Pub Date : 2017-01-01Epub Date: 2017-07-19DOI: 10.15226/2374-6858/4/1/00132
Jonathan R Brent, P Hande Ozdinler
Recent advances in the genetics of ALS have bolstered hope that a molecular logic for the pathogenesis of the disease is fast approaching. An emerging challenge is the dissection of the common and unique molecular pathways altered by ALS gene mutations. Disease modeling in rodents has yielded many important insights, but as the genetic complexity of the disease grows, additional models with improved speed, cost and genetic tractability will be increasingly necessary. Models such as fruitfly, nematode, and zebrafish have been important for diagramming the molecular pathways that underlie many fundamental biological processes, but have been comparatively underutilized in the study of neurodegeneration. Here we highlight the benefits and opportunities for increased diversity in the models used to study ALS.
{"title":"Deciphering the molecular logic of ALS using model organisms: \"A family affair.\"","authors":"Jonathan R Brent, P Hande Ozdinler","doi":"10.15226/2374-6858/4/1/00132","DOIUrl":"https://doi.org/10.15226/2374-6858/4/1/00132","url":null,"abstract":"<p><p>Recent advances in the genetics of ALS have bolstered hope that a molecular logic for the pathogenesis of the disease is fast approaching. An emerging challenge is the dissection of the common and unique molecular pathways altered by ALS gene mutations. Disease modeling in rodents has yielded many important insights, but as the genetic complexity of the disease grows, additional models with improved speed, cost and genetic tractability will be increasingly necessary. Models such as fruitfly, nematode, and zebrafish have been important for diagramming the molecular pathways that underlie many fundamental biological processes, but have been comparatively underutilized in the study of neurodegeneration. Here we highlight the benefits and opportunities for increased diversity in the models used to study ALS.</p>","PeriodicalId":87364,"journal":{"name":"SOJ neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7943172/pdf/nihms-1676131.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25471336","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}
Pub Date : 2015-11-11DOI: 10.15226/2374-6858/2/2/00118
Tai T. Nguyen, J. Ugwu, S. Madhavan
Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique increasingly investigated an adjunct modality to enhance the effects of motor therapy. Although the safety of tDCS in relation to cognition, sensation and perception has been well reviewed, there still exists limited information regarding its effects on blood pressure and heart rate. As tDCS is being largely used in conjunction with stroke rehabilitation, it is important that we understand the effects of tDCS on autonomic function in the stroke population. In this retrospective study, we examined the acute effects of tDCS of the lower limb motor cortex in healthy and post stroke individuals using clinical measurements of blood pressure and heart rate. Fifteen minutes of 1 mA anodal tDCS did not cause any clinically detectable changes in blood pressure or heart rate. This is the first study to report the cardiovascular autonomic effects of tDCS of the lower limb M1 in healthy and post stroke individuals. Further studies are needed to examine if these safety effects are preserved during repeated applications of tDCS.
{"title":"Anodal tDCS of the lower limb M1 does not acutely affect clinical blood pressure and heart rate in healthy and post stroke individuals.","authors":"Tai T. Nguyen, J. Ugwu, S. Madhavan","doi":"10.15226/2374-6858/2/2/00118","DOIUrl":"https://doi.org/10.15226/2374-6858/2/2/00118","url":null,"abstract":"Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique increasingly investigated an adjunct modality to enhance the effects of motor therapy. Although the safety of tDCS in relation to cognition, sensation and perception has been well reviewed, there still exists limited information regarding its effects on blood pressure and heart rate. As tDCS is being largely used in conjunction with stroke rehabilitation, it is important that we understand the effects of tDCS on autonomic function in the stroke population. In this retrospective study, we examined the acute effects of tDCS of the lower limb motor cortex in healthy and post stroke individuals using clinical measurements of blood pressure and heart rate. Fifteen minutes of 1 mA anodal tDCS did not cause any clinically detectable changes in blood pressure or heart rate. This is the first study to report the cardiovascular autonomic effects of tDCS of the lower limb M1 in healthy and post stroke individuals. Further studies are needed to examine if these safety effects are preserved during repeated applications of tDCS.","PeriodicalId":87364,"journal":{"name":"SOJ neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67332196","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}
Pub Date : 2014-03-17DOI: 10.15226/2374-6858/1/1/00105
N. Soundarya, Dm Lawrence, Jb Samip, Av Stacy, J. Robert, R. Leroy, R. Alan
INTRODUCTION To determine the clinical significance of elevation of Troponin-I [cTn-I] during prolonged status epilepticus [pSE] SE is known to be accompanied by an increase in sympathetic outflow. Elevation of cTn-I has been linked to myocardial stress. We hypothesize that in patients with risk factors for coronary artery disease[CAD], pSE may lead to myocardial stress and an elevation of cTn-I. METHODS This is a retrospective study of patients over the age of 18 years who were presented to Virginia Commonwealth University with SE between 2005 and 2010. Data was evaluated using the 30-minute definition for SE and 30 day mortality. Risk factors for CAD and cTn-I levels within the first 24 hours of diagnosis of pSE were analyzed. KEY FINDINGS There were a total of 435 patients with a confirmed diagnosis of pSE, of which 266 had cTn-I concentrations reported. Statistical analysis showed a significant association between CAD risk factors and cTn-I elevation (χ2 =12.87, p-value <0.01), with Crude Odds Ratio of 4.7. In patients with a CAD risk factor, an elevation of cTn-I is associated with a significantly increased risk of mortality, with an Odds ratio of 8.0, (χ2 =40, [95% CI 4.1-15.9] p-value < 0.01). Mortality was higher in those with an elevation of cTn-I [54.65%] as opposed to those who did not have an elevation [15.08%], irrespective of CAD risk factors. OR=6.7, (χ2 =45, [95% CI=3.7-12.2] p-value < 0.01). CONCLUSIONS In patients with pSE values, elevated cTn-I values are seen four to five time more often in those with CAD risk factors, as opposed to those without the risks. An elevation of cTn-I in this subgroup of patients with CAD risk factors was associated with an eight to nine fold increase in their 30 day mortality as compared to patients with pSE, who did not have an elevation of cTn-I.
{"title":"Elevation of Cardiac Troponins in Prolonged Status Epilepticus: A Retrospective Chart Analysis.","authors":"N. Soundarya, Dm Lawrence, Jb Samip, Av Stacy, J. Robert, R. Leroy, R. Alan","doi":"10.15226/2374-6858/1/1/00105","DOIUrl":"https://doi.org/10.15226/2374-6858/1/1/00105","url":null,"abstract":"INTRODUCTION\u0000To determine the clinical significance of elevation of Troponin-I [cTn-I] during prolonged status epilepticus [pSE] SE is known to be accompanied by an increase in sympathetic outflow. Elevation of cTn-I has been linked to myocardial stress. We hypothesize that in patients with risk factors for coronary artery disease[CAD], pSE may lead to myocardial stress and an elevation of cTn-I.\u0000\u0000\u0000METHODS\u0000This is a retrospective study of patients over the age of 18 years who were presented to Virginia Commonwealth University with SE between 2005 and 2010. Data was evaluated using the 30-minute definition for SE and 30 day mortality. Risk factors for CAD and cTn-I levels within the first 24 hours of diagnosis of pSE were analyzed.\u0000\u0000\u0000KEY FINDINGS\u0000There were a total of 435 patients with a confirmed diagnosis of pSE, of which 266 had cTn-I concentrations reported. Statistical analysis showed a significant association between CAD risk factors and cTn-I elevation (χ2 =12.87, p-value <0.01), with Crude Odds Ratio of 4.7. In patients with a CAD risk factor, an elevation of cTn-I is associated with a significantly increased risk of mortality, with an Odds ratio of 8.0, (χ2 =40, [95% CI 4.1-15.9] p-value < 0.01). Mortality was higher in those with an elevation of cTn-I [54.65%] as opposed to those who did not have an elevation [15.08%], irrespective of CAD risk factors. OR=6.7, (χ2 =45, [95% CI=3.7-12.2] p-value < 0.01).\u0000\u0000\u0000CONCLUSIONS\u0000In patients with pSE values, elevated cTn-I values are seen four to five time more often in those with CAD risk factors, as opposed to those without the risks. An elevation of cTn-I in this subgroup of patients with CAD risk factors was associated with an eight to nine fold increase in their 30 day mortality as compared to patients with pSE, who did not have an elevation of cTn-I.","PeriodicalId":87364,"journal":{"name":"SOJ neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67332105","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}
Ng Soundarya, Dm Lawrence, Jb Samip, Av Stacy, Jc Robert, Rt Leroy, Rt Alan
Introduction: To determine the clinical significance of elevation of Troponin-I [cTn-I] during prolonged status epilepticus [pSE] SE is known to be accompanied by an increase in sympathetic outflow. Elevation of cTn-I has been linked to myocardial stress. We hypothesize that in patients with risk factors for coronary artery disease[CAD], pSE may lead to myocardial stress and an elevation of cTn-I.
Methods: This is a retrospective study of patients over the age of 18 years who were presented to Virginia Commonwealth University with SE between 2005 and 2010. Data was evaluated using the 30-minute definition for SE and 30 day mortality. Risk factors for CAD and cTn-I levels within the first 24 hours of diagnosis of pSE were analyzed.
Key findings: There were a total of 435 patients with a confirmed diagnosis of pSE, of which 266 had cTn-I concentrations reported. Statistical analysis showed a significant association between CAD risk factors and cTn-I elevation (χ2 =12.87, p-value <0.01), with Crude Odds Ratio of 4.7. In patients with a CAD risk factor, an elevation of cTn-I is associated with a significantly increased risk of mortality, with an Odds ratio of 8.0, (χ2 =40, [95% CI 4.1-15.9] p-value < 0.01). Mortality was higher in those with an elevation of cTn-I [54.65%] as opposed to those who did not have an elevation [15.08%], irrespective of CAD risk factors. OR=6.7, (χ2 =45, [95% CI=3.7-12.2] p-value < 0.01).
Conclusions: In patients with pSE values, elevated cTn-I values are seen four to five time more often in those with CAD risk factors, as opposed to those without the risks. An elevation of cTn-I in this subgroup of patients with CAD risk factors was associated with an eight to nine fold increase in their 30 day mortality as compared to patients with pSE, who did not have an elevation of cTn-I.
{"title":"Elevation of Cardiac Troponins in Prolonged Status Epilepticus: A Retrospective Chart Analysis.","authors":"Ng Soundarya, Dm Lawrence, Jb Samip, Av Stacy, Jc Robert, Rt Leroy, Rt Alan","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>To determine the clinical significance of elevation of Troponin-I [cTn-I] during prolonged status epilepticus [pSE] SE is known to be accompanied by an increase in sympathetic outflow. Elevation of cTn-I has been linked to myocardial stress. We hypothesize that in patients with risk factors for coronary artery disease[CAD], pSE may lead to myocardial stress and an elevation of cTn-I.</p><p><strong>Methods: </strong>This is a retrospective study of patients over the age of 18 years who were presented to Virginia Commonwealth University with SE between 2005 and 2010. Data was evaluated using the 30-minute definition for SE and 30 day mortality. Risk factors for CAD and cTn-I levels within the first 24 hours of diagnosis of pSE were analyzed.</p><p><strong>Key findings: </strong>There were a total of 435 patients with a confirmed diagnosis of pSE, of which 266 had cTn-I concentrations reported. Statistical analysis showed a significant association between CAD risk factors and cTn-I elevation (χ<sup>2</sup> =12.87, p-value <0.01), with Crude Odds Ratio of 4.7. In patients with a CAD risk factor, an elevation of cTn-I is associated with a significantly increased risk of mortality, with an Odds ratio of 8.0, (χ<sup>2</sup> =40, [95% CI 4.1-15.9] p-value < 0.01). Mortality was higher in those with an elevation of cTn-I [54.65%] as opposed to those who did not have an elevation [15.08%], irrespective of CAD risk factors. OR=6.7, (χ<sup>2</sup> =45, [95% CI=3.7-12.2] p-value < 0.01).</p><p><strong>Conclusions: </strong>In patients with pSE values, elevated cTn-I values are seen four to five time more often in those with CAD risk factors, as opposed to those without the risks. An elevation of cTn-I in this subgroup of patients with CAD risk factors was associated with an eight to nine fold increase in their 30 day mortality as compared to patients with pSE, who did not have an elevation of cTn-I.</p>","PeriodicalId":87364,"journal":{"name":"SOJ neurology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4327831/pdf/nihms649400.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33385700","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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