scholarly journals Postnatal Role of the Cytoskeleton in Adult Epileptogenesis

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Cezar Gavrilovici ◽  
Yulan Jiang ◽  
Ivana Kiroski ◽  
G Campbell Teskey ◽  
Jong M Rho ◽  
...  
Keyword(s):  
Animal Models ◽  
Neuronal Activity ◽  
Causative Factor ◽  
Cytoskeletal Proteins ◽  
Human Studies ◽  
Pathogenic Mechanism ◽  
Neuronal Connectivity ◽  
Cytoskeletal Disruption

Abstract Mutations in cytoskeletal proteins can cause early infantile and childhood epilepsies by misplacing newly born neurons and altering neuronal connectivity. In the adult epileptic brain, cytoskeletal disruption is often viewed as being secondary to aberrant neuronal activity and/or death, and hence simply represents an epiphenomenon. Here, we review the emerging evidence collected in animal models and human studies implicating the cytoskeleton as a potential causative factor in adult epileptogenesis. Based on the emerging evidence, we propose that cytoskeletal disruption may be an important pathogenic mechanism in the mature epileptic brain.

Role of dendritic cells in the lung:in vitromodels, animal models and human studies

2008 ◽  
Vol 2 (2) ◽  
pp. 215-233 ◽  
Author(s):  
Fabian Blank ◽  
Christophe von Garnier ◽  
Carolina Obregon ◽  
Barbara Rothen-Rutishauser ◽  
Peter Gehr ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Animal Models ◽  
Human Studies

scholarly journals Silencing neuronal activity is required for developmental circuit remodeling

2021 ◽  
Author(s):  
Oded Mayseless ◽  
El-Yazid Rachad ◽  
Gal Shapira ◽  
Andre Fiala ◽  
Oren Schuldiner
Keyword(s):  
Nervous System ◽  
Neuronal Activity ◽  
Mushroom Body ◽  
Excitatory Synapses ◽  
Neuronal Connectivity ◽  
Axon Pruning ◽  
Kenyon Cells ◽  
Inward Rectifying Potassium Channel ◽  
Developmental Remodeling

Postnatal refinement of neuronal connectivity shapes the mature nervous system. Pruning of exuberant connections involves both cell autonomous and non-cell autonomous mechanisms, such as neuronal activity. While the role of neuronal activity in the plasticity of excitatory synapses has been extensively studied, the involvement of inhibition is less clear. Furthermore, the role of activity during stereotypic developmental remodeling, where competition is not as apparent, is not well understood. Here we use the Drosophila mushroom body as a model to show that regulated silencing of neuronal activity is required for developmental axon pruning of the γ-Kenyon cells. We demonstrate that silencing neuronal activity is mechanistically achieved by cell autonomous expression of the inward rectifying potassium channel (irk1) combined with inhibition by the GABAergic APL neuron. These results support the Hebbian-like rule 'use it or lose it', where inhibition can destabilize connectivity and promote pruning while excitability stabilizes existing connections.

scholarly journals Animal Models to Study the Role of Long-Term Hypergastrinemia in Gastric Carcinogenesis

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Reidar Fossmark ◽  
Gunnar Qvigstad ◽  
Tom Chr. Martinsen ◽  
Øyvind Hauso ◽  
Helge L. Waldum
Keyword(s):  
Animal Models ◽  
Causative Factor ◽  
Chronic Atrophic Gastritis ◽  
Gastric Carcinogenesis ◽  
Oxyntic Mucosa ◽  
Increased Risk ◽  
Short Period ◽  
Gastric Malignancy

Patients with chronic hypergastrinemia due to chronic atrophic gastritis or gastrinomas have an increased risk of developing gastric malignancy, and it has been questioned whether also patients with hypergastrinemia caused by long-term use of acid inhibiting drugs are at risk. Gastric carcinogenesis in humans is affected by numerous factors and progresses slowly over years. When using animal models with the possibility of intervention, a complex process can be dissected by studying the role of hypergastrinemia in carcinogenesis within a relatively short period of time. We have reviewed findings from relevant models where gastric changes in animal models of long-term hypergastrinemia have been investigated. In all species where long-term hypergastrinemia has been induced, there is an increased risk of gastric malignancy. There is evidence that hypergastrinemia is a common causative factor in carcinogenesis in the oxyntic mucosa, while other cofactors may vary in the different models.

Role of Brain Iron Accumulation in Cognitive Dysfunction: Evidence from Animal Models and Human Studies

2013 ◽  
Vol 34 (4) ◽  
pp. 797-812 ◽  
Author(s):  
Nadja Schröder ◽  
Luciana Silva Figueiredo ◽  
Maria Noêmia Martins de Lima
Keyword(s):  
Animal Models ◽  
Cognitive Dysfunction ◽  
Human Studies ◽  
Iron Accumulation ◽  
Brain Iron

Cellular and animal models in pheochromocytoma/paragangliomas research: role of microenvironment

2016 ◽  
Author(s):  
M Mannelli ◽  
E Rapizzi ◽  
L Canu ◽  
T Ercolino ◽  
V Giache
Keyword(s):  
Animal Models

The role of vinpocetine in the treatment of cerebrovascular diseases based on human studies

2007 ◽  
Vol 148 (29) ◽  
pp. 1353-1358 ◽  
Author(s):  
Edit Bagoly ◽  
Gergely Fehér ◽  
László Szapáry
Keyword(s):  
Cerebrovascular Diseases ◽  
Human Studies

Az agyérbetegségek jelentőségét jelzi, hogy a cardiovascularis és tumoros betegségek után a stroke jelenti a harmadik leggyakoribb halálokot világszerte. Mivel stroke során az érintett agyállomány irreverzíbilisen károsodik, az infarktust övező épen maradt, de általában hipoperfundált agyterületek működésének serkentésével lehet a betegek állapotán javítani. Az agyi véráramlás növelése révén várható javulás a stroke-on még át nem esett, de krónikus agyi hipoperfúzióban szenvedő betegek tüneteiben is. Célkitűzés, módszer: Jelen tanulmány célja, hogy áttekintse a vinpocetin akut és krónikus agyérbetegségekben történő alkalmazásának eddig publikált humán vizsgálati eredményeit, és összefoglaló képet adjon a gyógyszer főbb indikációs területeiről, az ott mutatott hatékonyságról. Eredmények: A vinpocetin akut ischaemiás stroke-ban történő alkalmazását vizsgáló tanulmányok száma csekély, eredményeik pedig ellentmondásosak. Krónikus agyérbetegek esetében mind az egyszeri, mind a hosszú távú vinpocetinkezelést követően PET-, SPECT-, TCD- és NIRS-vizsgálatokkal a laesio körüli ép agyterületek perfúziónövekedése, fokozott glükóz- és O 2 -felhasználása igazolódott, és jelentős javulás volt észlelhető a vér reológiai paramétereiben is. A klinikai hatékonyságot értékelő nemzetközi tanulmányok metaanalízise alapján a gyógyszer per os alkalmazásával szignifikáns javulás jelentkezik a kognitív teljesítményben és a napi aktivitásban. Következtetések: A fenti vizsgálatok eredményei alapján kimondható, hogy a vinpocetin sokrétű farmakológiai hatása révén kedvezően befolyásolja az agy ép területeinek perfúzióját és metabolizmusát, a vér áramlási viszonyait, javítva ezzel a krónikus agyérbetegek életminőségét.

Bioengineered in vitro Vascular Models for Applications in Interventional Radiology

2019 ◽  
Vol 24 (45) ◽  
pp. 5367-5374 ◽  
Author(s):  
Xiaoyun Li ◽  
Seyed M. Moosavi-Basri ◽  
Rahul Sheth ◽  
Xiaoying Wang ◽  
Yu S. Zhang
Keyword(s):  
Interventional Radiology ◽  
Animal Models ◽  
Blood Vessels ◽  
In Vitro Models ◽  
The Past ◽  
Endovascular Interventions ◽  
Conventional Animal ◽  
Vascular Structures

The role of endovascular interventions has progressed rapidly over the past several decades. While animal models have long-served as the mainstay for the advancement of this field, the use of in vitro models has become increasingly widely adopted with recent advances in engineering technologies. Here, we review the strategies, mainly including bioprinting and microfabrication, which allow for fabrication of biomimetic vascular models that will potentially serve to supplement the conventional animal models for convenient investigations of endovascular interventions. Besides normal blood vessels, those in diseased states, such as thrombosis, may also be modeled by integrating cues that simulate the microenvironment of vascular disorders. These novel engineering strategies for the development of biomimetic in vitro vascular structures will possibly enable unconventional means of studying complex endovascular intervention problems that are otherwise hard to address using existing models.

scholarly journals The Role of the Transsulfuration Pathway in Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol 10 (5) ◽  
pp. 1081
Author(s):  
Mikkel Parsberg Werge ◽  
Adrian McCann ◽  
Elisabeth Douglas Galsgaard ◽  
Dorte Holst ◽  
Anne Bugge ◽  
...  
Keyword(s):  
Liver Disease ◽  
Animal Models ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Precise Control ◽  
Transsulfuration Pathway ◽  
Global Population ◽  
Alcoholic Fatty Liver Disease

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing and approximately 25% of the global population may have NAFLD. NAFLD is associated with obesity and metabolic syndrome, but its pathophysiology is complex and only partly understood. The transsulfuration pathway (TSP) is a metabolic pathway regulating homocysteine and cysteine metabolism and is vital in controlling sulfur balance in the organism. Precise control of this pathway is critical for maintenance of optimal cellular function. The TSP is closely linked to other pathways such as the folate and methionine cycles, hydrogen sulfide (H2S) and glutathione (GSH) production. Impaired activity of the TSP will cause an increase in homocysteine and a decrease in cysteine levels. Homocysteine will also be increased due to impairment of the folate and methionine cycles. The key enzymes of the TSP, cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), are highly expressed in the liver and deficient CBS and CSE expression causes hepatic steatosis, inflammation, and fibrosis in animal models. A causative link between the TSP and NAFLD has not been established. However, dysfunctions in the TSP and related pathways, in terms of enzyme expression and the plasma levels of the metabolites (e.g., homocysteine, cystathionine, and cysteine), have been reported in NAFLD and liver cirrhosis in both animal models and humans. Further investigation of the TSP in relation to NAFLD may reveal mechanisms involved in the development and progression of NAFLD.

scholarly journals Inflammation and Atherosclerosis

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1197
Author(s):  
Klaus Ley
Keyword(s):  
Clinical Trials ◽  
Animal Models ◽  
Basic Science ◽  
Translational Science ◽  
Special Issue

This 11-chapter Special Issue of Cells spans the gamut from basic science in mechanistic animal models to translational science to outcomes of clinical trials, all focused on the role of inflammation in atherosclerosis [...]

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