Pub Date : 2018-01-01DOI: 10.21088/I6NNS.0975.0223.10318.2
Adimoolam Sendilkumar, M. Narayanan, S. Syamala
{"title":"Analysis of Montreal Cognitive Assessment and Minimental State Examination in Patients with Mild Traumatic Brain Injury","authors":"Adimoolam Sendilkumar, M. Narayanan, S. Syamala","doi":"10.21088/I6NNS.0975.0223.10318.2","DOIUrl":"https://doi.org/10.21088/I6NNS.0975.0223.10318.2","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"13 1","pages":"145-150"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80047788","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 : 2018-01-01DOI: 10.15436/2377-1348.18.1978
Zhiquan Jiang, Shan Xie, Yinglei Du, Jincheng Fang, Song Bai, Nan Li, Jiwei Sun, Ommega Internationals
GH adenomas account for about 10% 15% of all benign pituitary tumors[1]. Its incidence is second only to the prolactinomas. GH adenomas secrete excessive growth hormone ,which causes acromegaly in adults, and before puberty, the patients with unfused epiphysis present as gigantism[2]. The most common cause of acromegaly is the growth hormone pituity adenomas by excessive GH secretion[3]. Continued secretion of GH may affect the cardiovascular system, leading to such conditions increased as hypertension, cardiomyopathy, valvular heart disease, and premature death[4,5]. Reports have shown that acromegaly can significantly increase the incidence of respiratory disease and therioma[6-8]. Some retrospective studies have shown that the mortality of acromegalyis at least twice as high as in normal people[9]. Surgical resection is the preferred treatment for GH pituitary adenoma. There are transsphenoidal and transcranial surgery. Butterflies are divided into endoscopic transsphenoidal and microscopical transsphenoidal. In general, surgery can only enable 50% patients to reach the clinical level and biochemical remission[10]. Giant or invasive GH adenoma is more difficult to treat. Abstract Background: Growth hormone pituity adenomas account for about 10% 15% of all benign pituitary tumors ,over-secreted growth hormone leads to acromegaly, significantly increased incidence of respiratory, cardiovascular and malignant tumors, severely affected people’s health. But the pathogenesis of GH adenomas is complex, it is not completely understood so far. Gene HS3ST2is one kind of sulfonyl transferase, which is inactivated by hypermethylation of the gene in most tumors. However, the expression and role of the gene HS3ST2 in pituitary adenomas have not been reported in the literature. It was found that the gene was highly expressed in GH adenoma and interacted with WNT pathway and ECMreceptor. Therefore, gene HS3ST2 may be the key gene for the occurrence and development of GH adenoma. The purpose of this study was to investigate the difference of gene HS3ST2 expression between invasive and noninvasive growth hormone pituitary adenomas, to explore the role of the gene in GH adenomas . Methods: Collected specimens of normal pituitary tissues (n = 3), and invasive and non invasive pituitary growth hormone adenoma (n = 6 in each group), according to the inclusion and exclusion criteria, the application of RT-qPCR method and Western Blot to detect the expression of gene HS3ST2 between normal pituitary tissues group and GH adenoma group. Results: The level of gene HS3ST2 expression in GH adenomas (non-invasive and invasive) and normal pituity tissues is different. We found that the expression of HS3ST2 in tumor tissues was higher than that in normal pituitary tissues (P < 0.05), and the expression in noninvasive growth hormone pituitary adenomas was higher than that in invasive GH pituitary adenomas (P < 0.05). Conclusion: Gene HS3ST2 may be related to the pathogenesis o
{"title":"The Relationship between Expression of HS3ST2 and the Invasiveness in Growth Hormone Adenomas","authors":"Zhiquan Jiang, Shan Xie, Yinglei Du, Jincheng Fang, Song Bai, Nan Li, Jiwei Sun, Ommega Internationals","doi":"10.15436/2377-1348.18.1978","DOIUrl":"https://doi.org/10.15436/2377-1348.18.1978","url":null,"abstract":"GH adenomas account for about 10% 15% of all benign pituitary tumors[1]. Its incidence is second only to the prolactinomas. GH adenomas secrete excessive growth hormone ,which causes acromegaly in adults, and before puberty, the patients with unfused epiphysis present as gigantism[2]. The most common cause of acromegaly is the growth hormone pituity adenomas by excessive GH secretion[3]. Continued secretion of GH may affect the cardiovascular system, leading to such conditions increased as hypertension, cardiomyopathy, valvular heart disease, and premature death[4,5]. Reports have shown that acromegaly can significantly increase the incidence of respiratory disease and therioma[6-8]. Some retrospective studies have shown that the mortality of acromegalyis at least twice as high as in normal people[9]. Surgical resection is the preferred treatment for GH pituitary adenoma. There are transsphenoidal and transcranial surgery. Butterflies are divided into endoscopic transsphenoidal and microscopical transsphenoidal. In general, surgery can only enable 50% patients to reach the clinical level and biochemical remission[10]. Giant or invasive GH adenoma is more difficult to treat. Abstract Background: Growth hormone pituity adenomas account for about 10% 15% of all benign pituitary tumors ,over-secreted growth hormone leads to acromegaly, significantly increased incidence of respiratory, cardiovascular and malignant tumors, severely affected people’s health. But the pathogenesis of GH adenomas is complex, it is not completely understood so far. Gene HS3ST2is one kind of sulfonyl transferase, which is inactivated by hypermethylation of the gene in most tumors. However, the expression and role of the gene HS3ST2 in pituitary adenomas have not been reported in the literature. It was found that the gene was highly expressed in GH adenoma and interacted with WNT pathway and ECMreceptor. Therefore, gene HS3ST2 may be the key gene for the occurrence and development of GH adenoma. The purpose of this study was to investigate the difference of gene HS3ST2 expression between invasive and noninvasive growth hormone pituitary adenomas, to explore the role of the gene in GH adenomas . Methods: Collected specimens of normal pituitary tissues (n = 3), and invasive and non invasive pituitary growth hormone adenoma (n = 6 in each group), according to the inclusion and exclusion criteria, the application of RT-qPCR method and Western Blot to detect the expression of gene HS3ST2 between normal pituitary tissues group and GH adenoma group. Results: The level of gene HS3ST2 expression in GH adenomas (non-invasive and invasive) and normal pituity tissues is different. We found that the expression of HS3ST2 in tumor tissues was higher than that in normal pituitary tissues (P < 0.05), and the expression in noninvasive growth hormone pituitary adenomas was higher than that in invasive GH pituitary adenomas (P < 0.05). Conclusion: Gene HS3ST2 may be related to the pathogenesis o","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"42 1","pages":"15-21"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88035511","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 : 2018-01-01DOI: 10.21088/IJNNS.0975.0223.10418.2
L. Sankar
{"title":"Drainage Pattern in Venous Sinuses within the Tentorium Cerebelli in 100 Cases of Autopsy","authors":"L. Sankar","doi":"10.21088/IJNNS.0975.0223.10418.2","DOIUrl":"https://doi.org/10.21088/IJNNS.0975.0223.10418.2","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"49 1","pages":"103-107"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74944732","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 : 2018-01-01DOI: 10.21088/IJNNS.0975.0223.10418.11
A. Chugh
{"title":"Neuroendoscopic Excision of Third Ventricular Colloid Cysts","authors":"A. Chugh","doi":"10.21088/IJNNS.0975.0223.10418.11","DOIUrl":"https://doi.org/10.21088/IJNNS.0975.0223.10418.11","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"15 1","pages":"157-164"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89662710","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 : 2018-01-01DOI: 10.21088/IJNNS.0975.0223.10218.9
A. Nandy, S. Jakobsen
{"title":"Patent Foramen Ovale (PFO) and Association with Cryptogenic Stroke in Young Patients","authors":"A. Nandy, S. Jakobsen","doi":"10.21088/IJNNS.0975.0223.10218.9","DOIUrl":"https://doi.org/10.21088/IJNNS.0975.0223.10218.9","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"167 1","pages":"121-123"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77303866","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 : 2018-01-01DOI: 10.21088/IJNNS.0975.0223.10218.7
M. Jaiswal, Somil Jaiswal, B. Ojha, S. Singh, A. Chandra, C. Srivastava
{"title":"How to Improve the outcome of Unidentified/ Unaccompanied Patient of Traumatic Brain Injury: An Institutional Study for Proposal of Framework","authors":"M. Jaiswal, Somil Jaiswal, B. Ojha, S. Singh, A. Chandra, C. Srivastava","doi":"10.21088/IJNNS.0975.0223.10218.7","DOIUrl":"https://doi.org/10.21088/IJNNS.0975.0223.10218.7","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"57 1","pages":"113-117"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83122922","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 : 2018-01-01DOI: 10.21088/IJNNS.0975.0223.10218.3
A. Sunil, C. Dinesh, J. Rahul, L. Akshay
{"title":"Clinical, Electroencephalographic and Radiological Profile of Epilepsy in A Tertiary Care Hospital from Central India","authors":"A. Sunil, C. Dinesh, J. Rahul, L. Akshay","doi":"10.21088/IJNNS.0975.0223.10218.3","DOIUrl":"https://doi.org/10.21088/IJNNS.0975.0223.10218.3","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"75 1","pages":"83-89"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79495390","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 : 2018-01-01DOI: 10.21088/ijnns.0975.0223.10218.10
A. M. Reddy, Dr. abhishek, A. L. Rao, G. Venugopal
{"title":"Frontal Radiation Induced Meningioma","authors":"A. M. Reddy, Dr. abhishek, A. L. Rao, G. Venugopal","doi":"10.21088/ijnns.0975.0223.10218.10","DOIUrl":"https://doi.org/10.21088/ijnns.0975.0223.10218.10","url":null,"abstract":"","PeriodicalId":14163,"journal":{"name":"International journal of neurology","volume":"281 1","pages":"124-128"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76805014","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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