{"title":"The Heredity of Beauty","authors":"M. Sasaki, Aliss D. Abdel, E. Dinu","doi":"10.22186/JYI.34.4.1-6","DOIUrl":"https://doi.org/10.22186/JYI.34.4.1-6","url":null,"abstract":"","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42020454","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}
artery disease, hypertension, metabolic syndrome, gall bladder disease, cancer, osteoarthritis and type 2 diabetes (Rodriguez-Hernandez, Simental-Mendia, Rodriguez-Ramirez, & Reyes-Romero, 2013). Among the obesity related diseases, type 2 diabetes has recently been classified an autoimmune disease involving inflammation through NLRP3 activation (Bray, 2004; Gunter & Leitzmann, 2006; Hajer, Haeften, & Visseren 2008). Studies have investigated the relationship between type 2 diabetes, insulin resistance and IL1β expression (Gao et al, 2014; Larsen et al, 2007). Larsen et al.’s experimental results (2007) showed that blockade of IL-1β expression in patients with type 2 diabetes improved β-cell function and promoted glycemic control while Goa et al.’s results (2014) showed that IL-1β presence in human adipocytes significantly reduced the gene expression of insulin signaling molecules and its absence improved insulin sensitivity. The secretion of IL-1β is regulated by the Nod-Like Receptor protein 3 (NLRP3) inflammasome. IL-1β secretion is carried out in two steps. The first signal, also known as the priming step, consists of activation of Nod-Like Receptor protein 3 (NLRP3) coupled with accumulation of proIL-1β the inactivated precursor protein for IL-1β. Upon accumulation of the precursor, a second signal is needed to recruit the NLRP3 inflammasome complex, consisting of (NLRP3), adaptor protein apoptosis speck-like Protein (ASC) and activated caspase 1, consequently responsible for cleavage of pro-IL-1β to secretion as Il-1β (Figure 1). When NLRP3/IL-1β pathway is activated, ROS production is also observed (Jo, Kim, Shin, & Sasakawa et al, 2016). An article (Tschopp & Schroder, 2010) suggested that mitochondrial ROS is not only correlated with NLRP3 activation, but is involved in assembling the NLRP3 inflammasome complex. Mitochondria are considered the main source of ROS in INTRODUCTION Western culture has adopted a diet rich in energy-loaded carbohydrates. This increased consumption of high-energy foods has been accompanied by reliance on mechanical technology to do work, reducing necessary physical activity (Popkin, 2001). The ratio of energy consumed to energy spent is imbalanced in favor of consumption, which results in storage of fat cells as adipose tissue and uncontrolled deposition of fats could lead to an individual carrying an excess amount of weight, referred to as being overweight or obese. This condition can be defined using the body mass index (BMI) of an individual (Finucane et al, 2011). Higher BMIs correspond to excess weight and obesity. Studies (Finucane et al, 2011) show that the mean BMI worldwide has increased over the years and so has the rate of obesity. In 2008, over 500 million people worldwide were considered obese and about 1.46 billion were overweight (Finucane et al, 2011). In obese individuals, enlarged fat cells secrete fatty acids and cytokine factors such as tumor necrosis factor-α (TNF-α), that are capable of cau
动脉疾病、高血压、代谢综合征、胆囊疾病、癌症、骨关节炎和2型糖尿病(Rodriguez-Hernandez, simmental - mendia, Rodriguez-Ramirez， & Reyes-Romero, 2013)。在肥胖相关疾病中，2型糖尿病最近被归类为一种通过NLRP3激活引起炎症的自身免疫性疾病(Bray, 2004;Gunter & Leitzmann, 2006;Hajer, Haeften， & Visseren 2008)。有研究调查了2型糖尿病、胰岛素抵抗和il - 1β表达之间的关系(Gao et al .， 2014;Larsen et al, 2007)。Larsen等(2007)的实验结果表明，阻断2型糖尿病患者IL-1β的表达可改善β细胞功能，促进血糖控制。Goa等(2014)的研究结果表明，人脂肪细胞中IL-1β的存在可显著降低胰岛素信号分子的基因表达，IL-1β的缺失可改善胰岛素敏感性。IL-1β的分泌受nod样受体蛋白3 (NLRP3)炎性体的调节。IL-1β的分泌分两步进行。第一个信号，也被称为启动步骤，包括nod样受体蛋白3 (NLRP3)的激活以及IL-1β (IL-1β的失活前体蛋白)的积累。在前体积累后，需要第二个信号来招募NLRP3炎性小体复合物，该复合物由NLRP3、接头蛋白凋亡斑点样蛋白(ASC)和活化的caspase 1组成，因此负责切割Il-1β前体并以Il-1β的形式分泌(图1)。当NLRP3/ Il-1β途径被激活时，也可以观察到ROS的产生(Jo, Kim, Shin， & Sasakawa等，2016)。一篇文章(Tschopp & Schroder, 2010)认为线粒体ROS不仅与NLRP3激活相关，还参与了NLRP3炎性体复合物的组装。线粒体被认为是活性氧的主要来源。西方文化已经采用了富含能量的碳水化合物的饮食。高能量食物的消费增加伴随着对机械技术的依赖来完成工作，减少了必要的身体活动(Popkin, 2001)。消耗的能量和消耗的能量的比例是不平衡的，有利于消耗，这导致脂肪细胞作为脂肪组织储存，脂肪不受控制的沉积可能导致个体携带过量的体重，被称为超重或肥胖。这种情况可以用个体的身体质量指数(BMI)来定义(Finucane et al, 2011)。较高的bmi与超重和肥胖相对应。研究(Finucane et al, 2011)表明，多年来，全球平均体重指数有所上升，肥胖率也有所上升。2008年，全世界有超过5亿人被认为肥胖，约14.6亿人超重(Finucane et al, 2011)。在肥胖个体中，增大的脂肪细胞分泌脂肪酸和肿瘤坏死因子-α (TNF-α)等细胞因子，能够引起广泛的下游效应，如冠状动脉等多种疾病的高风险
{"title":"Effects of High Fructose/Glucose on Nlrp3/Il1ß Inflammatory Pathway","authors":"E. Araoye, K. Ckless","doi":"10.22186/jyi.31.5.25-30","DOIUrl":"https://doi.org/10.22186/jyi.31.5.25-30","url":null,"abstract":"artery disease, hypertension, metabolic syndrome, gall bladder disease, cancer, osteoarthritis and type 2 diabetes (Rodriguez-Hernandez, Simental-Mendia, Rodriguez-Ramirez, & Reyes-Romero, 2013). Among the obesity related diseases, type 2 diabetes has recently been classified an autoimmune disease involving inflammation through NLRP3 activation (Bray, 2004; Gunter & Leitzmann, 2006; Hajer, Haeften, & Visseren 2008). Studies have investigated the relationship between type 2 diabetes, insulin resistance and IL1β expression (Gao et al, 2014; Larsen et al, 2007). Larsen et al.’s experimental results (2007) showed that blockade of IL-1β expression in patients with type 2 diabetes improved β-cell function and promoted glycemic control while Goa et al.’s results (2014) showed that IL-1β presence in human adipocytes significantly reduced the gene expression of insulin signaling molecules and its absence improved insulin sensitivity. The secretion of IL-1β is regulated by the Nod-Like Receptor protein 3 (NLRP3) inflammasome. IL-1β secretion is carried out in two steps. The first signal, also known as the priming step, consists of activation of Nod-Like Receptor protein 3 (NLRP3) coupled with accumulation of proIL-1β the inactivated precursor protein for IL-1β. Upon accumulation of the precursor, a second signal is needed to recruit the NLRP3 inflammasome complex, consisting of (NLRP3), adaptor protein apoptosis speck-like Protein (ASC) and activated caspase 1, consequently responsible for cleavage of pro-IL-1β to secretion as Il-1β (Figure 1). When NLRP3/IL-1β pathway is activated, ROS production is also observed (Jo, Kim, Shin, & Sasakawa et al, 2016). An article (Tschopp & Schroder, 2010) suggested that mitochondrial ROS is not only correlated with NLRP3 activation, but is involved in assembling the NLRP3 inflammasome complex. Mitochondria are considered the main source of ROS in INTRODUCTION Western culture has adopted a diet rich in energy-loaded carbohydrates. This increased consumption of high-energy foods has been accompanied by reliance on mechanical technology to do work, reducing necessary physical activity (Popkin, 2001). The ratio of energy consumed to energy spent is imbalanced in favor of consumption, which results in storage of fat cells as adipose tissue and uncontrolled deposition of fats could lead to an individual carrying an excess amount of weight, referred to as being overweight or obese. This condition can be defined using the body mass index (BMI) of an individual (Finucane et al, 2011). Higher BMIs correspond to excess weight and obesity. Studies (Finucane et al, 2011) show that the mean BMI worldwide has increased over the years and so has the rate of obesity. In 2008, over 500 million people worldwide were considered obese and about 1.46 billion were overweight (Finucane et al, 2011). In obese individuals, enlarged fat cells secrete fatty acids and cytokine factors such as tumor necrosis factor-α (TNF-α), that are capable of cau","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46974596","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}
With regards to the correlations between TEC and pre-earthquake and seismic activities, the TEC is an important parameter of study because it has the potential for showing the changes in the ionosphere due to these activities. It is because seismic and pre-earthquake activities create stress in rocks in the earth’s crust. These stresses are known to positively charge the rocks on the earth’s crust. As the positive charges accumulate at the rocks outer surfaces, they create a difference in potential which in turn creates a flow of charges that can travel fast and far from their point of origin. As the charges travel upward under the influence of the electric field lines between the surface of earth and the bottom of the ionosphere, they reach the bottom of the ionosphere, disturbing the equilibrium of the electrons in the ionosphere (Freund, Takeuchi & Lau, 2006). These disturbances can be seen in the TEC which makes TEC a potential candidate as an earthquake precursor. If TEC disturbances could be used as an earthquake precursor, tracking those disturbances could be used as part of an earthquake forecasting system which would improve earthquake warning systems, in turn saving countless lives. This study uses TEC data from Japan and current knowledge of the Tōhoku Japan earthquake to determine whether pre-earthquake and seismic activities correlate with TEC changes around the time of the earthquake.
{"title":"Total Electron Content (TEC) Variations and Correlation with Seismic Activity over Japan","authors":"Joseph A. Hammerstrom, P. Cornely","doi":"10.22186/jyi.31.4.13-16","DOIUrl":"https://doi.org/10.22186/jyi.31.4.13-16","url":null,"abstract":"With regards to the correlations between TEC and pre-earthquake and seismic activities, the TEC is an important parameter of study because it has the potential for showing the changes in the ionosphere due to these activities. It is because seismic and pre-earthquake activities create stress in rocks in the earth’s crust. These stresses are known to positively charge the rocks on the earth’s crust. As the positive charges accumulate at the rocks outer surfaces, they create a difference in potential which in turn creates a flow of charges that can travel fast and far from their point of origin. As the charges travel upward under the influence of the electric field lines between the surface of earth and the bottom of the ionosphere, they reach the bottom of the ionosphere, disturbing the equilibrium of the electrons in the ionosphere (Freund, Takeuchi & Lau, 2006). These disturbances can be seen in the TEC which makes TEC a potential candidate as an earthquake precursor. If TEC disturbances could be used as an earthquake precursor, tracking those disturbances could be used as part of an earthquake forecasting system which would improve earthquake warning systems, in turn saving countless lives. This study uses TEC data from Japan and current knowledge of the Tōhoku Japan earthquake to determine whether pre-earthquake and seismic activities correlate with TEC changes around the time of the earthquake.","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45661304","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}
2016). Alpha-synuclein aggregation leads to Lewy body formation, the characteristic pathological marker. It is currently unclear whether dopaminergic atrophy leads to alpha-synuclein aggregation or if it is the aggregates that lead to cell death. Few causative factors have thus far been supported, though some environmental toxins have been shown to cause disease symptomology (Pan-Montojo & Reichmann, 2014). For example, exposure to the herbicide Paraquat can result in dopaminergic degeneration and Lewy body formation in the substantia nigra by generating high levels of oxidative stress (Pan-Montojo & Reichmann, 2014). In addition, the production of the synthetic opioid drug MPPP can generate an accidental compound MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which quickly induces a Parkinsonian state when its toxic metabolite inhibits complex I of the electron transport chain (Pan-Montojo & Reichmann, 2014). The possibility of an endogenous neurotoxic mechanism that was acquired in early life has been contemplated for many years (Gibb & Lees, 1988). It is thought that this potential pathogen is transported from the gastrointestinal (GI) tract to the brain via the vagus nerve over the course of twenty years (Syensson et al., 2015). Svensson and colleagues (2015) examined a cohort of patients who underwent vagotomies. They found that patients who received a truncal vagotomy (i.e., the surgical severance of both vagal trunks) had a lower risk of Parkinson’s disease compared to a INTRODUCTION Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder in the elderly population, following Alzheimer’s disease (Lin et al., 2014). PD is a chronic disorder, characterized primarily by motor deficits including resting tremor, rigidity, bradykinesia, and postural instability (Burke & O’Malley, 2013; Choi et al., 2016; Lohr & Miller, 2014; Miller et al., 1999; Taylor et al., 2014). Although dopaminergic atrophy in the substantia nigra pars compacta mediates the presence of these motor deficits, the clinical indicators do not appear until over 70% of dopamine (DA) nerve terminals in the striatum have atrophied, suggesting the presence of compensatory mechanisms (Bezard et al., 2013). In disease propagation, alpha-synuclein proteins bind ubiquitin ligands and accumulate in damaged cells (Rao & Gershon, A New Perspective on Parkinson’s Disease: Pathology Begins in the Gastrointestinal Tract
2016)。-突触核蛋白聚集导致路易体形成，这是典型的病理标志。目前尚不清楚是多巴胺能萎缩导致α -突触核蛋白聚集，还是聚集导致细胞死亡。迄今为止，虽然一些环境毒素已被证明会导致疾病症状，但很少有致病因素得到支持(Pan-Montojo & Reichmann, 2014)。例如，暴露于除草剂百草枯可通过产生高水平的氧化应激导致黑质中多巴胺能变性和路易体形成(Pan-Montojo & Reichmann, 2014)。此外，合成阿片类药物MPPP的生产可以产生意外化合物MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶)，当其有毒代谢物抑制电子传递链的复合物I时，MPTP迅速诱导帕金森状态(Pan-Montojo & Reichmann, 2014)。在生命早期获得的内源性神经毒性机制的可能性已经被考虑了很多年(Gibb & Lees, 1988)。据认为，这种潜在的病原体在20年的时间里通过迷走神经从胃肠道运输到大脑(Syensson et al.， 2015)。Svensson及其同事(2015)研究了一组接受迷走神经切开术的患者。他们发现接受迷走神经截切术(即手术切除迷走神经主干)的患者患帕金森病的风险较低。帕金森病(PD)是老年人群中第二大常见的神经退行性疾病，仅次于阿尔茨海默病(Lin et al.， 2014)。PD是一种慢性疾病，主要以运动缺陷为特征，包括静息性震颤、强直、运动迟缓和姿势不稳定(Burke & O 'Malley, 2013;Choi et al.， 2016;Lohr & Miller, 2014;Miller et al.， 1999;Taylor et al.， 2014)。尽管黑质致密部多巴胺能萎缩介导了这些运动缺陷的存在，但直到纹状体中超过70%的多巴胺(DA)神经末梢萎缩后，临床指标才出现，这表明存在代偿机制(Bezard等人，2013)。在疾病传播过程中，α -突触核蛋白结合泛素配体并在受损细胞中积累(Rao & Gershon, A New Perspective on Parkinson 's disease: Pathology Begins In胃肠道)
{"title":"A new perspective on parkinson's disease: pathology begins in the gastrointestinal tract","authors":"Kianna J. Mau, N. Jadavji","doi":"10.22186/jyi.33.4.63-70","DOIUrl":"https://doi.org/10.22186/jyi.33.4.63-70","url":null,"abstract":"2016). Alpha-synuclein aggregation leads to Lewy body formation, the characteristic pathological marker. It is currently unclear whether dopaminergic atrophy leads to alpha-synuclein aggregation or if it is the aggregates that lead to cell death. Few causative factors have thus far been supported, though some environmental toxins have been shown to cause disease symptomology (Pan-Montojo & Reichmann, 2014). For example, exposure to the herbicide Paraquat can result in dopaminergic degeneration and Lewy body formation in the substantia nigra by generating high levels of oxidative stress (Pan-Montojo & Reichmann, 2014). In addition, the production of the synthetic opioid drug MPPP can generate an accidental compound MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), which quickly induces a Parkinsonian state when its toxic metabolite inhibits complex I of the electron transport chain (Pan-Montojo & Reichmann, 2014). The possibility of an endogenous neurotoxic mechanism that was acquired in early life has been contemplated for many years (Gibb & Lees, 1988). It is thought that this potential pathogen is transported from the gastrointestinal (GI) tract to the brain via the vagus nerve over the course of twenty years (Syensson et al., 2015). Svensson and colleagues (2015) examined a cohort of patients who underwent vagotomies. They found that patients who received a truncal vagotomy (i.e., the surgical severance of both vagal trunks) had a lower risk of Parkinson’s disease compared to a INTRODUCTION Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder in the elderly population, following Alzheimer’s disease (Lin et al., 2014). PD is a chronic disorder, characterized primarily by motor deficits including resting tremor, rigidity, bradykinesia, and postural instability (Burke & O’Malley, 2013; Choi et al., 2016; Lohr & Miller, 2014; Miller et al., 1999; Taylor et al., 2014). Although dopaminergic atrophy in the substantia nigra pars compacta mediates the presence of these motor deficits, the clinical indicators do not appear until over 70% of dopamine (DA) nerve terminals in the striatum have atrophied, suggesting the presence of compensatory mechanisms (Bezard et al., 2013). In disease propagation, alpha-synuclein proteins bind ubiquitin ligands and accumulate in damaged cells (Rao & Gershon, A New Perspective on Parkinson’s Disease: Pathology Begins in the Gastrointestinal Tract","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":"1 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41303740","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}
where m is the mass of a particle which moves under the influence of a real potential V(r) (ħ is the reduced Planck constant h/2π). When V(r) does not depend on time t the eigenvalues En of the Hermitian Hamiltonian H are the energy levels of a system. (d) The time evolution of the wave function is given by the timedependent Schrödinger equation Introduction In 1926, Erwin Schrödinger formulated his famous non-relativistic equation for matter waves. In this form quantum mechanics (QM) has since then remained a never-ending success. It expands the classical Newtonian mechanics for particle orbitals into the world of quantum matter as atoms, molecules, solid matter, microand nano-scale devices, etc., in which particles acquire wave properties. For this reason it is also referred to, particularly in the early years of the new theory, as wave mechanics (WM) with reference to common wave phenomena present in acoustics, electromagnetism, vibrational structures as membranes and drums, hydrodynamics and more. The predictive power of QM is, as well known, overwhelming. In short, traditional QM as above rests solidly on a number of postulates as (Schiff, 1968):
{"title":"Non-Hermitian Wave Mechanics: An Unorthodox Way into Embedded Systems","authors":"Felix Tellander, K. Berggren","doi":"10.22186/jyi.33.4.87-90","DOIUrl":"https://doi.org/10.22186/jyi.33.4.87-90","url":null,"abstract":"where m is the mass of a particle which moves under the influence of a real potential V(r) (ħ is the reduced Planck constant h/2π). When V(r) does not depend on time t the eigenvalues En of the Hermitian Hamiltonian H are the energy levels of a system. (d) The time evolution of the wave function is given by the timedependent Schrödinger equation Introduction In 1926, Erwin Schrödinger formulated his famous non-relativistic equation for matter waves. In this form quantum mechanics (QM) has since then remained a never-ending success. It expands the classical Newtonian mechanics for particle orbitals into the world of quantum matter as atoms, molecules, solid matter, microand nano-scale devices, etc., in which particles acquire wave properties. For this reason it is also referred to, particularly in the early years of the new theory, as wave mechanics (WM) with reference to common wave phenomena present in acoustics, electromagnetism, vibrational structures as membranes and drums, hydrodynamics and more. The predictive power of QM is, as well known, overwhelming. In short, traditional QM as above rests solidly on a number of postulates as (Schiff, 1968):","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43714012","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 use of the Global Workspace Theory. A good example of the interjection of neuroscience and architecture can be found in spatial navigation research. Scientific authors are capable of identifying floor patterns that are most and least useful to way-finding. Studies have also found that computer game and virtual reality architects may play an integral role in retaining memory and attention in elderly populations (Optale et al., 2010). Architectural students can benefit from a greater understanding of the impact of environmental stressors on biological mechanisms. Chronic stress response is one of the most pressing design problems as it may increase the risk of psychobiological disorders such as immune deficiencies, irritable bowel syndrome, depression, and anxiety (Hammen, 2015). Neuroscience research permits an objective review of the usability and mental health impacts of space. “An informed architect could use this research as a means for evidence-based design (EBD), a concept which seeks to ratify design standards of the built environment by incorporating research from multiple disciplines into the design process.” However, of the 113 post-secondary architecture institutions in North America, only the New School of San Diego offers students a certification program, which applies neuroscience principles to evidence-based practice (“Certificate in Neuroscience for Architecture” 2017). Although EBD is currently taught in many programs geared towards renewable/sustainable/green buildings, a truly multidisciplinary approach to EBD involves neuroscientific, psychological and economic research to guide design, a method commonly used in healthcare facilities today (Ulrich, Zimring, & Zhu, 2008). Students in architecture are entering a field which is now exploring ways to make use of neurobiological data analysis involvINTRODUCTION Architects have long sought to inspire creativity, ingenuity, worship, community and awe using the tools at their disposal. Homo faber, “Man the Maker”, crafts his environment, thereby controlling his fate. As a result of human ingenuity, we now spend over 90% of our time within a built environment crafted to suit our needs (Janda & Janda, 2017). Design is inspired by societal reform and scientific exploration expressed as an art form in itself. If architecture is an expression of creativity as a mean to reflect on the human condition, one might argue that such a reflection can also be found within neuroscientific exploration of the mind. As we come to understand the biological mechanisms of perception, consciousness and their residual impacts on mental and physical health, there is question of how our environment might in turn affect those mechanisms. Perception of space relies upon conscious awareness: the ability to receive and comprehend exterior and interior stimuli through Application of Neuroscience Principles for Evidence-based Design in Architectural Education
{"title":"Application of Neuroscience Principles for Evidence-based Design in Architectural Education","authors":"Andrea Mcintosh, N. Jadavji","doi":"10.22186/jyi.33.4.71-76","DOIUrl":"https://doi.org/10.22186/jyi.33.4.71-76","url":null,"abstract":"the use of the Global Workspace Theory. A good example of the interjection of neuroscience and architecture can be found in spatial navigation research. Scientific authors are capable of identifying floor patterns that are most and least useful to way-finding. Studies have also found that computer game and virtual reality architects may play an integral role in retaining memory and attention in elderly populations (Optale et al., 2010). Architectural students can benefit from a greater understanding of the impact of environmental stressors on biological mechanisms. Chronic stress response is one of the most pressing design problems as it may increase the risk of psychobiological disorders such as immune deficiencies, irritable bowel syndrome, depression, and anxiety (Hammen, 2015). Neuroscience research permits an objective review of the usability and mental health impacts of space. “An informed architect could use this research as a means for evidence-based design (EBD), a concept which seeks to ratify design standards of the built environment by incorporating research from multiple disciplines into the design process.” However, of the 113 post-secondary architecture institutions in North America, only the New School of San Diego offers students a certification program, which applies neuroscience principles to evidence-based practice (“Certificate in Neuroscience for Architecture” 2017). Although EBD is currently taught in many programs geared towards renewable/sustainable/green buildings, a truly multidisciplinary approach to EBD involves neuroscientific, psychological and economic research to guide design, a method commonly used in healthcare facilities today (Ulrich, Zimring, & Zhu, 2008). Students in architecture are entering a field which is now exploring ways to make use of neurobiological data analysis involvINTRODUCTION Architects have long sought to inspire creativity, ingenuity, worship, community and awe using the tools at their disposal. Homo faber, “Man the Maker”, crafts his environment, thereby controlling his fate. As a result of human ingenuity, we now spend over 90% of our time within a built environment crafted to suit our needs (Janda & Janda, 2017). Design is inspired by societal reform and scientific exploration expressed as an art form in itself. If architecture is an expression of creativity as a mean to reflect on the human condition, one might argue that such a reflection can also be found within neuroscientific exploration of the mind. As we come to understand the biological mechanisms of perception, consciousness and their residual impacts on mental and physical health, there is question of how our environment might in turn affect those mechanisms. Perception of space relies upon conscious awareness: the ability to receive and comprehend exterior and interior stimuli through Application of Neuroscience Principles for Evidence-based Design in Architectural Education","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44347989","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}
been found (Harbo, Gold, & Tintoré, 2013). Genetically, MS is best characterized by a mutation on the human leukocyte antigen (HLA) gene locus, which causes abnormal antigen recognition of T cells leading to attacks on myelin proteins (Raffel et al., 2016). These findings have not been conclusive, as many other genes involved in immunological roles have also been found to play a role in contributing to MS. Environmental risk factors include smoking ,sunlight exposure, and vitamin D deficiency (Raffel et al., 2016). Currently, there are no treatments that cure MS (Ziemssen et al., 2016). Instead, treatments target symptom management to increase patients’ quality of life. These include high doses of corticosteroids such as methylprednisolone (Jongen et al., 2016), Disease modifying Treatments (DMTs) such as interferon β-1a, interferon β-1b, alemtuzumab, fingolimod and natalizumab (Carrithers et al., 2014; Gajofatto & Benedetti, 2015), and neuro-rehabilitation (Dasari, Wootla, Warrington, & Rodriguez, 2016). All of these treatment options have adverse effects or are not particularly effective in the long term (Jongen et al., 2016; Ontaneda, Fox, & Chataway, 2015; Schäcke, Döcke, & Asadullah, 2002; Ziemssen et al., 2016). There is a considerable need for new treatment options that are more effective, while reducing the adverse side-effects. A potential therapy for MS-affected individuals may be the therapeutic application of optogenetics. Optogenetics is a novel method that utilizes photoreceptors to selectively activate neurons (Hegemann & Nagel, 2013). The genetic code of these receptors is delivered either virally or nonvirally to be expressed on the cells of interest. Once expressed, Introduction Multiple Sclerosis (MS) is a chronic autoimmune disease that leads to focal and diffuse neurodegenration and myelination throughout the nervous system (Kolasinski et al., 2012; Siffrin, Vogt, Radbruch, Nitsch, & Zipp, 2010). In its most common form, relapseremitting MS, it is characterized by high inflammation levels that lead to a continuous cycle of relapse and remission (Raffel, Wakerley, & Nicholas, 2016). These relapses, called exacerbations, may come in the form of new or worsening of old symptoms that are largely neurological such as visual impairment and imbalance that worsen over days or weeks, then recover spontaneously (Wingerchuk et al., 2014). Other common symptoms are cognitive impairment, loss of bladder control, leg weakness and sensory symptoms (Raffel et al., 2016). Genetic and environmental factors both have a role in MS development; however, a specific link to the disease has not Therapeutic Potential of Optogenetic Treatment for Individuals with Multiple Sclerosis
{"title":"Therapeutic potential of optogenetic treatment for individuals with multiple sclerosis","authors":"Mohamed M. El Koussy, N. Jadavji","doi":"10.22186/jyi.33.4.77-82","DOIUrl":"https://doi.org/10.22186/jyi.33.4.77-82","url":null,"abstract":"been found (Harbo, Gold, & Tintoré, 2013). Genetically, MS is best characterized by a mutation on the human leukocyte antigen (HLA) gene locus, which causes abnormal antigen recognition of T cells leading to attacks on myelin proteins (Raffel et al., 2016). These findings have not been conclusive, as many other genes involved in immunological roles have also been found to play a role in contributing to MS. Environmental risk factors include smoking ,sunlight exposure, and vitamin D deficiency (Raffel et al., 2016). Currently, there are no treatments that cure MS (Ziemssen et al., 2016). Instead, treatments target symptom management to increase patients’ quality of life. These include high doses of corticosteroids such as methylprednisolone (Jongen et al., 2016), Disease modifying Treatments (DMTs) such as interferon β-1a, interferon β-1b, alemtuzumab, fingolimod and natalizumab (Carrithers et al., 2014; Gajofatto & Benedetti, 2015), and neuro-rehabilitation (Dasari, Wootla, Warrington, & Rodriguez, 2016). All of these treatment options have adverse effects or are not particularly effective in the long term (Jongen et al., 2016; Ontaneda, Fox, & Chataway, 2015; Schäcke, Döcke, & Asadullah, 2002; Ziemssen et al., 2016). There is a considerable need for new treatment options that are more effective, while reducing the adverse side-effects. A potential therapy for MS-affected individuals may be the therapeutic application of optogenetics. Optogenetics is a novel method that utilizes photoreceptors to selectively activate neurons (Hegemann & Nagel, 2013). The genetic code of these receptors is delivered either virally or nonvirally to be expressed on the cells of interest. Once expressed, Introduction Multiple Sclerosis (MS) is a chronic autoimmune disease that leads to focal and diffuse neurodegenration and myelination throughout the nervous system (Kolasinski et al., 2012; Siffrin, Vogt, Radbruch, Nitsch, & Zipp, 2010). In its most common form, relapseremitting MS, it is characterized by high inflammation levels that lead to a continuous cycle of relapse and remission (Raffel, Wakerley, & Nicholas, 2016). These relapses, called exacerbations, may come in the form of new or worsening of old symptoms that are largely neurological such as visual impairment and imbalance that worsen over days or weeks, then recover spontaneously (Wingerchuk et al., 2014). Other common symptoms are cognitive impairment, loss of bladder control, leg weakness and sensory symptoms (Raffel et al., 2016). Genetic and environmental factors both have a role in MS development; however, a specific link to the disease has not Therapeutic Potential of Optogenetic Treatment for Individuals with Multiple Sclerosis","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46305361","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":"Brain Tumor Segmentation Using Morphological Processing and the Discrete Wavelet Transform","authors":"Joshua Michael Lojzim, M. Fries","doi":"10.22186/jyi.33.3.55-62","DOIUrl":"https://doi.org/10.22186/jyi.33.3.55-62","url":null,"abstract":"","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41556561","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}
J. Keating, B. Patterson, R. Speir, C. Wiswell, L. A. Gonzalez, H. Kundargi, Tugba Bayrak, C. Lasalle
ability in the U.S (USBDC, 2013), the importance of this research cannot be overstated. Although the blueprint outlining the microbial role within gut-brain axis regulation is far from maturation, the current understanding is that certain microbial strains are able to induce measurable neurologic and behavioral effect through the modulation of inflammatory response, neurochemical concentration, barrier-integrity, and interaction with the vagus nerve. In order to understand, and potentially utilize these microbial capabilities, it is essential to distinguish between which microbes are inducing behavioral and or neurologic effect, and which pathway each microbe is using to do so. The complexity of this task resides in the significant microbial distinction expressed not only on a species level, but amongst microbial strains (Greenblum, Rogan, & Borenstein, 2015). Among the more than 7,000 microbial strains (Ley, Peterson, & Gordon, 2006), majority have not demonstrated direct behavioral or neurologic effect. The collection of strains that have been shown to induce measurable neurologic and behavioral manipulation belong to one of the three genus types Lactobacillus, Bifidobacterium, and Bacteroides (Mayer, Knight, Mazmanian, Cryan, & Tillisch, 2014). Amongst these genus types, a plethora of biologic and behavioral variances have been expressed on both a species and strain level. While variation across differing genus and species type is expected, differences expressed between microbial strains belonging to the same genus and species type is a surprising find in light of the genomic similarity expressed between them. Further investigation into these microbial variances can explain questions such as why, despite genomic similarities, only certain microbial strains are able to induce behavioral and neurologic effect. Why INTRODUCTION Despite the myriad of pills and procedures aiming to treat psychiatric abnormalities and conditions, there is still much to be discovered about the brain. Fortunately, exploration into the effect upon commensal microbiota within behavioral and neurologic regulation has created a path in which to further decode and explore this enigmatic terrain. Recent in vitro and in vivo experimentation has demonstrated microbial influence within complex emotive states such as depression, chronic stress, anxiety, and psychiatric disorder (Bailey et al., 2011; Bercik et al., 2010; Maes, Kubera, Leunis, & Berk, 2012; Rook & Lowry, 2008). While this field is emerging and many mechanistic factors facilitating the microbial influence within gut-brain axis regulation have yet to be identified, the work done thus far suggest a future in which the brain can be indirectly targeted for therapeutic benefit through manipulation of commensal microbiota (Clarke et al., 2014; Cryan & Dinan, 2012). At a time when neuropsychiatric disorders are the leading cause of disStrain Specific: Microbial Strains Involved in Gut-Brain Signaling
{"title":"Strain specific: microbial strains involved in gut-brain signaling","authors":"J. Keating, B. Patterson, R. Speir, C. Wiswell, L. A. Gonzalez, H. Kundargi, Tugba Bayrak, C. Lasalle","doi":"10.22186/jyi.33.3.49-54","DOIUrl":"https://doi.org/10.22186/jyi.33.3.49-54","url":null,"abstract":"ability in the U.S (USBDC, 2013), the importance of this research cannot be overstated. Although the blueprint outlining the microbial role within gut-brain axis regulation is far from maturation, the current understanding is that certain microbial strains are able to induce measurable neurologic and behavioral effect through the modulation of inflammatory response, neurochemical concentration, barrier-integrity, and interaction with the vagus nerve. In order to understand, and potentially utilize these microbial capabilities, it is essential to distinguish between which microbes are inducing behavioral and or neurologic effect, and which pathway each microbe is using to do so. The complexity of this task resides in the significant microbial distinction expressed not only on a species level, but amongst microbial strains (Greenblum, Rogan, & Borenstein, 2015). Among the more than 7,000 microbial strains (Ley, Peterson, & Gordon, 2006), majority have not demonstrated direct behavioral or neurologic effect. The collection of strains that have been shown to induce measurable neurologic and behavioral manipulation belong to one of the three genus types Lactobacillus, Bifidobacterium, and Bacteroides (Mayer, Knight, Mazmanian, Cryan, & Tillisch, 2014). Amongst these genus types, a plethora of biologic and behavioral variances have been expressed on both a species and strain level. While variation across differing genus and species type is expected, differences expressed between microbial strains belonging to the same genus and species type is a surprising find in light of the genomic similarity expressed between them. Further investigation into these microbial variances can explain questions such as why, despite genomic similarities, only certain microbial strains are able to induce behavioral and neurologic effect. Why INTRODUCTION Despite the myriad of pills and procedures aiming to treat psychiatric abnormalities and conditions, there is still much to be discovered about the brain. Fortunately, exploration into the effect upon commensal microbiota within behavioral and neurologic regulation has created a path in which to further decode and explore this enigmatic terrain. Recent in vitro and in vivo experimentation has demonstrated microbial influence within complex emotive states such as depression, chronic stress, anxiety, and psychiatric disorder (Bailey et al., 2011; Bercik et al., 2010; Maes, Kubera, Leunis, & Berk, 2012; Rook & Lowry, 2008). While this field is emerging and many mechanistic factors facilitating the microbial influence within gut-brain axis regulation have yet to be identified, the work done thus far suggest a future in which the brain can be indirectly targeted for therapeutic benefit through manipulation of commensal microbiota (Clarke et al., 2014; Cryan & Dinan, 2012). At a time when neuropsychiatric disorders are the leading cause of disStrain Specific: Microbial Strains Involved in Gut-Brain Signaling","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41496499","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}
Dallon C Knight, Nicole A Ramos, Chris R Iceman, Sarah M Hayes
Recent studies highlight the health risks associated with toxic metal(loid)s [e.g., arsenic (As), zinc (Zn), and lead (Pb)] in dust from mining operations, urban settings, and rural roads. To have a deleterious health effect, inhaled or ingested metal(loid)s must dissolve under conditions in the lung or gastrointestinal tract. In this study, we determined total and physiologically-soluble fractions of metal(loid)s in road dust from four sites in east-central interior Alaska. Total As and antimony (Sb) were enriched up to 26.2 and 53.7, respectively in dusts relative to average crustal abundance. Several elements such as nickel (Ni), As, and Sb were highly to moderately soluble in simulated lung fluids (7-80%, 15-51%, and 5-42%, respectively). Nickel and As exceeded the EPA inhalation risk unit, which is an exposure level of minimal risk. Despite several elements being highly soluble in simulated gastric fluids, including Ni, Cu, As, and Pb, only As samples exceeded the oral reference dose for children (based on total elemental concentrations) in some samples. The highest exposure risks identified in this study are inhalation of As and Ni present in road dust and ingestion of As-containing dust, especially by children. Additional studies would be needed to further quantify the health risk posed by road dust in this region.
{"title":"Is Unpaved Road Dust Near Fairbanks, Alaska a Health Concern? Examination of the Total and Bioaccessible Metal(loid)s.","authors":"Dallon C Knight, Nicole A Ramos, Chris R Iceman, Sarah M Hayes","doi":"10.22186/jyi.33.1.8-18","DOIUrl":"10.22186/jyi.33.1.8-18","url":null,"abstract":"<p><p>Recent studies highlight the health risks associated with toxic metal(loid)s [e.g., arsenic (As), zinc (Zn), and lead (Pb)] in dust from mining operations, urban settings, and rural roads. To have a deleterious health effect, inhaled or ingested metal(loid)s must dissolve under conditions in the lung or gastrointestinal tract. In this study, we determined total and physiologically-soluble fractions of metal(loid)s in road dust from four sites in east-central interior Alaska. Total As and antimony (Sb) were enriched up to 26.2 and 53.7, respectively in dusts relative to average crustal abundance. Several elements such as nickel (Ni), As, and Sb were highly to moderately soluble in simulated lung fluids (7-80%, 15-51%, and 5-42%, respectively). Nickel and As exceeded the EPA inhalation risk unit, which is an exposure level of minimal risk. Despite several elements being highly soluble in simulated gastric fluids, including Ni, Cu, As, and Pb, only As samples exceeded the oral reference dose for children (based on total elemental concentrations) in some samples. The highest exposure risks identified in this study are inhalation of As and Ni present in road dust and ingestion of As-containing dust, especially by children. Additional studies would be needed to further quantify the health risk posed by road dust in this region.</p>","PeriodicalId":74021,"journal":{"name":"Journal of young investigators","volume":"33 1","pages":"8-18"},"PeriodicalIF":0.0,"publicationDate":"2017-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e5/1e/nihms965844.PMC6208360.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36634616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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