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1Ischemia/reperfusion injury and cardioprotective mechanisms:Role of mitochondria and reactive oxygen species显示文摘Reperfusion therapy must be applied as soon as possible to attenuate the ischemic insult of acute myocardial infarction(AMI).However reperfusion is responsible for additional myocardial damage,which likely involves opening of the mitochondrial permeability transition pore(mPTP).In reperfusion injury,mitochondrial damage is a determining factor in causing loss of cardiomyocyte function and viability.Major mechanisms of mitochondrial dysfunction include the long lasting opening of mPTPs and the oxidative stress resulting from formation of reactive oxygen species(ROS).Several signaling cardioprotective pathways are activated by stimuli such as preconditioning and postconditioning,obtained with brief intermittent ischemia or with pharmacological agents.These pathways converge on a common target,the mitochondria,to preserve their function after ischemia/reperfusion.The present review discusses the role of mitochondria in cardioprotection,especially the involvement of adenosine triphosphate-dependent potassium channels,ROS signaling,and the mPTP.Ischemic postconditioning has emerged as a new way to target the mitochondria,and to drastically reduce lethal reperfusion injury.Several clinical studies using ischemic postconditioning during angioplasty now support its protective effects,and an interesting alternative is pharmacological postconditioning.In fact ischemic postconditioning and the mPTP desensitizer,cyclosporine A,have been shown to induce comparable protection in AMI patients.Maria-Giulia Perrelli Pasquale Pagliaro Claudia Penna 2011World Journal of Cardiology2011,3,6:64
2Draining Tangjiashan Barrier Lake after Wenchuan Earthquake and the flood propagation after the dam break显示文摘Tangjiashan Barrier Lake is one of the largest barrier lakes caused by the Wenchuan Earthquake. Its risk analysis, emergency plan and effect of the emergency plan are introduced in this paper. The dam height of Tangjiashan Barrier Dam is about 105 m, and the reservoir storage capacity is 3.2×108 m3. When the dam broke the flood peak were estimated to be larger than 48000 m3/s, which might cause a enormous disaster to the downstream cities and residents. A discharge channel with 13 m deep and 8 m wide was drug, so that the water may flow out of the lake before the dam breaks. As a result, the drainage and risk mitigation project are successful. During the drainage process, the flood peak was about 6500 m3/s, and about 1.6×108 m3 of water was drained off and the residual reservoir capacity was only 8.97×107 m3. A new channel with average width 100 m was formed, which can bear floods of 200 years frequency. The successful experience and the collected data can be used to deal with the similar natural disasters in future.LIU Ning1, ZHANG JianXin2, LIN Wei3, CHENG WuYI4 & CHEN ZuYu5 1 Ministry of Water Resources of the People’s Republic of China, Beijing 100053, China 2 Bureau of Hydrology of the Ministry of Water Resources of the People’s Republic of China, Beijing 100053, China 3 Sichuan Hydrographic and Water Resources Survey Bureau Chengdu 610031, China 4 HydroChina Chengdu Engineering Corporation, Chengdu 610072, China 5 China Institute of Water Resources and Hydropower Research, Beijing 100044, China 2009Science China(Technological Sciences)2009,52,4:29
3Parishin C's prevention of Aβ_(1–42)-induced inhibition of long-term potentiation is related to NMDA receptors显示文摘The rhizome of Gastrodia elata(GE), a herb medicine, has been used for treatment of neuronal disorders in Eastern Asia for hundreds of years. Parishin C is a major ingredient of GE. In this study, the i.c.v. injection of soluble Aβ1–42oligomers model of LTP injury was used. We investigated the effects of parishin C on the improvement of LTP in soluble Aβ1–42oligomer–injected rats and the underlying electrophysiological mechanisms. Parishin C(i.p. or i.c.v.) significantly ameliorated LTP impairment induced by i.c.v. injection of soluble Aβ1–42oligomers. In cultured hippocampal neurons,soluble Aβ1–42oligomers significantly inhibited NMDAR currents while not affecting AMPAR currents and voltage-dependent currents. Pretreatment with parishin C protected NMDA receptor currents from the damage induced by Aβ. In summary, parishin C improved LTP deficits induced by soluble Aβ1–42oligomers. The protection by parishin C against Aβ-induced LTP damage might be related to NMDA receptors.Zhihui Liu Weiping Wang Nan Feng Ling Wang Jiangong Shi Xiaoliang Wang 2016Acta Pharmaceutica Sinica B2016,6,3:25
4Ion channels in neuronal survival显示文摘The study of ion channels represents one of the most active fields in neuroscience research in China.In the last 10 years,active research in various Chinese neuroscience institutions has sought to understand the mechanisms responsible for sensory processing,neural development and neurogenesis,neural plasticity,as well as pathogenesis.In addition,extensive studies have been directed to measure ion channel activity,structure-function relationships,as well as many other biophysical and biochemical properties.This review focuses on the progress achieved in the investigation of ion channels in neuronal survival during the past 10 years in China.WANG YiZheng & XU TianLe Institute of Neuroscience and State Key Laboratory of Neuroscience,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 2010Science China(Life Sciences)2010,53,3:24
5Plant salt tolerance and Na^+ sensing and transport显示文摘Salinity is a global challenge to agricultural production. Understanding Na^+ sensing and transport in plants under salt stress will be of benefit for breeding robustly salt-tolerant crop species. In this review, first, possible salt stress sensor candidates and the root meristem zone as a tissue harboring salt stress-sensing components are proposed. Then,the importance of Na^+ exclusion and vacuolar Na^+ sequestration in plant overall salt tolerance is highlighted. Other Na^+ regulation processes, including xylem Na^+ loading and unloading, phloem Na^+ recirculation, and Na^+ secretion, are discussed and summarized.Along with a summary of Na^+ transporters and channels, the molecular regulation of Na^+ transporters and channels in response to salt stress is discussed. Finally, some largely neglected issues in plant salt stress tolerance, including Na^+ concentration in cytosol and the role of Na^+ as a nutrient, are reviewed and discussed.Honghong Wu 2018The Crop Journal2018,6,3:20
6Role of ion channels in gastrointestinal cancer显示文摘In their seminal papers Hanahan and Weinberg described oncogenic processes a normal cell undergoes to be transformed into a cancer cell.The functions of ion channels in the gastrointestinal(GI)tract influence a variety of cellular processes,many of which overlap with these hallmarks of cancer.In this review we focus on the roles of the calcium(Ca^2+),sodium(Na^+),potassium(K^+),chloride(Cl^-)and zinc(Zn^2+)transporters in GI cancer,with a special emphasis on the roles of the KCNQ1 K+channel and CFTR Cl-channel in colorectal cancer(CRC).Ca^2+is a ubiquitous second messenger,serving as a signaling molecule for a variety of cellular processes such as control of the cell cycle,apoptosis,and migration.Various members of the TRP superfamily,including TRPM8,TRPM7,TRPM6 and TRPM2,have been implicated in GI cancers,especially through overexpression in pancreatic adenocarcinomas and down-regulation in colon cancer.Voltage-gated sodium channels(VGSCs)are classically associated with the initiation and conduction of action potentials in electrically excitable cells such as neurons and muscle cells.The VGSC NaV1.5 is abundantly expressed in human colorectal CRC cell lines as well as being highly expressed in primary CRC samples.Studies have demonstrated that conductance through NaV1.5 contributes significantly to CRC cell invasiveness and cancer progression.Zn2+transporters of the ZIP/SLC39A and ZnT/SLC30A families are dysregulated in all major GI organ cancers,in particular,ZIP4 up-regulation in pancreatic cancer(PC).More than 70 K+channel genes,clustered in four families,are found expressed in the GI tract,where they regulate a range of cellular processes,including gastrin secretion in the stomach and anion secretion and fluid balance in the intestinal tract.Several distinct types of K+channels are found dysregulated in the GI tract.Notable are hERG1 upregulation in PC,gastric cancer(GC)and CRC,leading to enhanced cancer angiogenesis and invasion,and KCNQ1 down-regulation in CRC,where KCNQ1 expression is associated with enhanced disease-free survival in stage II,III,and IV disease.Cl-channels are critical for a range of cellular and tissue processes in the GI tract,especially fluid balance in the colon.Most notable is CFTR,whose deficiency leads to mucus blockage,microbial dysbiosis and inflammation in the intestinal tract.CFTR is a tumor suppressor in several GI cancers.Cystic fibrosis patients are at a significant risk for CRC and low levels of CFTR expression are associated with poor overall disease-free survival in sporadic CRC.Two other classes of chloride channels that are dysregulated in GI cancers are the chloride intracellular channels(CLIC1,3&4)and the chloride channel accessory proteins(CLCA1,2,4).CLIC1&4 are upregulated in PC,GC,gallbladder cancer,and CRC,while the CLCA proteins have been reported to be down-regulated in CRC.In summary,it is clear,from the diverse influences of ion channels,that their aberrant expression and/or activity can contribute to malignant transformation and tumor progression.Further,because ion channels are often localized to the plasma membrane and subject to multiple layers of regulation,they represent promising clinical targets for therapeutic intervention including the repurposing of current drugs.Kyle J Anderson Robert T Cormier Patricia M Scott 2019World Journal of Gastroenterology2019,25,38:19
7Potassium Channels: A Potential Therapeutic Target for Parkinson's Disease显示文摘The pathogenesis of the second major neurodegenerative disorder, Parkinson's disease(PD), is closely associated with the dysfunction of potassium(K^+ ) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K^+ channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K^+ channels enhances the spontaneous firing frequency of nigral dopamine(DA)neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the striatum.Recently, three K^+ channels have been identified to protect DA neurons and to improve the motor and non-motor symptoms in PD animal models: small conductance(SK)channels, A-type K^+ channels, and KV7/KCNQ channels.In this review, we summarize the physiological and pharmacological effects of the three K^+ channels. We also describe in detail the laboratory investigations regarding K^+ channels as a potential therapeutic target for PD.Xiaoyan Chen Bao Xue Jun Wang Haixia Liu Limin Shi Junxia Xie 2018Neuroscience Bulletin2018,34,2:13
8Mechanisms mediating CCK-8S-induced contraction of proximal colon in guinea pigs显示文摘AIM:To investigate the effects of sulfated cholecystokinin octapeptide (CCK-8S) on the contractile activity of guinea-pig proximal colon.METHODS:Proximal colonic smooth muscle (PCSM) strips were obtained from adult female guinea pigs and contractile response of PCSM strips was recorded using a polyphysiograph.PCSM cells were isolated by enzymatic digestion.Resting potential (RP),action potential (AP),large conductance potassium channel currents (IBKCa) and L-type calcium currents (ICa-L) were recorded by patch-clamp techniques.RESULTS:(1) CCK-8S (10-7 mol/L) enhanced the mean contractile amplitude of colonic circular muscle and longitudinal muscle (LM) strips by 56.53% ± 11.92%(P=0.038) and 65.93% ± 12.98% (P=0.019),respectively,as well as the mean frequency of LM by 31.69% ± 13.58% (P=0.023),which were significantly attenuated by pretreating strips with devazepide,nifedipine,iberiotoxin,thapsigargin (TG) and BAPTA-AM (BA) respectively;(2) CCK-8S (10-7 mol/L) increased the AP amplitude by 38.6% ± 3.2% (P=0.015),decreased AP duration by 36.9% ± 8.7% (P=0.026),and depolarized the RP from-61.3 ± 2.7 mV to-29.8 ± 5.9 mV (P=0.032);and (3) Compared with the normal control group,CCK-8S (10-7 mol/L) enhanced the peak current of IBKCa by 18.7% ± 2.1% (from 916 ± 183 pA to 1088 ± 226 pA;at +60 mV;P=0.029),which was inhibited by respective pretreatment with iberiotoxin and devazepide.Additionally,CCK-8S (10-7 mol/L) intensif ied the peak current of ICa-L by 40% (from 60 ± 8 pA to 84 ± 11 pA;at +10 mV;P=0.012),compared to the normal control group,which was apparently suppressed by respective pretreatment with nifedipine,devazepide,TG and BA.In the respective presence of heparin and staurosporine,CCK-8S did not signif icantly enhance IBKCa and ICa-L.CONCLUSION:The results suggest that CCK-8S promotes guinea-pig proximal colon contraction by CCK1 receptors,following activation of the inositol triphosphate-protein kinase C signal transduction pathway.Zhu, Jie Chen, Ling Xia, Hong Luo, He-Sheng 2010World Journal of Gastroenterology2010,16,9:8
9Possible mechanism underlying analgesic effect of Tuina in rats may involve piezo mechanosensitive channels within dorsal root ganglia axon显示文摘OBJECTIVE: To demonstrate the analgesic effect of Tuina mainly from mechanically sensitive ion channels in peripheral myelinated nerve fibers.METHODS: A total of 40 healthy and pathogen-free adult male Sprague-Dawley rats were used in the study [weight:(220.0 ± 1.4) g, Shanghai Slac Laboratory Animal Co., Ltd., Shanghai, China; license No. Shanghai ICP 05033115]. The rats were housed in cages with free access to water and food in a temperature-controlled room [(22 ± 1) ℃] and12-h/12-h light-dark cycle. Thirty-two rats were randomly divided into five groups: naive, sham, chronic compression of dorsal root ganglion(CCD), Tuina(7 d) and Tuina(21 d). CCD rat model was established via unilateral DRG compression by'L'liked steel bar. Chinese Tuina treatment was accepted once per day. Behavior monitoring of paw withdrawal threshold(PWT) and paw withdrawal latency(PWL) were tested. The expression of Piezo1 and Piezo2 in myelinated nerve fiber were analyzed by immunohistochemistry and Western-blotting.RESULTS: There was a high expression of Piezo2 and a low expression of Piezo1 in the naive and CCD groups. In contrast, the expression of Piezo2 was down regulated and Piezo1 was increased after a period of Tuina. There was significant difference(P ≤ 0.05) between the groups.CONCLUSION: Our findings suggest that Tuina therapy can increase the expression of Piezo2 and decrease the expression of Piezo1 in the test rats.The different changes in the expressions of Piezo1 and Piezo2 may play an important role in alleviating CCD-induced allodynia and hyperalgesia.Song Pengfei Lin Zhigang Zhu Qingguang Jiang Shichao Zhang Hao Cheng Yanbin Sun Wuquan Wu Zhiwei Zhou Xin Lv Zhizhen Fang Min 2018Journal of Traditional Chinese Medicine2018,38,6:6
10Quantum-confined ion superfluid in nerve signal transmission显示文摘We propose a process of quantum-confined ion superfluid (QISF),which is enthalpy-driven confined ordered fluid,to explain the transmission of nerve signals.The ultrafast Na^+ and K^+ ions transportation through all sodium-potassium pump nanochannels simultaneously in the membrane is without energy loss,and leads to QISF wave along the neuronal axon,which acts as an information medium in the ultrafast nerve signal transmission.The QISF process will not only provide a new view point for a reasonable explanation of ultrafast signal transmission in the nerves and brain,but also challenge the theory of matter wave for ions,molecules and particles.Xiqi Zhang Lei Jiang 2019Nano Research2019,12,6:6
11含双重植物明渠水流特性研究显示文摘以典型沉水植物狐尾藻和挺水植物菖蒲为研究对象,采用三维多普勒超声测速仪(ADV)对含双重植物明渠恒定水流的水力特性进行了试验研究,分析了含双重植物明渠水流的水力学特性及阻力特性并得出其曼宁糙率n的变化规律。结果表明,含双重植物的垂向流速分布基本呈'3'型分布,其紊流具有明显的各向异性特性,底层狐尾藻仅对其高度区域内的流速有较大影响,对高于其植物高度区域的断面流速影响不大。王忖 2010水电能源科学2010,28,9:6
12Monetary policy and dynamic adjustment of corporate investment: A policy transmission channel perspective显示文摘We investigate monetary policy effects on corporate investment adjustment,using a sample of China's A-share listed firms(2005–2012), under an asymmetic framework and from a monetary policy transmission channel perspective. We find that corporate investment adjustment is faster in expansionary than contractionary monetary policy periods. Monetary policy has a significant effect on adjustment speed through monetary and credit channels. An increase in the growth rate of money supply or credit accelerates adjustment.Both effects are significantly greater during tightening than expansionary periods. The monetary channel has significant asymmetry, whereas the credit channel has none. Leverage moderates the relationship between monetary policy and adjustment, with a greater effect in expansionary periods. This study enriches the corporate investment behavior literature and can help governments develop and optimize macro-control policies.Qiang Fu Xing Liu 2015China Journal of Accounting Research2015,,2:5
13Tandem pore TWIK-related potassium channels and neuroprotection显示文摘TWIK-related potassium channels (TREK) belong to a subfamily of the two-pore domain potassium channels family with three members, TREK1, TREK2 and TWIK-related arachidonic acid-activated potassium channels. The two-pore domain potassium channels is the last big family of channels being discovered, therefore it is not surprising that most of the information we know about TREK channels predominantly comes from the study of heterologously expressed channels. Notw让hstanding, in this review we pay special attention to the limited amount of information available on native TREK-like channels and real neurons in relation to neuroprotection. Mainly we focus on the role of free fatty acids, lysophospholipids and other neuroprotective agents like riluzole in the modulation of TREK channels, emphasizing on how important this modulation may be for the development of new therapies against neuropathic pain, depression, schizophrenia, epilepsy, ischemia and cardiac complications.J.Antonio Lamas Diego Fernández-Fernández 2019Neural Regeneration Research2019,14,8:5
14Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension显示文摘Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS),hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.Wen Wu Yan Li Dunquan Xu 2017Chinese Medical Sciences Journal2017,32,4:5
15Mechanism for chronic pain generation显示文摘Neuropathic pain and the other abnormalities of sensation induced by axon injury or by peripheral nerve inflammation should result from functional compensations of the injured neurons during their regeneration. Ectopic distribution of proteins related to Na+, K+ and Ca2+ channels as well as of receptors on both membranes of injured axon and its cell body becomes a main pacemaker from which spontaneous ectopic afferent of primary sensatory neurons and crosstalk between neurons occur. Abnormal ectopic afferent activities lead to disorders of the sensation, such as hyperalgesia, allodynia, spontaneous pain and paraesthesia. Administration of some ion channel agents and/or α2-adrenergic blockers has shown efficiency in preventing neuropathic pain development and in relieving neuropathic pain.XIE YikuanInstitute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005. 2000Chinese Science Bulletin2000,45,9:4
16Event-trigger-based consensus secure control of linear multi-agent systems under DoS attacks over multiple transmission channels显示文摘This paper proposes a consensus secure control scheme in the presence of denial-of-service(DoS)attacks based on an event-trigger mechanism. In contrast to a scenario in which attacks are the same and simultaneously paralyze all channels, the DoS attack addressed in this paper occurs aperiodically and results in the independent interruption of multiple transmission channels. A sufficient condition for the attack duration is designed and a distributed event-triggered control scheme is proposed, where the updated instants are triggered aperiodically to reduce the required communication resources. It is shown that the overall system is stable with the proposed scheme according to the Lyapunov stability theory and that Zeno behavior is excluded. Finally, a numerical example is presented to verify the effectiveness of the proposed scheme.Yang YANG Yanfei LI Dong YUE 2020Science China(Information Sciences)2020,63,5:4
17Cellular and Molecular Mechanisms Underlying Arterial Baroreceptor Remodeling in Cardiovascular Diseases and Diabetes显示文摘Clinical trials and animal experimental studies have demonstrated an association of arterial baroreflex impairment with the prognosis and mortality of cardiovascular diseases and diabetes. As a primary part of the arterial baroreflex arc, the pressure sensitivity of arterial baroreceptors is blunted and involved in arterial baroreflex dysfunction in cardiovascular diseases and diabetes.Changes in the arterial vascular walls, mechanosensitive ion channels, and voltage-gated ion channels contribute to the attenuation of arterial baroreceptor sensitivity. Some endogenous substances(such as angiotensin II and superoxide anion) can modulate these morphological and functional alterations through intracellular signaling pathways in impaired arterial baroreceptors. Arterial baroreceptors can be considered as a potential therapeutic target to improve the prognosis of patients with cardiovascular diseases and diabetes.Huiyin Tu Dongze Zhang Yu-Long Li 2019Neuroscience Bulletin2019,35,1:4
18Polydatin attenuated food allergy via store-operated calcium channels in mast cell显示文摘AIM: To investigate the effect of polydatin (PD), a resveratrol glucoside, on mast cell degranulation and antiallergic activity. METHODS: After the rats were orally sensitized with ovalbumin (OVA) for 48 d and underwent PD treatment for 4 d, all the rats were stimulated by 100 mg/mL OVA for24 h and then sacrificed for the following experiments. The small intestines from all the groups were prepared for morphology examination by hematoxylin and eosin staining. We also used a smooth muscle organ bath to evaluate the motility of the small intestines. The OVA-specific immunoglobulin E (IgE) production and interleu-kin-4 (IL-4) levels in serum or supernatant of intestinal mucosa homogenates were analyzed by enzyme-linked immunosorbent assay (ELISA). Using toluidine blue stain, the activation and degranulation of isolated rat peritoneal mast cells (RPMCs) were analyzed. Release of histamine from RPMCs was measured by ELISA, and regulation of PD on intracellular Ca 2+ mobilization was investigated by probing intracellular Ca 2+ with fluo-4 fluo-rescent dye, with the signal recorded and analyzed. RESULTS: We found that intragastric treatment with PD significantly reduced loss of mucosal barrier integrity in the small intestine. However, OVA-sensitization caused significant hyperactivity in the small intestine of allergic rats, which was attenuated by PD administration by 42% (1.26 ± 0.13 g vs OVA 2.18 ± 0.21 g, P < 0.01). PD therapy also inhibited IgE production (3.95 ± 0.53 ng/mL vs OVA 4.53 ± 0.52 ng/mL, P < 0.05) by suppressing the secretion of Th2-type cytokine, IL-4, by 34% (38.58 ± 4.41 pg/mLvs OVA 58.15 ± 6.24 pg/mL, P < 0.01). The ratio of degranulated mast cells, as indicated by vehicles (at least five) around the cells, dramatically increased in the OVA group by 5.5 fold (63.50% ± 15.51% vs phosphate-buffered saline 11.15% ± 8.26%, P < 0.001) and fell by 65% after PD treatment (21.95% ± 4.37% vs OVA 63.50% ± 15.51%, P < 0.001). PD mediated attenuation of mast cell degranulation was further confirmed by decreased histamine levels in both serum (5.98 ± 0.17 vs OVA 6.67 ± 0.12, P < 0.05) and intestinal mucosa homogenates (5.83 ± 0.91 vs OVA 7.35 ± 0.97, P < 0.05). Furthermore, we demonstrated that administration with PD significantly decreased mast cell degranulation due to reduced Ca 2+ influx through store-operated calcium channels (SOCs) (2.35 ± 0.39vs OVA 3.51 ± 0.38,P < 0.01).CONCLUSION: Taken together, our data indicate that PD stabilizes mast cells by suppressing intracellular Ca 2+ mobilization, mainly through inhibiting Ca 2+ entry via SOCs, thus exerting a protective role against OVA-sensitized food allergy.Bo Yang Jian-Jie Li Ji-Juan Cao Cheng-Bin Yang Jie Liu Qiong-Mei Ji Zhi-Gang Liu 2013World Journal of Gastroenterology2013,19,25:4
19TYPES AND DISTRIBUTION PATTERNS OF MODERN TIDAL CHANNELS ALONG THE HUANGHE RIVER DELTA COAST显示文摘There are three major types of tidal channels along the coast of the Huanghe (Yellow) River Delta: tidal inlets, tidal creeks, and tidal channels developed from abandoned river channels. The tidal inlets develop mainly in two areas with weak erosion and barrier islands. The tidal channels formed from abandoned river channels mainly developed in the area of the new delta lobes formed since 1934. Tidal creeks developed in the intertidal zone and distributed along almost all parts of the Huanghe River Delta coast, but their scales and features are different.尹延鸿 王玉荣 刘宪启 1999Chinese Journal of Oceanology and Limnology1999,17,4:3
20Mechanism of persistent hyperalgesia in neuropathic pain caused by chronic constriction injury显示文摘Transmembrane member 16 A(TMEM16 A) is involved in many physiological functions, such as epithelial secretion, sensory conduction, nociception, control of neuronal excitability, and regulation of smooth muscle contraction, and may be important in peripheral pain transmission. To explore the role of TMEM16 A in the persistent hyperalgesia that results from chronic constriction injury-induced neuropathic pain, a rat model of the condition was established by ligating the left sciatic nerve. A TMEM16 A selective antagonist(10 μg T16 Ainh-A01) was intrathecally injected at L5–6. For measurement of thermal hyperalgesia, the drug was administered once at 14 days and thermal withdrawal latency was recorded with an analgesia meter. For measurement of other indexes, the drug was administered at 12 days,once every 6 hours, totally five times. The measurements were performed at 14 days. Western blot assay was conducted to analyze TMEM16 A expression in the L4–6 dorsal root ganglion. Immunofluorescence staining was used to detect the immunoreactivity of TMEM16 A in the L4–6 dorsal root ganglion on the injured side. Patch clamp was used to detect electrophysiological changes in the neurons in the L4–6 dorsal root ganglion. Our results demonstrated that thermal withdrawal latency was shortened in the model rats compared with control rats.Additionally, TMEM16 A expression and the number of TMEM16 A positive cells in the L4–6 dorsal root ganglion were higher in the model rats, which induced excitation of the neurons in the L4–6 dorsal root ganglion. These findings were inhibited by T16 Ainh-A01 and confirm that TMEM16 A plays a key role in persistent chronic constriction injury-induced hyperalgesia. Thus, inhibiting TMEM16 A might be a novel pharmacological intervention for neuropathic pain. All experimental protocols were approved by the Animal Ethics Committee at the First Affiliated Hospital of Shihezi University School of Medicine, China(approval No. A2017-170-01) on February 27, 2017.Qin-Yi Chen Chao-Yang Tan Yang Wang Ke-Tao Ma Li Li Jun-Qiang Si 2019Neural Regeneration Research2019,14,6:3
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