Journal of Cellular Neuroscience and Oxidative Stress最新文献

{"title":"Involvement of Thermo TRP channels on chemothrepeutic agents-induced peripheral pain","authors":"M. K. Yıldırım","doi":"10.37212/jcnos.610118","DOIUrl":"https://doi.org/10.37212/jcnos.610118","url":null,"abstract":"Accumulating evidences have indicated that  disturbances in intracellular free calcium ([Ca2+]i)  concentration play an important role in the  pathophysiology of peripheral pain. Ca2+ passes cell  membrane via different channels such as chemical and  voltage gated channels. Apart from the well-known  cation channels, there is recently discovered channels  namely transient receptor potential (TRP) family. At  least, 11 TRP channels in mammalian cells have been  identified as thermosensitive TRP (thermo-TRP)  channels (Uchida et al. 2017). Two TRP channels  (TRPV1 and TRPV2) are activated by high  temperatures. Five TRP channels (TRPV1-4 and  TRPM2) are activated by different heat temperatures,  although two of TRP channels (TRPA1 and TRPM8)  are activated by cold and cool temperatures,  respectively (Naziroglu and Braidy, 2017). It is well  known that increase of [Ca2+]i concentration but  decrease of intracellular Mg2+ levels induces activation  of nitric oxide synthase (NOS) enzyme. By catalytic  activity of NOS, nitric oxide synthetizes in neurons. In  turn, it induces pain through production of excitatory  amino acids and substance P (Medvedeva et al. 2008).  Results of recent studies indicated involvement of  chemothrepeutic agents (i.e. cisplatin, oxaliplatin and  paclitaxel)-induced mitochondrial oxidative stress  through activation of Thermo TRP channels such as  TRPA1, TRPV1 and TRPM8, although antioxidants  induced protective action on the pain induction through  inhibition of the TRP channels in the experimental  animals (Materazzi et al. 2012). In the oral presentation,  I discussed novel effects of chemotherapeutic agents on  the peripheral pain by the regulation of TRP channels.  I concluded that the chemotherapeutic agents  cause TRP channel activation and oxidative stress,  which may lead to the pathology of peripheral pain. It seems to that the exact relationship between TRP  channel activation and chemotherapeutic agents still  remain to be determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44584648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voltage gated sodium channels and epilepsy","authors":"S. Hebeisen","doi":"10.37212/JCNOS.584668","DOIUrl":"https://doi.org/10.37212/JCNOS.584668","url":null,"abstract":"Epilepsy is the fourth most common neurological disorder and affects people of all ages. Medication for epilepsy is often life-long and has a major impact on the quality of life - mostly being related to substantial adverse effects. Therefore, over 30% of people with epilepsy do not achieve sufficient seizure control whilst effective medication being available.  Ion channels are often primary targets of anticonvulsant drugs. They can either act as blockers for voltage gated sodium and calcium channels or as activators for potassium or chloride channels. Additionally, modulators of ligand gated ion channels (GABA or Glutamate receptors) are frequently used to treat epilepsy.  Employing a panel of functional electrophysiological assays using fluorescence based methods and patch-clamping on a broad range of voltage and ligand gated ion channels, we were able to successfully screen for drugs with a beneficial action profile. In successful leads we found drugs that selectively interacted with TTX sensitive, neuronal voltage gated sodium channels. Activation and fast inactivation were unchanged, while an increased affinity in the slow inactivated state was observed. This profile is in contrast to traditional anticonvulsant drugs which show their major effects on the fast inactivated state of voltage gated sodium channels. One drug showed substantial shifts of the voltage dependence of the slow inactivation only for NaV1.2 and 1.6. This favours this drug for treating patients with diseases with compromised NaV1.1 function in interneurons, such as Alzheimer's disease.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43904538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPV1 channel is a potential drug discovery channel for epilepsy","authors":"Ahmet Özşimşek","doi":"10.37212/JCNOS.610113","DOIUrl":"https://doi.org/10.37212/JCNOS.610113","url":null,"abstract":"Epilepsy is one of the most frequent and  heterogeneous neurological disorders and it is  characterized by several disabilities. Epilepsy is  affecting about 3% of people worldwide. Current antiepileptic  drugs are only effective in 60% of individuals  and many drugs can induce several unwanted side  effects in patients. Etiology of epilepsy has not been  clarified fully. However, increased intracellular calcium  ion (Ca 2+ ) concentration has main role in etiology of  epilepsy. Ca2+ passes the cell membrane through  different cell membrane channels. One of the channels  is TRP superfamily. The family is containing six  subfamilies. TRPV1 channel is a member of TRPV  subfamily. Capsaicin is a component of hot chili pepper.  The TRPV1 channels is activated by different stimuli  such as acidic pH, high temperature (≥ 42° C) and  capsaicin, causing pain, inflammation and hyperalgesia  in peripheral nervous system (Caterina et al. 1997). Is  has been well known that hippocampus is main area in  the brain for induction of epilepsy. Expression levels of  TRPV1 channels in different areas of hippocampus are  high (Gonzalez-Reyes et al. 2013). Results of recent  studies indicated involvement of TRPV1 channels in  epilepsy (Naziroglu and Ovey, 2015; Cho et al. 2018).  In the oral presentation, I discussed novel roles of  TRPV1 on the epilepsy induction by the capsaicin.  Results of a recent study indicated increased levels  of intracellular Ca2+ concentration in hippocampus of  epilepsy induced rats (Naziroglu and Ovey, 2015).  They also observed increased levels of intracellular  mitochondrial oxidative stress and apoptosis levels in  the neurons by the capsaicin stimulation. However, their  levels were decreased by inhibition of TRPV1 channel  blocker, capsazepine.  I concluded that the results of recent studies  suggest that TRPV1 stimulation through capsaicin  causes oxidative stress and  intracellular Ca2+ signaling  in epileptic rats. It seems to that the certain role of  TRPV1 channel activation in in the epilepsy still  remains to be determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47496251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of desflurane on oxidative stress in neuroscience","authors":"Mustafa Kütük","doi":"10.37212/jcnos.610129","DOIUrl":"https://doi.org/10.37212/jcnos.610129","url":null,"abstract":"Oxidative stress in a neuron is induced by several  physiological and pathological processes. Within the  pathophysiological processes, ischemia-reperfusion  injury has major role in the neurons and brain, because  the neurons and brain are very sensitive to oxidative  stress as compared to other tissues due to their high  oxygen consumption rate and rich poly unsaturated fatty  acid content but low antioxidant levels. Results of  rodent studies indicated that exposure to volatile  anesthetics as a result of ischemia-reperfusion injury  can active leukocytes or alveolar macrophages, which,  in turn, release inflammatory mediators and reactive  oxygen species (ROS). This release of inflammatory  mediators, ischemia/reperfusion injury, and ROS has  been clearly demonstrated in generalized inflammatory  reactions involving the production of phagocytic cells  such as leucocytes and microglia. A common volatile  general anesthetic is desflurane and results of several  recent papers indicated that it  an increase oxidative  stress but can decrease antioxidant defense mechanisms  through ischemia/reperfusion injury mechanisms.  The excessive production of ROS is scavenged by  enzymatic and non-enzymatic antioxidants. Major  enzymatic antioxidants are vitamin A, vitamin C,  vitamin E, glutathione, alpha lipoic acid and melatonin.  Major non enzymatic antioxidants are glutathione  peroxidase (GSH-Px), superoxide dismutase (SOD) and  catalase (CAT). Superoxide radical is converted to  hydrogen peroxide by SOD enzyme and then the  hydrogen peroxide is converted to water by CAT and  GSH-Px enzymes. Results of papers indicated that the  CAT, GSH-Px, SOD, vitamin A, vitamin E and vitamin  C values were decreased in plasma and erythrocytes of  human and animals by desflurane anesthesia, but  oxidative stress levels were increased by desflurane  anesthesia (Allaouchiche et al. 2001; Ceylan et al. 2011;  Yalcin et al. 2013). In the oral presentation, I will  summarize the results of recent papers on oxidative  stress and antioxidants in human and rodents.  In conclusion, it seems that desflurane anesthesia  has oxidant effects through down-regulating the  enzymatic and non-enzymatic antioxidants but upregulating  of lipid peroxidation.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43896770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of TRP channels on fibromyalgiainduced pain","authors":"A. Doğru","doi":"10.37212/JCNOS.610116","DOIUrl":"https://doi.org/10.37212/JCNOS.610116","url":null,"abstract":"Fibromyalgia (FM) is a common chronic pain  syndrome affecting up to 2% of the adult population. Several factors such as excessive oxidative stress and  overload calcium ion (Ca2+) influx play main roles in  the etiology of FM. Several pharmaceutical drugs such  as antidepressants and voltage-gated calcium channel  blockers are recommended for the treatment of FM;  however, they fail to produce a satisfactory response in  patients with FM because of the unclear etiology of the  disease. Transient receptor potential (TRP) channels  have six subfamilies and 27 members in human. Most of  these channels are responsible in dorsal root ganglia  (DRG) neurons for the Ca2+ permeation especially in  neuronal cells. Expression level of the TRPM2 and  TRPV1 channels are high in the DRG neurons and they  show oxidative stress dependent activation (Tan and  McNaughton 2016; Santos et al. 2018). The TRPM2  and TRPV1 channel expression levels in the DRG  increased in different types of pain. Selenium as an  antioxidant trace element is implicated as a  neuroprotective agent in peripheral pain through the  inhibition of apoptosis and regulation of the TRPM2  and TRPV1 channels (Kahya et al. 2017). Since a  decade, a recent theory have argued that both supporting  of intracellular antioxidant system and extracellular  antioxidant administration may helpful in fibromyalgia  for the inhibition of TRP channels mediated Ca2+ influx  (Yuksel et al. 2017). In the oral presentation, I discussed  novel effects of selenium on the treatment of irregular  oxidative status and fibromyalgia by the regulation of  TRPM2 and TRPV1 channels in rats.  In conclusion, present literature information  indicated that protective effects of selenium on TRPM2  and TRPV1 channels may novel approach to treat FM induced  pain and mitochondrial oxidative stress.  However, the subject should be clarified by further  studies.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42696323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Western-blot, PCR and immunofluorescence analysis in mitochondrial biogenesis studies","authors":"D. Rousseau","doi":"10.37212/jcnos.609964","DOIUrl":"https://doi.org/10.37212/jcnos.609964","url":null,"abstract":"Mitochondria are providing an essential amount of  energy to the cell, to achieve in homeostasis, metabolic  increases, proliferation and differentiation processes.  Also, mitochondrial deficiencies have severe or lethal  impacts on cell viability. Among the 3000 proteins  involved in mitochondrial activities, ATAD3 is a major  one as essential for mitochondrial biogenesis, vital as  early as embryonic implantation.  In order to see its  impact at animal level, we have  used ATAD3+/- mice to investigate its role in running  training and in high calorie diet.  We found here that ATAD3 expression level  avoids running capacity improvement and has a strong  effect on weight increase, underlying its important role  in mitochondrial mass regulations.  Prior to this presentation we will emphasize on the  potential of Western-blot, PCR and  immunofluorescence analysis in biomedical researches.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47187816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experimental Parkinson’s disease models","authors":"E. İpek","doi":"10.37212/jcnos.610154","DOIUrl":"https://doi.org/10.37212/jcnos.610154","url":null,"abstract":"Parkinson's disease (PD) is a neurodegenerative  disease that develops slowly; however, there is no  efficient method of early diagnosis, nor is there a cure.  It is characterized by the relatively selective loss of  dopaminergic neuronal cells in the substantia nigra pars  compacta and the presence of alpha-synuclein  aggregation named as Lewy bodies and Lewy neurites  in surviving affected neurons. Nigrostriatal  dopaminergic neurodegeneration is shared with other  parkinsonian disorders, including some genetic forms of  parkinsonism, but many of these disorders do not have  Lewy bodies. An ideal animal model for PD, therefore,  should exhibit age-dependent and progressive  dopaminergic neurodegeneration, motor and non-motor  dysfunction, and abnormal alpha-synuclein pathology.  A wide range of neurotoxic agents are used to  induce PD, alterations that are similar with dose  observed in human PD. These agents are classified  mainly by administration route and the species involved.  The toxins that are mainly used in present 6-  hydroxydopamine, 1-Methyl-4-phenyl-1,2,3,6- tetrahydropyridine, rotenone, paraquat, reserpine,  methamphetamine, 3-nitrotyrosine and isoquinoline  derivatives (Tieu, 2011; McDowell and Chesselet, 2012;  Bezard et al. 2013). In addition, viral mediated  expression of human α-synuclein, as well as the  inoculation of pathogenic α-synuclein species from  Lewy bodies of PD patients, for accurately modelling  progressive self-propagating neurodegeneration and  genetic LRRK2 models (PARK8 gene mutation) has  been used (Jiang and Dickson, 2018).  In conclusion, these models are only  approximations, each possibly holding a certain degree  of relevance. Thus, researchers should select models  whose characteristics are most suitable for addressing  the experimental question.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70024659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology of cation channels in pain: Focus on TRP Channels","authors":"M. Naziroğlu","doi":"10.37212/JCNOS.609840","DOIUrl":"https://doi.org/10.37212/JCNOS.609840","url":null,"abstract":"In neurons such as dorsal root ganglion (DRG) and trigeminal ganglia, calcium (Ca2+) and sodium ion concentrations are higher in in outside than in cytosol, although potassium ion concentration was higher in inside of the neurons than outside of the neurons. Within the ions, it has been suggested that a dysregulation of Ca2+ homeostasis acts a key role in the pathogenesis of oxidative stress associated nerve damage. Ca2+ is a main intracellular messenger involved in several physiological functions of neurons such survival, death, synaptic plasticity and neurotransmitter release. It has specific role in induction of peripheral pain. Ca2+ passes cell membrane via different channels such as chemical and voltage gated channels. Apart from the well-known cation channels, there is recently discovered channels namely transient receptor potential (TRP) family. The TRP superfamily is containing 6 subfamilies with 28 members in mammalian. Activation and inhibition mechanisms of the TRP channels are very different from the voltage gated calcium channels. Some TRP channels such as TRP melastatin 2 (TRPM2), melastatin 7 (TRPM7) and TRP ankyrin 1 (TRPA1) are activated by oxidative stress. Expression levels of TRPA1, TRPM2 and TRPM7 are high in DRG, phagocytic cells and hippocampus, respectively. Therefore, TRPM2 is important channels in physiological activity of phagocytic cells such as neutrophil and monocytes (Heiner et al. 2006). TRPM7 and TRPA1 have main roles in cerebral ischemia and peripheral pain molecular pathways, respectively (Carrasco et al. 2018; Sun, 2017). Till today specific antagonists of most TRP channels have not been discovered yet and they have potential targets for discovering drugs in neuroscience. In pain etiology, Ca2+ is important and it has been demonstrated in some studies that the administration of an antagonist to Ca2+ channels induces a reduction in chemotherapeutic   agents-induced neuropathic pain.  In the presentation, I discussed novel results of Ca2+ on the peripheral pain by the regulation of TRP channels.  I concluded that the results of recent studies suggest that increased cytosolic Ca2+ has through inhibition of TRP channels main role in etiology of peripheral pain. It seems to that the TRP channels are potential target for treatment of peripheral pain.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42072456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of dexmedetomidine and calcium signaling in cerebral ischemia: Focus TRP channels","authors":"Hacı Ömer Osmanlioğlu","doi":"10.37212/jcnos.610107","DOIUrl":"https://doi.org/10.37212/jcnos.610107","url":null,"abstract":"An accumulating body of evidence indicates that  abnormalities of intracellular free calcium ([Ca2+]i)  concentration is caused by excessive levels of reactive  oxygen species (ROS) in rats with cerebral ischemia in  play an important role in the pathophysiology of  cerebral ischemia (Miyanohara et al. 2015; Belrose and  Jackson, 2018). Ca2+ passes cell membrane via different  channels such as chemical and voltage gated channels.  Apart from the well-known cation channels, there is  recently discovered channels namely transient receptor  potential (TRP) family. The TRP superfamily is  containing 7 subfamilies with 28 members in  mammalian. Activation and inhibition mechanisms of  the TRP channels are very different from the voltage  gated calcium channels. For example, TRPM2 channel  is activated by ADP-ribose and oxidative stress, but  TRPV1 channel is activated several stimuli, including  capsaicin and oxidative stress (Belrose and Jackson,  2018). Dexmedetomidine (DEX) is an important drug  for long-term sedation in intensive care patients because  it induces a rapid response and is easily controllable.  There is some modulator role of DEX on the [Ca2+]i  concentration in several neurons (Akpinar et al. 2016).   Results of a recent study indicated that DEX induced  modulator role on cerebral ischemia-induced ROS,  TRPM2 and TRPV1 channel activation in hippocampus of rats.  I concluded that the results of recent studies  suggest that DEX treatment reduces cerebral ischemiainduced  oxidative stress and intracellular Ca2+ signaling  through inhibition of TRP channels. It seems to that the  exact relationship between TRP channel activation and  DEX in cerebral ischemia still remains to be  determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44872714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depression models in experimental animals","authors":"Arif Demirdaş","doi":"10.37212/JCNOS.610108","DOIUrl":"https://doi.org/10.37212/JCNOS.610108","url":null,"abstract":"Depression is a mental disorder that is estimated  by the World Health Organization to affect 350 million  people worldwide. But its pathogenesis and underlying  mechanisms have not been understood yet. To present a  satisfying explanation for the causes and treatments of  these sorts of diseases animal models can be a powerful  model for the researchers.  Experimental animal research has been frequently  used, in related with clinical studies, to test a number of  hypotheses regarding the etiology of depression and its  related behaviors. In the literature, experimental animal  models about depression were described. These are  chronic mild stress, forced swimming test, learned  helplessness, tail suspension test, psycho-stimulant drug  withdrawal and olfactory bulbectomy. In the oral  presentation, it was summarized the experimental  animal models that are used most commonly for  depression, and discussed their advantages and  limitations.  In conclusion, it seems that some experimental  animal models such as chronic mild stress and forced  swimming test in several experiments have been using  for investigating depression etiology and treatment and  the models are very useful for searching the disease.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44062072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}