Calcium imaging is a scientific technique which is designed to measure the intracellular free calcium concentration (Ca2+) in an isolated cell or tissue. Calcium imaging techniques utilizes fluorescent molecules so called Ca2+ indicators that can respond to the binding of Ca2+ ions by changing heir fluorescence properties. Binding of a Ca2+ ion to a fluorescent indicator molecule leads to either an elevation in its fluorescence intensity or emission/excitation wavelength shift. Two main classes of calcium indicators are chemical indicators and genetically encoded calcium indicators. Chemical indicators are small molecules that can bind calcium ions. This group of indicators includes Fura-2, Fluo-3, Fluo-4, Rhod-2. These dyes are often used with acetoxymethyl esters, in order to render the molecule lipophilic and to allow easy entrance into the cell. Genetically encoded indicators do not need to be loaded onto cells, instead the genes encoding for these proteins can be easily transfected to cells. These indicators are fluorescent proteins derived from green fluorescent protein (GFP). The time-scan mode of laser confocal microscopy is often used for calcium imaging. Intracellular Ca 2+ ions generate versatile intracellular signals that control key functions in all types of cells. In sensory neurons Ca2+ signals are associated with pain transmission.
{"title":"Calcium imaging techniques in cell lines","authors":"L. Pecze","doi":"10.37212/jcnos.609922","DOIUrl":"https://doi.org/10.37212/jcnos.609922","url":null,"abstract":"Calcium imaging is a scientific technique which is designed to measure the intracellular free calcium concentration (Ca2+) in an isolated cell or tissue. Calcium imaging techniques utilizes fluorescent molecules so called Ca2+ indicators that can respond to the binding of Ca2+ ions by changing heir fluorescence properties. Binding of a Ca2+ ion to a fluorescent indicator molecule leads to either an elevation in its fluorescence intensity or emission/excitation wavelength shift. Two main classes of calcium indicators are chemical indicators and genetically encoded calcium indicators. Chemical indicators are small molecules that can bind calcium ions. This group of indicators includes Fura-2, Fluo-3, Fluo-4, Rhod-2. These dyes are often used with acetoxymethyl esters, in order to render the molecule lipophilic and to allow easy entrance into the cell. Genetically encoded indicators do not need to be loaded onto cells, instead the genes encoding for these proteins can be easily transfected to cells. These indicators are fluorescent proteins derived from green fluorescent protein (GFP). The time-scan mode of laser confocal microscopy is often used for calcium imaging. Intracellular Ca 2+ ions generate versatile intracellular signals that control key functions in all types of cells. In sensory neurons Ca2+ signals are associated with pain transmission.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46226517","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}
Nicotinamide adenine dinucleotide (NAD+) serves important roles in hydrogen transfer and as the cosubstrate for poly(ADP-ribose) polymerase (PARPs), the sirtuin (SIRT1-7) family of enzymes, and CD38 glycohydrolases. Recently, intravenous (IV) NAD+ therapy has been used as a holistic approach to treat withdrawal from addiction, overcome anxiety and depression, and improve overall quality of life with minimal symptoms between 3-7 days of treatment. We evaluated repeat dose IV NAD+ (1000 mg) for 6 days in a population of 8 healthy adults between the ages of 70 and 80 years. Our data is the first to show that IV NAD+ increases the blood NAD+ metabolome in elderly humans. We found increased concentrations of glutathione peroxidase -3 and paraoxonase-1, and decreased concentrations of 8-iso-prostaglandin F2α, advanced oxidative protein products, protein carbonyl, C-reactive protein and interleukin 6. We report significant increases in mRNA expression and activity of SIRT1, and Forkhead box O1, and reduced acetylated p53 in peripheral blood mononuclear cells isolated from these subjects. No major adverse effects were reported in this study. The study shows that repeat IV dose of NAD+ is a safe and efficient way to slow down age-related decline in NAD+.
{"title":"Intravenous NAD+ effectively increased the NAD metabolome, reduced oxidative stress and inflammation, and increased expression of longevity genes safely in elderly humans","authors":"N. Braidy","doi":"10.37212/JCNOS.610084","DOIUrl":"https://doi.org/10.37212/JCNOS.610084","url":null,"abstract":"Nicotinamide adenine dinucleotide (NAD+) serves important roles in hydrogen transfer and as the cosubstrate for poly(ADP-ribose) polymerase (PARPs), the sirtuin (SIRT1-7) family of enzymes, and CD38 glycohydrolases. Recently, intravenous (IV) NAD+ therapy has been used as a holistic approach to treat withdrawal from addiction, overcome anxiety and depression, and improve overall quality of life with minimal symptoms between 3-7 days of treatment. We evaluated repeat dose IV NAD+ (1000 mg) for 6 days in a population of 8 healthy adults between the ages of 70 and 80 years. Our data is the first to show that IV NAD+ increases the blood NAD+ metabolome in elderly humans. We found increased concentrations of glutathione peroxidase -3 and paraoxonase-1, and decreased concentrations of 8-iso-prostaglandin F2α, advanced oxidative protein products, protein carbonyl, C-reactive protein and interleukin 6. We report significant increases in mRNA expression and activity of SIRT1, and Forkhead box O1, and reduced acetylated p53 in peripheral blood mononuclear cells isolated from these subjects. No major adverse effects were reported in this study. The study shows that repeat IV dose of NAD+ is a safe and efficient way to slow down age-related decline in NAD+.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45745097","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}
Evidence suggests that intestinal microbiota, especially in the case of dysbiosis, may affect the progression of neurological diseases and may even lead to the formation of the disease. It has been realized that decreasing diversity in aging gut of the microbiota may be an important factor in the development of neurodegeneration. Neuroinflammation is one of the major mechanisms that associate microbiota with agerelated diseases. Intestinal microbiota; plays a key role in the activation of microglia and it is suggested that manipulation of intestinal microbiota, especially with short chain fatty acid producing bacteria, may modulate neuroimmun activation (Westfall et al. 2017). On the clinical and scientific level, most neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Disease related pathology may spread across the nervous system in a self-propagative fashion. Importantly, there is a strong bidirectional interaction between gut microbiota and the central nervous system, a connection recently termed the “microbiota-gut-brainaxis” (Jiang et al. 2017; Houser and Tansey, 2017). While the effects of the autonomic nervous system on gut physiology have been known for a long time, we are just beginning to understand that gut microbiota has strong effects on CNS physiology as well. The vast number of ways through which gut microbiota affects the host shows intriguing overlaps with pathways previously implicated in neurodegeneration. Although evidence for involvement of microbiota in neurodegenerative diseases is still very preliminary, initial findings are extremely promising (Zhu et al. 2017). This presentation will give an overview of recent findings regarding the connections between gutmicrobiota and neurodegenerative disorders and how this may reshape our understanding of these diseases.
有证据表明，肠道微生物群，尤其是在微生态失调的情况下，可能会影响神经系统疾病的进展，甚至可能导致疾病的形成。人们已经意识到，衰老肠道微生物群多样性的降低可能是神经退行性变发展的一个重要因素。神经炎症是将微生物群与年龄相关疾病联系起来的主要机制之一。肠道微生物群；在小胶质细胞的激活中起着关键作用，有人认为，对肠道微生物群的操纵，特别是对产生短链脂肪酸的细菌的操纵，可能会调节神经免疫的激活（Westfall等人，2017）。在临床和科学层面上，大多数神经退行性疾病，如阿尔茨海默病、帕金森病和肌萎缩侧索硬化症。与疾病相关的病理学可能以自我传播的方式在整个神经系统中传播。重要的是，肠道微生物群和中枢神经系统之间存在强烈的双向相互作用，这种联系最近被称为“微生物群-肠-脑轴”（Jiang et al.2017；Houser和Tansey，2017）。虽然自主神经系统对肠道生理学的影响已经知道很长时间了，但我们才刚刚开始了解肠道微生物群对中枢神经系统生理学也有很强的影响。肠道微生物群影响宿主的大量途径与以前涉及神经退行性变的途径有着有趣的重叠。尽管微生物群参与神经退行性疾病的证据仍然非常初步，但初步发现非常有希望（Zhu等人，2017）。本报告将概述有关骨微生物群与神经退行性疾病之间联系的最新发现，以及这可能如何重塑我们对这些疾病的理解。
{"title":"Neurodegenerative disease and microbiota","authors":"O. Akpınar","doi":"10.37212/jcnos.610095","DOIUrl":"https://doi.org/10.37212/jcnos.610095","url":null,"abstract":"Evidence suggests that intestinal microbiota, especially in the case of dysbiosis, may affect the progression of neurological diseases and may even lead to the formation of the disease. It has been realized that decreasing diversity in aging gut of the microbiota may be an important factor in the development of neurodegeneration. Neuroinflammation is one of the major mechanisms that associate microbiota with agerelated diseases. Intestinal microbiota; plays a key role in the activation of microglia and it is suggested that manipulation of intestinal microbiota, especially with short chain fatty acid producing bacteria, may modulate neuroimmun activation (Westfall et al. 2017). On the clinical and scientific level, most neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Disease related pathology may spread across the nervous system in a self-propagative fashion. Importantly, there is a strong bidirectional interaction between gut microbiota and the central nervous system, a connection recently termed the “microbiota-gut-brainaxis” (Jiang et al. 2017; Houser and Tansey, 2017). While the effects of the autonomic nervous system on gut physiology have been known for a long time, we are just beginning to understand that gut microbiota has strong effects on CNS physiology as well. The vast number of ways through which gut microbiota affects the host shows intriguing overlaps with pathways previously implicated in neurodegeneration. Although evidence for involvement of microbiota in neurodegenerative diseases is still very preliminary, initial findings are extremely promising (Zhu et al. 2017). This presentation will give an overview of recent findings regarding the connections between gutmicrobiota and neurodegenerative disorders and how this may reshape our understanding of these diseases.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46562767","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}
Traumatic brain injury (TBI) is induced in the brain by external forces such as traffic accidents and heat trauma. Death and disability are induced by the TBI. Indeed, worldwide, about 10 million people are annually deaths or hospitalizations annually by the TBI exposures. In addition, about 57 million exposed to brain injury after TBI annually (Xiong et al. 2013). There is no direct treatment method for the TBI. After the TBI, different pathological processes such as oxidative stress, inflammation and apoptosis are induced by the brain injury. Hence, investigations of new treatment methods in rodent models have important role for inhibition of the pathological processes of human. Marmarou method has been used to make a diffuse head trauma (Marmarou et al. 1994) and it is popular for induction of TBI in rats. Before induction of TBI, the animals should anesthetized by anesthetics such as ketamine and xylazine combination. The animals are placed in prone position on the trauma table under the anesthesia. After skin incision, a steel disc (10 mm X 3 mm) is placed midline between coronal and lambdoid sutures on the animal’s skull, and a 250-300 g weight is freely dropped through a cylindrical tube, with 19 mm inner diameter, from 2 m height onto the head of the animal (Marmarou et al. 1994). In the presentation, a selection of the principal models is described and the model was compared
外伤性脑损伤（TBI）是由交通事故和热创伤等外力在大脑中诱发的。TBI会导致死亡和残疾。事实上，全世界每年约有1000万人因TBI暴露而死亡或住院。此外，每年约有5700万人在TBI后受到脑损伤（Xiong等人，2013）。TBI没有直接的治疗方法。TBI后，脑损伤会诱导不同的病理过程，如氧化应激、炎症和细胞凋亡。因此，在啮齿类动物模型中研究新的治疗方法对抑制人类的病理过程具有重要作用。Marmarou方法已被用于制造弥漫性头部创伤（Marmarou等人，1994），并且它在大鼠中广泛用于诱导TBI。在诱导TBI之前，应使用氯胺酮和甲苯噻嗪等麻醉剂对动物进行麻醉。在麻醉下将动物以俯卧姿势放置在创伤台上。皮肤切开后，将一个钢制圆盘（10 mm X 3 mm）放置在动物头骨上冠状和lambdoid缝合线之间的中线上，并将250-300 g的重物通过内径为19 mm的圆柱形管从2 m高自由下落到动物头部（Marmarou等人，1994）。在演示中，对主要模型的选择进行了描述，并对模型进行了比较
{"title":"Traumatic brain injury models in rats","authors":"Kemal Ertilav","doi":"10.37212/jcnos.610092","DOIUrl":"https://doi.org/10.37212/jcnos.610092","url":null,"abstract":"Traumatic brain injury (TBI) is induced in the brain by external forces such as traffic accidents and heat trauma. Death and disability are induced by the TBI. Indeed, worldwide, about 10 million people are annually deaths or hospitalizations annually by the TBI exposures. In addition, about 57 million exposed to brain injury after TBI annually (Xiong et al. 2013). There is no direct treatment method for the TBI. After the TBI, different pathological processes such as oxidative stress, inflammation and apoptosis are induced by the brain injury. Hence, investigations of new treatment methods in rodent models have important role for inhibition of the pathological processes of human. Marmarou method has been used to make a diffuse head trauma (Marmarou et al. 1994) and it is popular for induction of TBI in rats. Before induction of TBI, the animals should anesthetized by anesthetics such as ketamine and xylazine combination. The animals are placed in prone position on the trauma table under the anesthesia. After skin incision, a steel disc (10 mm X 3 mm) is placed midline between coronal and lambdoid sutures on the animal’s skull, and a 250-300 g weight is freely dropped through a cylindrical tube, with 19 mm inner diameter, from 2 m height onto the head of the animal (Marmarou et al. 1994). In the presentation, a selection of the principal models is described and the model was compared","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46794731","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}
Humans coexist in a mutualistic relationship with the intestinal microbiota, a complex microbial ecosystem that resides largely in the distal bowel. The lower gastrointestinal tract contains almost 100 trillion microorganisms, most of which are bacteria. More than 1,000 bacterial species have been identified in this microbiota. The intestinal microbiota lives in a symbiotic relationship with the host. A bidirectional neurohumoral communication system, known as the gut–brain axis, integrates the host gut and brain activities (Mayer et al. 2015). Communication between the brain and gut occurs along a network of pathways collectively termed the brain-gut axis. The brain-gut axis encompass the CNS, ENS, sympathetic and parasympathetic branches of the autonomic nervous system, neuroendocrine and neuroimmune pathways, and the gut microbiota (Colins et al. 2012). The gut microbiota can signal to the brain via a number of pathways which include: regulating immune activity and the production of roinflammatory cytokines that can either stimulate the HPA axis to produce CRH, ACTH and cortisol, or directly impact on CNS immune activity; through the production of SCFAs such as propionate, butyrate, and acetate; the production of neurotransmitters which may enter circulation and cross the blood brain barrier; by modulating tryptophan metabolism and downstream metabolites, serotonin, kynurenic acid and quinolinic acid. Neuronal and spinal pathways, particularly afferent signaling pathways of the vagus nerve, are critical in mediating the effect of the gut microbiota on brain function and behavior. Microbial produced SCFAs and indole also impact on EC cells of the enteric nervous system (Romijn et al. 2008; Cani et al. 2013). The purpose of this presentation was to summarize our current knowledge regarding the role of microbiota in bottom-up pathways of communication in the gutbrain axis.
人类与肠道微生物群共存，肠道微生物群是一个复杂的微生物生态系统，主要位于远端肠道。下胃肠道含有近100万亿个微生物，其中大部分是细菌。在这个微生物群中已经发现了1000多种细菌。肠道菌群与宿主是一种共生关系。被称为肠脑轴的双向神经体液通讯系统整合了宿主肠道和大脑活动(Mayer et al. 2015)。大脑和肠道之间的交流发生在一个被统称为脑肠轴的通路网络上。脑肠轴包括中枢神经系统、ENS、自主神经系统的交感神经和副交感神经分支、神经内分泌和神经免疫途径以及肠道微生物群(collins et al. 2012)。肠道微生物群可以通过多种途径向大脑发出信号，其中包括:调节免疫活性和炎症细胞因子的产生，这些细胞因子可以刺激HPA轴产生CRH, ACTH和皮质醇，或直接影响CNS免疫活性;通过生产丙酸、丁酸和醋酸酯等短链脂肪酸;神经递质的产生可能进入血液循环并穿过血脑屏障;通过调节色氨酸代谢和下游代谢物，血清素，犬尿酸和喹啉酸。神经元和脊髓通路，特别是迷走神经的传入信号通路，在调节肠道微生物群对脑功能和行为的影响方面至关重要。微生物产生的短链脂肪酸和吲哚也会影响肠神经系统的EC细胞(Romijn et al. 2008;Cani et al. 2013)。本报告的目的是总结我们目前关于微生物群在肠脑轴自下而上的沟通途径中的作用的知识。
{"title":"The gut-brain axis: interactions between microbiota and nervous systems","authors":"O. Akpınar","doi":"10.37212/JCNOS.610103","DOIUrl":"https://doi.org/10.37212/JCNOS.610103","url":null,"abstract":"Humans coexist in a mutualistic relationship with the intestinal microbiota, a complex microbial ecosystem that resides largely in the distal bowel. The lower gastrointestinal tract contains almost 100 trillion microorganisms, most of which are bacteria. More than 1,000 bacterial species have been identified in this microbiota. The intestinal microbiota lives in a symbiotic relationship with the host. A bidirectional neurohumoral communication system, known as the gut–brain axis, integrates the host gut and brain activities (Mayer et al. 2015). Communication between the brain and gut occurs along a network of pathways collectively termed the brain-gut axis. The brain-gut axis encompass the CNS, ENS, sympathetic and parasympathetic branches of the autonomic nervous system, neuroendocrine and neuroimmune pathways, and the gut microbiota (Colins et al. 2012). The gut microbiota can signal to the brain via a number of pathways which include: regulating immune activity and the production of roinflammatory cytokines that can either stimulate the HPA axis to produce CRH, ACTH and cortisol, or directly impact on CNS immune activity; through the production of SCFAs such as propionate, butyrate, and acetate; the production of neurotransmitters which may enter circulation and cross the blood brain barrier; by modulating tryptophan metabolism and downstream metabolites, serotonin, kynurenic acid and quinolinic acid. Neuronal and spinal pathways, particularly afferent signaling pathways of the vagus nerve, are critical in mediating the effect of the gut microbiota on brain function and behavior. Microbial produced SCFAs and indole also impact on EC cells of the enteric nervous system (Romijn et al. 2008; Cani et al. 2013). The purpose of this presentation was to summarize our current knowledge regarding the role of microbiota in bottom-up pathways of communication in the gutbrain axis.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44445093","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}
Stroke is the second cause of death worldwide. Stroke induces cerebral ischemia. The cerebral ischemia is a neurodegenerative disease that causes disability and mortality. An accumulating body of evidence indicates that abnormalities of Ca2+ homeostasis are caused by excessive levels of free oxygen radicals in rats with cerebral ischemia. Occlusion of middle cerebral artery in human induces cerebral ischemic stroke. In experimental animals, best model of induction of cerebral ischemic stroke is occlusion of middle cerebral artery for 30 min (Canazza et al. 2014). In cerebral ischemia stoke model, right or left middle cerebral artery is exposed through a ventral midline incision in the neck and it is loosely encircled with sutures for further occlusion. Following a midline incision, the skull is craniectomized to expose the right or left common carotid artery. A 3-0 suture is positioned so that it encircled the middle cerebral artery for further occlusion. Cerebral ischemic surgery is performed through occlusion of the right or left middle cerebral artery for 30 min (Akpinar et al. 2016). In addition to the best model, there are also other models of cerebral stroke in rodents such as the intra-luminal suture, thromboembolic, the coagulation or ligation, the endothelin-1, and the distal artery compression models (Canazza et al. 2014). In the presentation, a selection of the principal models is described and the model was compared with the other models.
{"title":"Cerebral ischemia models in rats","authors":"Zeki Serdar Ataizi","doi":"10.37212/jcnos.610115","DOIUrl":"https://doi.org/10.37212/jcnos.610115","url":null,"abstract":"Stroke is the second cause of death worldwide. Stroke induces cerebral ischemia. The cerebral ischemia is a neurodegenerative disease that causes disability and mortality. An accumulating body of evidence indicates that abnormalities of Ca2+ homeostasis are caused by excessive levels of free oxygen radicals in rats with cerebral ischemia. Occlusion of middle cerebral artery in human induces cerebral ischemic stroke. In experimental animals, best model of induction of cerebral ischemic stroke is occlusion of middle cerebral artery for 30 min (Canazza et al. 2014). In cerebral ischemia stoke model, right or left middle cerebral artery is exposed through a ventral midline incision in the neck and it is loosely encircled with sutures for further occlusion. Following a midline incision, the skull is craniectomized to expose the right or left common carotid artery. A 3-0 suture is positioned so that it encircled the middle cerebral artery for further occlusion. Cerebral ischemic surgery is performed through occlusion of the right or left middle cerebral artery for 30 min (Akpinar et al. 2016). In addition to the best model, there are also other models of cerebral stroke in rodents such as the intra-luminal suture, thromboembolic, the coagulation or ligation, the endothelin-1, and the distal artery compression models (Canazza et al. 2014). In the presentation, a selection of the principal models is described and the model was compared with the other models.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43232881","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}
The trachea has a composite structure with individual and incomplete cartilaginous rings. Deformation of trachea through surgical process and mechanical applications induces injury of laryngotracheal mucosa (Hussain et al. 2015). Results of recent studies studying the oxidative related values in larynx cancer indicated the importance of oxidative stress. Main reactive oxygen species (ROS) are superoxide radical, hydroxyl radical and singlet oxygen. Production normal level of ROS is a physiological process, because the ROS has been using for physiological functions such as killing bacteria and viruses in the body. The excessive production of ROS is scavenged by enzymatic and non-enzymatic antioxidants. 900 and 1800 MHz frequencies are used in cell phones in several countries including Turkey, although 2450 MHz has been using as Wi-Fi frequency in the countries. The non-ionize cell phone and Wi-Fi frequencies induce their hazardous effects in cells including laryngeal mucosa by excessive production of ROS. Results of recent papers indicated that the antioxidant levels such as glutathione and glutathione peroxidase were decreased in the laryngeal mucosa of animals by the cell phone and Wi-Fi exposures, but oxidative stress levels were increased by the exposures (Aynali et al. 2013). In the oral presentation, I will summarize the results of recent papers on oxidative stress and antioxidants in neurons and cells including laryngeal mucosa. In conclusion, exposure to the frequencies is accompanied by increased oxidative stress, suggesting that oxidative stress is a cause of electromagnetic radiation-induced laryngotracheal pathophysiology. For clarifying the subject, future studies need on the Wi-Fi and mobile phone frequencies-induced oxidative stress in larynx of animal and human
{"title":"Effects of cell phone (900 and 1800 MHz) and Wi-Fi (2450 MHz) frequencies on oxidative stress in laryngeal mucosa","authors":"S. G. Kütük","doi":"10.37212/JCNOS.610132","DOIUrl":"https://doi.org/10.37212/JCNOS.610132","url":null,"abstract":"The trachea has a composite structure with individual and incomplete cartilaginous rings. Deformation of trachea through surgical process and mechanical applications induces injury of laryngotracheal mucosa (Hussain et al. 2015). Results of recent studies studying the oxidative related values in larynx cancer indicated the importance of oxidative stress. Main reactive oxygen species (ROS) are superoxide radical, hydroxyl radical and singlet oxygen. Production normal level of ROS is a physiological process, because the ROS has been using for physiological functions such as killing bacteria and viruses in the body. The excessive production of ROS is scavenged by enzymatic and non-enzymatic antioxidants. 900 and 1800 MHz frequencies are used in cell phones in several countries including Turkey, although 2450 MHz has been using as Wi-Fi frequency in the countries. The non-ionize cell phone and Wi-Fi frequencies induce their hazardous effects in cells including laryngeal mucosa by excessive production of ROS. Results of recent papers indicated that the antioxidant levels such as glutathione and glutathione peroxidase were decreased in the laryngeal mucosa of animals by the cell phone and Wi-Fi exposures, but oxidative stress levels were increased by the exposures (Aynali et al. 2013). In the oral presentation, I will summarize the results of recent papers on oxidative stress and antioxidants in neurons and cells including laryngeal mucosa. In conclusion, exposure to the frequencies is accompanied by increased oxidative stress, suggesting that oxidative stress is a cause of electromagnetic radiation-induced laryngotracheal pathophysiology. For clarifying the subject, future studies need on the Wi-Fi and mobile phone frequencies-induced oxidative stress in larynx of animal and human","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46204991","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}
Human gut microbiota (GM) has now been accepted as a potential modulator ofhuman biology. Although new to the world of science, GM's impaction brain and behavior has drawn great attention around the globe. Studies have now proven that GM can directly or indirectly modify brain neurochemistry via various mechanisms like neural, immune and endocrine. The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. This presentation is an overview of recent findings regarding the GM -brain axis in PD (Braniste et al. 2014; Sampson et al. 2016) Parkinson disease (PD) is the second-most common neurodegenerative disorder. PD patients show alpha-synuclein deposits and neurodegeneration in the enteric nervous system as well as breakdown of the mucosal barrier, bacterial invasion, and mucosal inflammation in the colon. Alterations in GM and increased gut permeability may influence PD pathophysiology via epigenetic processes that alter αSyn regulation (Matsumoto et al. 2010). Sampson et al. (2016) suggest that GM are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. They propose that GM regulate movement disorders and suggest that alterations in the human microbiome represent a risk factor for PD. GM do not only affect gut physiology, but there is also an intense bidirectional interaction with the brain influencing neuronal activity, behavior, as well as levels of neurotransmitter receptors, neurotrophic factors, and inflammation. Recently, gut microbiome alterations in PD subjects and a connection between GM and motoras well as non-motor symptoms have been described (Sampson et al. 2016; Parashar and Udayabanu 2017)
人类肠道菌群(GM)现已被认为是人类生物学的潜在调节剂。虽然转基因对科学界来说是一个新事物，但它对大脑和行为的影响已经引起了全球的极大关注。目前已有研究证明转基因可以通过神经、免疫、内分泌等多种机制直接或间接地改变脑神经化学。肠道微生物群影响神经发育，调节行为，并有助于神经系统疾病。本报告概述了PD中GM -脑轴的最新发现(Braniste et al. 2014;Sampson et al. 2016)帕金森病(PD)是第二常见的神经退行性疾病。PD患者表现为-突触核蛋白沉积和肠神经系统神经退行性变，以及粘膜屏障破坏、细菌侵袭和结肠粘膜炎症。GM的改变和肠道通透性的增加可能通过改变α - syn调节的表观遗传过程影响PD的病理生理(Matsumoto et al. 2010)。Sampson等人(2016)认为，通过影响神经炎症和αSyn聚集的微生物分子在出生后的肠-脑信号传导，转基因是PD小鼠模型中标志性的运动和GI功能障碍所必需的。他们提出转基因调节运动障碍，并提出人类微生物组的改变是帕金森病的一个危险因素。转基因不仅影响肠道生理，而且还与大脑产生强烈的双向相互作用，影响神经元活动、行为以及神经递质受体、神经营养因子和炎症的水平。最近，研究人员描述了PD患者肠道微生物组的改变以及GM与运动和非运动症状之间的联系(Sampson等人，2016;Parashar and Udayabanu 2017)
{"title":"Human gut microbiota and Parkinson Disease","authors":"M. Güzel","doi":"10.37212/jcnos.610152","DOIUrl":"https://doi.org/10.37212/jcnos.610152","url":null,"abstract":"Human gut microbiota (GM) has now been accepted as a potential modulator ofhuman biology. Although new to the world of science, GM's impaction brain and behavior has drawn great attention around the globe. Studies have now proven that GM can directly or indirectly modify brain neurochemistry via various mechanisms like neural, immune and endocrine. The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. This presentation is an overview of recent findings regarding the GM -brain axis in PD (Braniste et al. 2014; Sampson et al. 2016) Parkinson disease (PD) is the second-most common neurodegenerative disorder. PD patients show alpha-synuclein deposits and neurodegeneration in the enteric nervous system as well as breakdown of the mucosal barrier, bacterial invasion, and mucosal inflammation in the colon. Alterations in GM and increased gut permeability may influence PD pathophysiology via epigenetic processes that alter αSyn regulation (Matsumoto et al. 2010). Sampson et al. (2016) suggest that GM are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. They propose that GM regulate movement disorders and suggest that alterations in the human microbiome represent a risk factor for PD. GM do not only affect gut physiology, but there is also an intense bidirectional interaction with the brain influencing neuronal activity, behavior, as well as levels of neurotransmitter receptors, neurotrophic factors, and inflammation. Recently, gut microbiome alterations in PD subjects and a connection between GM and motoras well as non-motor symptoms have been described (Sampson et al. 2016; Parashar and Udayabanu 2017)","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47910351","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}
Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.
{"title":"Role of melatonin on oxidative stress in traumatic brain injury","authors":"Y. Akyuva","doi":"10.37212/jcnos.610135","DOIUrl":"https://doi.org/10.37212/jcnos.610135","url":null,"abstract":"Oxidative stress occurs in the several physiological processes such as phagocytic activity and mitochondrial membrane functions. Oxidative stress is controlled by several enzymatic and non-enzymatic antioxidants. Traumatic brain injury is one of the most common causes of the mortalities. Secondary events occur after primary events like shearing of nerve cells and blood vessels, cause posttraumatic neurodegenerations with an increase in ROS and ROSmediated lipid peroxidation. Melatonin is a member of non-enzymatic antioxidant group. The protective effects of melatonin on traumatic brain injury have been shown in vivo and in vitro studies (Barlow et al. 2018). Also melatonin has been shown to counteract oxidative stress-induced pathophysiologic conditions like ischemia/reperfusion injury, neuronal excitotoxicity and chronic inflammation. Recently, it was reported that TBI-induced oxidative stress in experimental TBI was inhibited by the melatonin treatment (Senol and Naziroglu, 2014). In the oral presentation, I will review recent studies on traumatic brain injury in human and rodents. I concluded that the oxidative stress causes changes through activation of second messengers, which may lead to the pathology of TBI, although melatonin has protective effects on the pathology. It seems to that the exact relationship between melatonin and TBI still remain to be determined.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47193673","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}
Alzheimer's Disease (AD) is a degenerative, chronic, progressive disease of CNS. Pathological changes that develop in the course of the disease lead to memory loss, alteration of thought, and deterioration of other brain functions. The disease progresses slowly, resulting in cell death and brain damage (Jiang 2017; Knopman 2016). Increased permeability of the intestinal and blood brain barrier due to microbial dysbosis plays a role in the pathogenesis of AD and other neurodegenerative disorders associated with aging. In addition, intestinal microbiota bacterial populations secrete amyloids and lipopolysaccharides in large quantities, which may contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD (Jiang 2017). Amyloid precursor protein (APP) , which constitutes Aβ plaques and is normally secreted by intestinal bacteria, is expressed by the enteric nervous system. However, the accumulation corrupts the CNS functions. Escherichia Coli and Salmonella Enterica are some of the many bacterial strains that express and secrete APP and play a role in the pathogenesis of AD (Tse 2017). Production and clearance of Aβ in CNS is a dynamic change and some bacteria and fungi are amyloid secretions, which disrupt the dynamic balance of Aβ protein in CNS and increase the amyloid levels. This causes Aβ protein accumulation in the brain and a high risk of AD (Hill 2015).It is very important for cognitive function in serotonin, 95% of serotonin is synthesized in intestines and intestinal microorganisms play an important role in the synthesis of serotonin. There is evidence that serotonin may reduce the formation of Aβ plaques and thus reduce AD risk (Hill 2015; Jiang 2017).
{"title":"Dysbiosis of gut microbiota and Alzheimer’s Disease","authors":"O. Akpınar","doi":"10.37212/jcnos.610150","DOIUrl":"https://doi.org/10.37212/jcnos.610150","url":null,"abstract":"Alzheimer's Disease (AD) is a degenerative, chronic, progressive disease of CNS. Pathological changes that develop in the course of the disease lead to memory loss, alteration of thought, and deterioration of other brain functions. The disease progresses slowly, resulting in cell death and brain damage (Jiang 2017; Knopman 2016). Increased permeability of the intestinal and blood brain barrier due to microbial dysbosis plays a role in the pathogenesis of AD and other neurodegenerative disorders associated with aging. In addition, intestinal microbiota bacterial populations secrete amyloids and lipopolysaccharides in large quantities, which may contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD (Jiang 2017). Amyloid precursor protein (APP) , which constitutes Aβ plaques and is normally secreted by intestinal bacteria, is expressed by the enteric nervous system. However, the accumulation corrupts the CNS functions. Escherichia Coli and Salmonella Enterica are some of the many bacterial strains that express and secrete APP and play a role in the pathogenesis of AD (Tse 2017). Production and clearance of Aβ in CNS is a dynamic change and some bacteria and fungi are amyloid secretions, which disrupt the dynamic balance of Aβ protein in CNS and increase the amyloid levels. This causes Aβ protein accumulation in the brain and a high risk of AD (Hill 2015).It is very important for cognitive function in serotonin, 95% of serotonin is synthesized in intestines and intestinal microorganisms play an important role in the synthesis of serotonin. There is evidence that serotonin may reduce the formation of Aβ plaques and thus reduce AD risk (Hill 2015; Jiang 2017).","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47368946","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}
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