今夜哪里有鬼》系列txt全集（今夜有鬼系列要台湾原版，无删减的）邮箱_百度知道
求《盗墓笔记》和《今夜哪里有鬼》系列txt全集（今夜有鬼系列要台湾原版，无删减的）邮箱
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好你要的资源已经发你了满意的话请有效率的采纳我的答案吧如果想表达你的谢意~~~那就加分吧(*^__^*)……~收件箱内没有，我会尽快解决的. 请看下垃圾箱如果没收到，请百度尽快HI我或者给我发邮件
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帮大忙了，太谢谢了。！
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出门在外也不愁Caveolin-1 in the anterior cingulate cortex modulates chronic neuropathic pain via regulation of NMDA receptor 2B subunit.
- PubMed - NCBI
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FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListChoose DestinationFileClipboardCollectionsE-mailOrderMy BibliographyCitation managerFormatSummary (text)Abstract (text)MEDLINEXMLPMID ListCSVCreate File1 selected item: FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListMeSH and Other DataE-mailSubjectAdditional textE-mailAdd to ClipboardAdd to CollectionsOrder articlesAdd to My BibliographyGenerate a file for use with external citation management software.Create File
2015 Jan 7;35(1):36-52. doi: 10.1523/JNEUROSCI.5.Caveolin-1 in the anterior cingulate cortex modulates chronic neuropathic pain via regulation of NMDA receptor 2B subunit.1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 1, 2.1Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical College, Xuzhou 221004, China, and.2Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou 221004, China, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical College, Xuzhou 221004, China, and Department of Anesthesiology, The Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China .AbstractChronic pain is still a basic science and clinical challenge. Unraveling of the neurobiological mechanisms involved in chronic pain will offer novel targets for the development of therapeutic strategies. It is well known that central sensitization in the anterior cingulate cortex (ACC) plays a critical role in initiation, development, and maintenance of chronic pain. However, the underlying mechanisms still remain elusive. Here, we reported that caveolin-1 (Cav-1), a scaffolding protein in membrane rafts, was persistently upregulated and activated in the ACC neurons after chronic constriction injury (CCI) in mice. Knockdown or blocking of Cav-1 in the contralateral ACC to the injury side reversed CCI-induced pain behavioral and neuronal sensitization and overexpression of Cav-1 in the ipsilateral ACC-induced pain behavior in the unaffected hindpaw. Furthermore, we found that Cav-1 directly binding with NMDA receptor 2B subunit (NR2B) and promotion of NR2B surface levels in the ACC contributed to modulation of chronic neuropathic pain. Disrupting the interaction of Cav-1 and NR2B through microinjection of a short peptide derived from the C-terminal of NR2B into the ACC exhibited a significant anti-nociception effect associated with decrease of surface NR2B expression. Moreover, Cav-1 increased intracellular Ca(2+) concentration and activated the ERK/CREB signaling pathway in an NR2B-dependent manner in the ACC. Our findings implicate that Cav-1 in the ACC neurons modulates chronic neuropathic pain via regulation of NR2B and subsequent activation of ERK/CREB signaling, suggesting a possible caveolin-mediated process would participate in neuronal transmission pathways implicated in pain modulation. Copyright (C) 2015 the authors /$15.00/0.KEYWORDS: NMDA receptor 2B anter caveolin-1; neuropathic painPMID:
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External link. Please review our .抱歉，根据相关法律法规和政策，本吧暂不开放。求 黯然销混蛋的《今夜有鬼系列》全集~全集呦 至邮箱： PS记得留下百度ID~_百度知道
求 黯然销混蛋的《今夜有鬼系列》全集~全集呦 至邮箱： PS记得留下百度ID~
我有更好的答案
合并我把他们都在排队的序列号？ 蛋南墓遇到鬼等着，你看到了吗？ 我有第二个结局的系列完成删除版本28
你好，欢迎提问，可以看看迅雷里或者旋风的资源分享
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出门在外也不愁Effect of stachydrine on endoplasmic reticulum stress-induced apoptosis in rat kidney after unilateral ureteral obstruction.
- PubMed - NCBI
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FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListChoose DestinationFileClipboardCollectionsE-mailOrderMy BibliographyCitation managerFormatSummary (text)Abstract (text)MEDLINEXMLPMID ListCSVCreate File1 selected item: FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListMeSH and Other DataE-mailSubjectAdditional textE-mailAdd to ClipboardAdd to CollectionsOrder articlesAdd to My BibliographyGenerate a file for use with external citation management software.Create File
):373-81. doi: 10.0.. Epub
2013 Mar 6.Effect of stachydrine on endoplasmic reticulum stress-induced apoptosis in rat kidney after unilateral ureteral obstruction.1, , , , , , .1College of Pharmacy, Harbin University of Commerce, Harbin 150076, China.AbstractOur study aimed at determining the effect of stachydrine on the PERK, CHOP, and caspase-3 in rat kidney with RIF. Rats were randomly divided into control group, model group, enalapril group, high stachydrine group, medium stachydrine group, and low stachydrine group. RIF models of five groups were developed by unilateral ureteral obstruction except the control group. The rats were sacrificed 12 days after surgery and blood samples were collected. Serum creatinine (Scr) and blood urea nitrogen (BUN) levels were detected. Renal tubular damage index was determined by HE staining. The area percentage of RIF was determined by the Masson method. Expressions of PERK, CHOP, and caspase-3 in kidney were determined by immunohistochemistry. Tubulointerstitial injury index, RIF, serum Scr, BUN level, and expressions of PERK, CHOP, and caspase-3 were different between the model and treatment groups (P & 0.05; P & 0.01). The expressions of PERK, CHOP, and caspase-3 in nephridial tissue were reduced (P & 0.05), tubulointerstitial injury and RIF were reduced (P & 0.05), and Scr and BUN were lower (P & 0.05) in the high stachydrine group than those in the enalapril group. The expressions of PERK, CHOP, and caspase-3 were reduced in the endoplasmic reticulum stress-related apoptosis pathway after stachydrine treatment. Consequently, apoptosis was prevented, and RIF was inhibited.PMID:
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