نتایج جستجو برای: neuronal death

تعداد نتایج: 382959  

Journal: :iranian journal of basic medical sciences 0
seung min park department of emergency medicine, school of medicine, kangwon national university, chuncheon 200-701, south korea department of emergency medicine, sacred heart hospital, college of medicine, hallym university, anyang431-796, south korea jae-chul lee department of neurobiology, school of medicine, kangwon national university, chuncheon 200-701, south korea bai hui chen department of physiology, college of medicine, hallym university, chuncheon 200-702, south korea bich-na shin department of physiology, college of medicine, hallym university, chuncheon 200-702, south korea jeong hwi cho department of neurobiology, school of medicine, kangwon national university, chuncheon 200-701, south korea

objective(s): the alteration of glucose transporters is closely related with the pathogenesis of brain edema. we compared neuronal damage/death in the hippocampus between adult and young gerbils following transient cerebral ischemia/reperfusion and changes of glucose transporter-1(glut-1)-immunoreactive microvessels in their ischemic hippocampal ca1 region. materials and methods: transient cere...

Journal: :مجله علوم اعصاب شفای خاتم 0
s kovac university hospital münster, münster, germany s williams university college london, london, uk am domijan university college london, london, uk mc walker university college london, london, uk ay abramov university college london, london, uk

seizure activity has been proposed to result in the generation of reactive oxygen species (ros), which then contribute to seizure-induced neuronal damage and eventually cell death. although the mechanisms of seizure-induced ros generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. we aim to determine the sources of seizure-induced ros and ...

Objective(s): To reach an evidence-based knowledge in the context of the temporal-spatial pattern of neuronal death and find appropriate time of intervention in order to preserve spared neurons and promote regeneration after traumatic spinal cord injury (TSCI). Materials and Methods: The study design was based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-guided...

Journal: :Cell Death & Disease 2010

Journal: :cell journal 0
marzieh panahi seyed hassan eftekhar vaghefi ali aboli dokht noughi zadeh

objective: morphological changes of ca1 neurons in rat hippocampus after transient and permanent focal cerebral ischemia were studied to clarify the nature of postischemic cell death in the subfield. materials and methods: male adult rats were divided into 3 groups: control (shamoperated), transient ischemic group (30 minutes of mcao followed by 48 hours of reperfusion), and permanent ischemic ...

Journal: :Japanese Journal of Pharmacology 1996

Ghadiri, Tahereh, Gorji, Ali, Hajali, Vahid, khodagholi, Fariba, Sharifzadeh, Mohammad, Vakilzadeh, Gelareh,

لطفاً به چکیده انگلیسی مراجعه شود.

AM Domijan, AY Abramov, MC Walker, S Kovac, S Williams,

Seizure activity has been proposed to result in the generation of reactive oxygen species (ROS), which then contribute to seizure-induced neuronal damage and eventually cell death. Although the mechanisms of seizure-induced ROS generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. We aim to determine the sources of seizure-induced ROS and ...

Leila Kamali Dolatabadi, Masoumeh Emamghoreishi, Mohammad Reza Namavar,

Global cerebral ischemia (GCI) leads to inflammation and neuronal death in CA1. Curcumin with neuroprotective and anti-inflammatory properties is a potential candidate for suppressing cell death. The aim of this study was to determine the effects of curcumin on neuronal number in the CA1 area following GCI. 28 Sprague-Dawley male rats were randomly assigned into four groups including sham, cont...

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