scholarly journals Zebrafish as an experimental model for the simulation of neurological and craniofacial disorders

2022 ◽  
pp. 22-29
Author(s):  
Ashwin Rohan Rai ◽  
Teresa Joy ◽  
K. S. Rashmi ◽  
Rajalakshmi Rai ◽  
N. A. Vinodini ◽  
...  
Keyword(s):  
Experimental Model ◽  
Neurological Disorders ◽  
Experimental Models ◽  
Research Techniques ◽  
Cellular Factors ◽  
Vertebrate Model

Zebrafish have gained momentum as a leading experimental model in recent years. At present, the zebrafish vertebrate model is increasingly used due to its multifactorial similarities to humans that include genetic, organ, and cellular factors. With the emergence of novel research techniques that are very expensive, it is necessary to develop affordable and valid experimental models. This review aimed to highlight some of the most important similarities between zebrafish and humans by emphasizing the relevance of the first in simulating neurological disorders and craniofacial deformity.

scholarly journals The Prion-Like Spreading of Alpha-Synuclein in Parkinson’s Disease: Update on Models and Hypotheses

2021 ◽  
Vol 22 (15) ◽  
pp. 8338
Author(s):  
Asad Jan ◽  
Nádia Pereira Gonçalves ◽  
Christian Bjerggaard Vaegter ◽  
Poul Henning Jensen ◽  
Nelson Ferreira
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Alpha Synuclein ◽  
Experimental Models ◽  
Cellular Factors ◽  
Recent Developments ◽  
Novel Targets ◽  
Presynaptic Protein

The pathological aggregation of the presynaptic protein α-synuclein (α-syn) and propagation through synaptically coupled neuroanatomical tracts is increasingly thought to underlie the pathophysiological progression of Parkinson’s disease (PD) and related synucleinopathies. Although the precise molecular mechanisms responsible for the spreading of pathological α-syn accumulation in the CNS are not fully understood, growing evidence suggests that de novo α-syn misfolding and/or neuronal internalization of aggregated α-syn facilitates conformational templating of endogenous α-syn monomers in a mechanism reminiscent of prions. A refined understanding of the biochemical and cellular factors mediating the pathological neuron-to-neuron propagation of misfolded α-syn will potentially elucidate the etiology of PD and unravel novel targets for therapeutic intervention. Here, we discuss recent developments on the hypothesis regarding trans-synaptic propagation of α-syn pathology in the context of neuronal vulnerability and highlight the potential utility of novel experimental models of synucleinopathies.

scholarly journals Evaluation of the heme oxygenase-1 expression in esophagitis and esophageal cancer induced by different reflux experimental models and diethylnitrosamine

2010 ◽  
Vol 25 (3) ◽  
pp. 304-310 ◽  
Author(s):  
Cleber Rosito Pinto Kruel ◽  
Luis Felipe Ribeiro Pinto ◽  
Tania Cristina Moita Blanco ◽  
Theresa Christina Barja-Fidalgo ◽  
Levi Lourenzo Melo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Model ◽  
Heme Oxygenase ◽  
Inflammatory Cells ◽  
Acid Reflux ◽  
Experimental Models ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Duodenal Reflux ◽  
Esophageal Carcinogenesis

PURPOSE: To study the expression of heme-oxygenase-1 (HO-1), an enzyme induced by oxidative stress, in specimens obtained from an experimental model in rats that evaluated the role of gastric and duodenal reflux in esophageal carcinogenesis. METHODS: Esophageal specimens embedded in paraffin obtained from different experimental groups of rats were used for immunohistochemistry analysis of HO-1 expression. The rats had been divided into the following groups and were killed after 22 weeks: (1) cardioplasty to induce acid reflux; (2) esophagoduodenal anastomosis to induce duodenal reflux; (3) no treatment; (4) cardioplasty + diethylnitrosamine (DEN); (5) esophagoduodenal anastomosis + DEN; and (6) DEN. The study sample comprised 3 specimens from each group with the most severe histopathological lesions found on each study branch. RESULTS: The expression of HO-1 was seen only in rat specimens submitted to esophagoduodenal anastomosis (Groups 2 and 5), and the analysis of mean fluorescence intensity revealed a significant increase of HO-1 expression (4.8 and 4.6 fold, respectively) when compared with the control group (Group 3) (p<0.05). The main target for HO-1 induction was the inflammatory cells inside the tumor or in subepithelial areas. Rats exposed to gastric reflux had no HO-1 expression. CONCLUSION: Reflux esophagitis induced by reflux of duodenal contents, which provoked considerable oxidative stress, may play an important role in esophageal carcinogenesis. Acid reflux did not induce oxidative stress in this experimental model.

Advances in the Experimental Models of HIV-Associated Neurological Disorders

2021 ◽  
Author(s):  
Susmita Sil ◽  
Palsamy Periyasamy ◽  
Annadurai Thangaraj ◽  
Fang Niu ◽  
Divya T. Chemparathy ◽  
...  
Keyword(s):  
Neurological Disorders ◽  
Experimental Models

Mitochondrial CHCHD2 and CHCHD10: Roles in Neurological Diseases and Therapeutic Implications

2019 ◽  
Vol 26 (2) ◽  
pp. 170-184
Author(s):  
Wei Zhou ◽  
Dongrui Ma ◽  
Eng-King Tan
Keyword(s):  
Neurological Disorders ◽  
Neurological Diseases ◽  
Mitochondrial Gene ◽  
Experimental Models ◽  
Loss Of Function ◽  
Motor Neuron Diseases ◽  
Therapeutic Implications ◽  
Mitochondrial Inner Membrane ◽  
Mitochondrial Defects ◽  
Neurological Conditions

CHCHD2 mutations have been identified in various neurological diseases such as Parkinson’s disease (PD), frontotemporal dementia (FTD), and Alzheimer’s disease (AD). It is also the first mitochondrial gene whose mutations lead to PD. CHCHD10 is a homolog of CHCHD2; similar to CHCHD2, various mutations of CHCHD10 have been identified in a broad spectrum of neurological disorders, including FTD and AD, with a high frequency of CHCHD10 mutations found in motor neuron diseases. Functionally, CHCHD2 and CHCHD10 have been demonstrated to interact with each other in mitochondria. Recent studies link the biological functions of CHCHD2 to the MICOS complex (mitochondrial inner membrane organizing system). Multiple experimental models suggest that CHCHD2 maintains mitochondrial cristae and disease-associated CHCHD2 mutations function in a loss-of-function manner. However, both CHCHD2 and CHCHD10 knockout mouse models appear phenotypically normal, with no obvious mitochondrial defects. Strategies to maintain or enhance mitochondria cristae could provide opportunities to correct the associated cellular defects in disease state and unravel potential novel targets for CHCHD2-linked neurological conditions.

Model Simplification for Offshore Platforms Using Model Refinement Scheme

2013 ◽  
Vol 284-287 ◽  
pp. 1436-1440 ◽  
Author(s):  
Min Zhang ◽  
Shu Qing Wang ◽  
Jia Li Fu ◽  
Xiao Long Xu
Keyword(s):  
Experimental Model ◽  
Degrees Of Freedom ◽  
Oil And Gas ◽  
Model Updating ◽  
Experimental Models ◽  
Offshore Platforms ◽  
Model Refinement ◽  
Jacket Platform ◽  
Cross Model ◽  
Offshore Oil And Gas

Offshore jacket platforms have been widely used in offshore oil and gas exploitation under hostile ocean environments. Finite element models of such structures need to have many degrees of freedom (DOFs) to represent the geometrical detail of complex structures, which leads to more computing power when performing the analysis and what’s more, the incompatibility in the number of degrees of freedom to the experimental models. Therefore, there is a need to simplify the analytical model by reducing the DOFs and in the process, making the essential eigen-properties agree with those of the experimental model is desired. In this paper, a scaled physical experimental model of an offshore jacket platform is simplified using the recently developed model refinement scheme. Mathematically, the procedure to implement the model refinement technique is an application of cross-model cross-mode (CMCM) method for model updating. The master degrees of freedom are chosen according to the placement of accelerometers in the experiment. Upon the completion of the refinement, the improved reduced jacket platform model matches the dynamic characteristics of the experimental model quite well.

scholarly journals Oxidative Stress Associated with Neuronal Apoptosis in Experimental Models of Epilepsy

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Marisela Méndez-Armenta ◽  
Concepción Nava-Ruíz ◽  
Daniel Juárez-Rebollar ◽  
Erika Rodríguez-Martínez ◽  
Petra Yescas Gómez
Keyword(s):  
Oxidative Stress ◽  
Neuronal Death ◽  
Neurological Disorders ◽  
Neuronal Apoptosis ◽  
Experimental Models ◽  
State Failure ◽  
Radical Production ◽  
Induction Of Apoptosis ◽  
Models Of Epilepsy

Epilepsy is considered one of the most common neurological disorders worldwide. Oxidative stress produced by free radicals may play a role in the initiation and progression of epilepsy; the changes in the mitochondrial and the oxidative stress state can lead mechanism associated with neuronal death pathway. Bioenergetics state failure and impaired mitochondrial function include excessive free radical production with impaired synthesis of antioxidants. This review summarizes evidence that suggest what is the role of oxidative stress on induction of apoptosis in experimental models of epilepsy.

scholarly journals Experimental model of induction of diabetes mellitus in rats

2003 ◽  
Vol 18 (spe) ◽  
pp. 60-64 ◽  
Author(s):  
Eliziane Nitz de Carvalho ◽  
Nestor Antônio Schmidt de Carvalho ◽  
Lydia Masako Ferreira
Keyword(s):  
Diabetes Mellitus ◽  
Experimental Model ◽  
Death Rate ◽  
Experimental Models ◽  
Morbid Condition ◽  
Reduced Dose ◽  
High Prevalence

Diabetes mellitus is a potentially morbid condition with high prevalence worldwide, thus being a major medical concern. Experimental models play an important role in understanding such a disease, which is treatable only. This study describes a rat diabetes mellitus model induced by administering a reduced dose of alloxan, thus greatly reducing the animals’ death rate.

scholarly journals Surface enlargement of a new arterialised venous flap by the surgical delay method

2014 ◽  
Vol 71 (6) ◽  
pp. 547-553 ◽  
Author(s):  
Mikica Lalkovic ◽  
Jefta Kozarski ◽  
Ljubomir Panajotovic ◽  
Milan Visnjic ◽  
Dragan Djurdjevic ◽  
...  
Keyword(s):  
Experimental Model ◽  
Experimental Models ◽  
Control Group ◽  
Average Weight ◽  
Surgical Delay ◽  
Surgical Method ◽  
Rabbit Ear ◽  
Group A ◽  
The Difference ◽  
Venous Flap

Background/Aim. The delay method is a surgical, pharmacological and combined method that includes two or more time separated phases, which gives bigger flap surface. In our research we explored the possibility of flap surface enlargement in a new arterialised venous flap (AVF) on an experimental rabbit ear model by the delay surgical method. The aim of this research was to establish vitality surface of our AVF and to maintain the difference in flap vital surface between AVF flaps, with or without performing the delay surgery method. Methods. We used both ears of ?Big Chinchilla? rabbits in 10 experimental male animals, divided into two groups, average weight 3-3.5 kg, and average age 8-10 months. In the first (experimental) group, a venous flap was arterialised by our method. In the second (control) group, the venous flap was arterialised 14 days after the delay surgical method. AVF surface was measured on the 1 and 14 days by the method of trapezoid rule. Results. Vital surface on our AVF experimental model was bigger than 87% of elevated flap surface after the delay surgical method. Vital surface on AVF without delay on our experimental model was bigger than 30% of elevated flap surface (p < 0.001). Conclusion. Analysis of previous experimental models on the rabbit ear, non-delayed and delayed (to enlarge flap surface) led us to conclusion that previously created experimental models of non-delayed AVF are hemodynamically negative. Our experimental non-delay AVF model is hemodynamically more positive than previously created models of non-delay AVF and provides better conditions for AVF survival and enlargement of vital flap surface of elevated flap. On the other hand, surgical delay method significantly enlarges vital surface of AFF.

scholarly journals Probing the Dynamics of Neuronal Proteins In Vivo Using Non-Canonical Amino Acids Tagging

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Kevin P. Lin ◽  
Aya M. Saleh ◽  
Kathryn R. Jacobson ◽  
Sarah Calve ◽  
Tamara L. Kinzer-Ursem
Keyword(s):  
Neurological Disorders ◽  
Temporal Dynamics ◽  
Click Reaction ◽  
Neurological Diseases ◽  
Experimental Models ◽  
Selective Enrichment ◽  
Neuronal Proteins ◽  
Canonical Amino Acid ◽  
Brain Tissues

Background and Hypothesis: More than 600 neurological disorders have been identified, each with varying degrees of complexity and level of molecular understanding. However, current approaches are inadequate to capture the complex progressive nature of most neurological diseases. Therefore, developing techniques capable of probing the temporal dynamics of neuronal proteins in rodents, the most commonly used experimental models, is imperative for proper understanding of mechanisms driving neurological disorders. In this project, a protein labeling technique that enables selective labeling of newly synthesized proteins in vivo is utilized. In this technique, the non-canonical amino acid azidohomoalanine (AHA) is injected into mice to achieve global proteome labeling. AHA is an azide-tagged methionine (Met) analog that is incorporated into the nascent proteins using endogenous translational mechanisms. The azide functional group of AHA allows selective enrichment of the newly synthesized proteins from brain tissues via click-chemistry using alkynebearing affinity tags. This will be followed by detecting the AHA-labeled protein using mass spectrometry. We hypothesize that this labeling technique will help map the dynamics of the brain proteome in health and disease. This will ultimately provide insights into mechanisms underlying complex neurological diseases. Experimental Design or Project Methods: C57Bl/6 murine dams were injected with 0.1 mg/g AHA for two days. Brain tissues were harvested, homogenized and lysates were reacted with biotin-alkyne using copper-catalyzed click reaction. Biotinylated proteins were then enriched using NeutrAvidin beads and eluted by boiling in 2% SDS. Results: Tissues were fractionated into different subcellular components (cytosolic, nuclear, membrane, cytoskeletal, and extracellular matrix) using buffers of different stringency. Western blot analysis of clicked tissues using Streptavidin-fluorophore indicated effective incorporation of AHA into different cellular fractions of brain tissues. Additionally, the analysis of eluted proteins revealed successful enrichment and elution of AHA-labeled proteins. Conclusion and Potential Impact: Successful incorporation of AHA in nascent neuronal proteins can lead to a comprehensive quantitative approach for elucidating changes in the regulation of neuronal proteins in disease states.

scholarly journals Kairiojo plaučio transplantacija žiurkei: eksperimentinio modelio paieškos

2006 ◽  
Vol 4 (3) ◽  
pp. 0-0
Author(s):  
Remigijus Sipavičius ◽  
Aleksejus Zorinas ◽  
Dalia Drobelytė ◽  
Rokas Šerpytis ◽  
Vytautas Sirvydis
Keyword(s):  
Lung Transplantation ◽  
Experimental Model ◽  
Heart Surgery ◽  
Left Lung ◽  
Experimental Models ◽  
Bronchial Anastomosis ◽  
G 21 ◽  
Vilnius University ◽  
Anesthetic Overdosage

Remigijus Sipavičius1, Aleksejus Zorinas1, Dalia Drobelytė2, Rokas Šerpytis2, Vytautas Sirvydis1.1 Vilniaus universiteto Širdies ir kraujagyslių ligų klinikos Širdies chirurgijos centras,Santariškių g. 2, LT-08661 Vilnius2 Vilniaus universiteto Medicinos fakultetas,M. K. Čiurlionio g. 21, LT-03101 VilniusEl. paštas: [email protected] Tikslas Sukurti ar pritaikyti esamus eksperimentinius modelius žiurkėms, tęsiant tyrinėjimus plaučių transplantacijos srityje. Metodai Žiurkėms atliekama kairiojo plaučio autotransplantacija arba ortotopinė transplantacija. Autotransplantacijos atveju atliekama kairiojo plaučio pulmoplegija, plautis paliekamas vietoje konservacijai norimam išemijos laikui. Jam praėjus atkuriama plaučio kraujotaka. Transplantacijos atveju donorui atliekama abiejų plaučių pulmoplegija, jie konservuojami norimą išemijos laiką. Recipientui pašalinamas kairysis plautis. Praėjus išemijos laikui, donoro kairysis plautis persodinamas recipientui, atkuriama plaučio kraujotaka. Rezultatai Atlikta 11 eksperimentų, penki iš jų – sėkmingai. Pagrindinės nesėkmių priežastys buvo broncho ar jo anastomozės plyšimas bei anestetikų perdozavimas. Išvados Esamus eksperimentinius modelius pavyko adaptuoti žiurkėms. Jie taikytini tolesnems plaučių transplantacijos tyrinėjimams. Pagrindiniai žodžiai: plaučių transplantacija, eksperimentinis modelis Left lung transplantation in rat: search for the experimental model Remigijus Sipavičius1, Aleksejus Zorinas1, Dalia Drobelytė2, Rokas Šerpytis2, Vytautas Sirvydis1.1 Vilnius University Clinic of Cardiovascular Diseases, Heart Surgery Centre,Santariškių str. 2, LT-08661 Vilnius, Lithuania2 Vilnius University Faculty of Medicine,M. K. Čiurlionio str. 21, LT-03101 Vilnius, LithuaniaE-mail: [email protected] Objective To design a new or to adapt the existing experimental models of rat lung transplantation. Methods Both left lung autotransplantation and orthotopic transplantation are implemented in rat. At autotransplantation, the left lung is left in situ after pulmoplegia. After a settled ischaemic time the lung perfusion is restored. At transplantation, pulmoplegia is performed in the donor. Lungs are separated and preserved for a settled ischaemic time. The recipient's left lung is removed and the donor's left lung transplantation is performed. The graft's perfusion is restored. Results Eleven experiments were carried out, 5 of them successfully. The main reasons for failure were bronchial anastomosis dehiscence or bronchial tear and anesthetic overdosage. Conclusion Existing experimental models were successfully adapted in rat, capacitating the further lung transplantation research. Key words: lung transplantation, experimental model

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