检索结果-南通市图书馆

Distinct and Additive Effects of Alcohol and thiamine deficiency in the Developing Brain: Relevance to Fetal Alcohol Spectrum Disorder

引用

Journal of Behavioral and Brain Science 2024年第6期14卷 161-186页

作者： Suzanne M. de la Monte Elizabeth Silbermann Ming Tong Departments of Pathology (Neuropathology) Neurology and Neurosurgery Brown University Providence RI USA Department of Medicine Brown University Providence RI USA Rhode Island Hospital Providence RI USA Women & Infants Hospital Providence RI USA Warren Alpert Medical School of Brown University Providence RI USA Portland VA Medical Center Oregon Health & Science University Portland OR USA

Background: Neurodevelopmental abnormalities in fetal alcohol spectrum disorder (FASD) are linked to brain insulin resistance and oxidative stress. However, the role of thiamine deficiency as a distinct or additive factor in the pathogenesis of the neurodevelopmental and metabolic derangements in FASD has not been determined. Methods: Control and ethanol-exposed human PNET2 cerebellar neuronal cells and rat cerebellar slice cultures were treated with vehicle or pyrithiamine (Pyr) to assess independent and additive effects of thiamine deficiency on ethanol-mediated neurotoxicity, mitochondrial dysfunction, insulin resistance, inhibition of neuronal and glial genes, and oxidative stress. Results: Pyr treatments (0 - 200 µM) caused dose-dependent cell loss (Crystal Violet assay) and reduced mitochondrial function (MTT assay) in PNET2 neuronal cultures. Ethanol alone (100 mM) significantly reduced PNET2 neuronal viability, MTT activity, and ATP production. Over the broad dose range of Pyr treatment, ethanol significantly reduced ATP content and cell number and increased mitochondrial mass (MitoTracker Green). Ex vivo cerebellar slice culture studies revealed ethanol-induced developmental architectural disruption that was substantially worsened by Pyr. The adverse effects of ethanol were linked to increased lipid peroxidation and inhibition of asparatyl-asparaginyl-β-hydroxylase (ASPH) expression. The independent and additive effects of Pyr were associated with increased cytotoxicity, lipid peroxidation, Caspase 3 activation, and Tau accumulation. Conclusions: During development, alcohol exposure and thiamine deficiency exert distinct but overlapping molecular pathologies that ultimately impair the structure and function of cerebellar neurons. While both insults drive cell loss and mitochondrial dysfunction with increased lipid peroxidation, ethanol’s additional inhibitory effects on ASPH reflect impairments in insulin and IGF signaling. In contrast, Pyr’s main adverse e

关键词： Fetal Alcohol Spectrum Disorder thiamine deficiency Cerebellum Slice Culture Pyrithiamine

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Interaction of thiamine deficiency and voluntary alcohol consumption disrupts rat corpus callosum ultrastructure

Interaction of thiamine deficiency and voluntary alcohol con...

引用

湖北省暨武汉市病理生理学会第十四届学术年会

作者： Edith V.Sullivan Roger K.Stankovic Clive G.Harper Adolf Pfefferbaum Department of Psychiatry & Behavioral Sciences Stanford University Schoolof MedicineStanfordCaliforniaU.S.A. Department of Pathology(D06) University of SydneyNSW2006Australia Department of Psychiatry & Behavioral Sciences Stanford University School of MedicineStanfordCaliforniaU.S.A.

The relative roles of alcohol and nutritional(thiamine)deficiency in causing brain damage remain controversial in alcoholics without history of Wernicke’s encephalopathy or signs of Korsakoff’s *** control over alco... 详细信息

关键词： electron microscopy alcohol thiamine deficiency alcohol-preferring(P)rat MRI brain white matter

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Wernicke encephalopathy in a patient after liver transplantation: A case report

引用

World Journal of Gastroenterology 2017年第47期23卷 8432-8436页

作者： Bin Xie Zhong-Zhou Si Wei-Ting Tang Hai-Zhi Qi Ting Li Organ Trans-plantation Center The Second Xiang-ya Hospital Central South University Department of Neurology Xiang-ya Hospital Central South University

Wernicke encephalopathy(WE) is an acute neurological disorder resulting from vitamin B1 deficiency, which is common in chronic alcoholism and is rare in acute liver failure. So far, there are 2 cases of WE reported after liver transplantation. Here, we report a case of a 45-year-old nonalcoholic male patient who developed psychiatric and neurological disturbance 15 d after receiving orthotopic liver transplantation because of hepatitis B-related cirrhosis and portal hypertension. Brain magnetic resonance imaging(MRI) showed symmetric high-signal intensities in the periaqueductal area. The patient was diagnosed with WE and given intravenous high-dose vitamin B1 immediately. His neurological disturbance resolved in 7 d after receiving the vitamin B1. Brain MRI after 5 mo showed nearly complete recovery. Most WE cases may be misdiagnosed in patients after liver transplantation, and we should pay more attention to its onset.

关键词： Liver transplantation thiamine deficiency Wernicke encephalopathy Magnetic resonance imaging Prevention Pharmacotherapy

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Non-alcoholic Wernicke encephalopathy in an esophageal cancer patient receiving radiotherapy:A case report

引用

World Journal of Clinical Cases 2022年第17期10卷 5810-5815页

作者： Ye Zhang Lei Wang Jin Jiang Wen-Yu Chen Department of General Practice The Affiliated Hospital of Jiaxing UniversityJiaxing 314000Zhejiang ProvinceChina Department of Oncology The Affiliated Hospital of Jiaxing UniversityJiaxing 314000Zhejiang ProvinceChina Department of Respiration The Affiliated Hospital of Jiaxing UniversityJiaxing 314000Zhejiang ProvinceChina

BACKGROUND, Wernicke encephalopathy is a rare but potentially fatal adverse event caused by thiamine deficiency. Reports of non-alcoholic Wernicke encephalopathy due to malignancy are scarce in the literature, with those reported mainly being on haematological cancer, followed by gastrointestinal cancer. As a result, there is considerable under-recognition and delay in the diagnosis and treatment of Wernicke encephalopathy in oncology departments. To our knowledge, there has been no report of Wernicke encephalopathy in a patient with esophageal cancer while receiving *** SUMMARY A 64-year-old man presented to the oncology outpatient clinic with a history of dysphagia for 2 mo, and was diagnosed with locally advanced esophageal squamous cell carcinoma(stage ⅢB). Radiotherapy was initiated to alleviate dysphagia due to malignant esophageal stenosis;however, the patient exhibited consciousness disturbances starting on day 10 of radiotherapy. Brain magnetic resonance imaging indicated the development of Wernicke encephalopathy. Subsequent treatment with thiamine led to rapid improvement in the patient’s neurological *** Wernicke encephalopathy may develop in non-alcoholic patients undergoing radiotherapy for esophageal cancer. Early diagnosis and sufficient thiamine supplementation during radiotherapy are essential.

关键词： Wernicke encephalopathy thiamine deficiency Esophageal cancer Radiotherapy Consciousness disturbance Case report

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Wernicke Encephalopathy in a Patient with Pulmonary and Abdominal Tuberculosis

引用

Chinese Medical Journal 2017年第22期130卷 2757-2758页

作者： Yun-Cui Gan Jing Jin Zhi-Xin Qiu Xue-Rong Chen Department of Pulmonary and Critical Care Medicine West China Hospital Sichuan University Chengdu Sichuan 610041 China

Wernicke encephalopathy （WE） is an acute or subacute neurological syndrome caused by thiamine （Vitamin B 1） deficiency and is usually underestimated in clinical practice. WE is suspected in merely about 6% of non-alcoholic patients and one-third of alcoholic patients, Non-alcoholic causes include gastrointestinal surgery and disease, malnutrition, cancer and chemotherapeutic treatments, and long-term parenteral ***, few cases were reported about WE in patients with tuberculosis. Early diagnosis and medication are vital for the prognosis of this disease.

关键词： Cerebellar Ataxia Mental Disorder Ophthalmoplegia thiamine deficiency Tuberculosis Wernicke Encephalopathy

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Neuronal MCP-1 mediates microglia recruitment and neurodegeneration induced by the mild impairment of oxidative metabolism

Neuronal MCP-1 mediates microglia recruitment and neurodegen...

引用

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Guang YANG,Ya MENG,Wenxia LI,Zhiqin FAN,Hanqing DING,Youzhen WEI,Jia LUO,Zun-Ji KE~* Key Laboratory of Nutrition and Metabolism,Institute for Nutritional Sciences,Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences,Graduate School of the Chinese Academy of Sciences,Shanghai 200031,China

＜正＞Chemokines are implicated in neuroinflammation of several chronic neurodegenerative disorders. However,the precise role of chemokines in neurodegeneration is *** deficiency（TD） causes abnormal oxidative metabolism in the brain as well as a well-defined microglia activation and neurodegeneration in the submedial thalamus nucleus（SmTN）,which are common features of neurodegenerative *** evaluated the role of chemokines in neurodegeneration and the underlying mechanism in a TD *** the chemokines examined,TD selectively induced neuronal expression of monocyte chemoattractant protein-1（MCP-1） in the SmTN prior to microglia activation and *** conditioned medium collected from TD-induced neurons caused microglia *** a neuron/microglia co-culture system,we showed that MCP-1-induced neurotoxicity required the presence of microglia and exogenous MCP-1 was able to activate microglia and stimulate microglia to produce cytokines.A MCP-1 neutralizing antibody inhibited MCP-1-induced microglia activation and neuronal death in culture and in the ***-1 knock-out mice were resistant to TD-induced neuronal death in *** selectively induced the accumulation of reactive oxygen species in neurons,and antioxidants blocked TDinduced MCP-1 ***,our results indicated an induction of neuronal MCP-1 during mild impairment of oxidative metabolism caused microglia recruitment/activation,which exacerbated neurodegeneration.

关键词： thiamine deficiency chemokines microglia activation neurodegeneration oxidative stress

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：