scholarly journals Diazepam Monotherapy or Diazepam-Ketamine Dual Therapy at Different Time Points Terminates Seizures and Reduces Mortality in a Status Epilepticus Animal Model

2021 ◽  
Vol 27 ◽  
Author(s):  
Ruijiao Zhou ◽  
Yanlin Wang ◽  
Xing Cao ◽  
Zhimin Li ◽  
Juming Yu
2020 ◽  
Vol 134 (7) ◽  
pp. 765-776 ◽  
Author(s):  
Monique Michels ◽  
Mariane Abatti ◽  
Andriele Vieira ◽  
Pricila Ávila ◽  
Amanda Indalécio Goulart ◽  
...  

Abstract Background: In order to modulate microglial phenotypes in vivo, M1 microglia were depleted by administration of gadolinium chloride and the expression of M2 microglia was induced by IL-4 administration in an animal model of sepsis to better characterize the role of microglial phenotypes in sepsis-induced brain dysfunction. Methods: Wistar rats were submitted to sham or cecal ligation and perforation (CLP) and treated with IL-4 or GdCl3. Animals were submitted to behavioral tests 10 days after surgery. In a separated cohort of animals at 24 h, 3 and 10 days after surgery, hippocampus was removed and cytokine levels, M1/M2 markers and CKIP-1 levels were determined. Results: Modulation of microglia by IL-4 and GdCl3 was associated with an improvement in long-term cognitive impairment. When treated with IL-4 and GdCl3, the reduction of pro-inflammatory cytokines was apparent in almost all analyzed time points. Additionally, CD11b and iNOS were increased after CLP at all time points, and both IL-4 and GdCl3 treatments were able to reverse this. There was a significant decrease in CD11b gene expression in the CLP+GdCl3 group. IL-4 treatment was able to decrease iNOS expression after sepsis. Furthermore, there was an increase of CKIP-1 in the hippocampus of GdCl3 and IL-4 treated animals 10 days after CLP induction. Conclusions: GdCl3 and IL-4 are able to manipulate microglial phenotype in an animal models of sepsis, by increasing the polarization toward an M2 phenotype IL-4 and GdCl3 treatment was associated with decreased brain inflammation and functional recovery.


2018 ◽  
Vol 29 (7) ◽  
pp. 757-770 ◽  
Author(s):  
Nikita Nirwan ◽  
Preeti Vyas ◽  
Divya Vohora

Abstract Temporal lobe epilepsy (TLE) is the chronic and pharmacoresistant form of epilepsy observed in humans. The current literature is insufficient in explicating the comprehensive mechanisms underlying its pathogenesis and advancement. Consequently, the development of a suitable animal model mimicking the clinical characteristics is required. Further, the relevance of status epilepticus (SE) to animal models is dubious. SE occurs rarely in people; most epilepsy patients never experience it. The present review summarizes the established animal models of SE and TLE, along with a brief discussion of the animal models that have the distinctiveness and carries the possibility to be developed as effective models for TLE. The review not only covers the basic requirements, mechanisms, and methods of induction of each model but also focuses upon their major limitations and possible modifications for their future use. A detailed discussion on chemical, electrical, and hypoxic/ischemic models as well as a brief explanation on the genetic models, most of which are characterized by development of SE followed by neurodegeneration, is presented.


2000 ◽  
Vol 98 (5) ◽  
pp. 561-567 ◽  
Author(s):  
Simon A. WEMYSS-HOLDEN ◽  
Gavin S. M. ROBERTSON ◽  
Ashley R. DENNISON ◽  
Paula S. VANDERZON ◽  
Pauline de la M. HALL ◽  
...  

The majority of liver tumours are inoperable and an alternative treatment to surgical resection is urgently needed. Electrolysis has been investigated in a rat model and the procedure is safe, with accurate and predictable effects. The necrosis produced has also been shown to cause destruction of tumour deposits in the rat liver. A similar evaluation in a large animal model was necessary before clinical trials could commence. Using platinum electrodes connected to a d.c. generator, areas of hepatic necrosis were created in the pig liver. Animals were killed at various time points after treatment to assess the extent of healing. Treatment was uneventful and all animals made a full recovery. No animal died from the treatment or had to be killed prematurely. After 2 days of treatment, healing was minimal but at successive time points there was progressive evidence of healing, such that after 4 months, the original electrolytic lesion was greatly reduced in size and the large area of necrosis seen at the early time points was largely replaced by a fibrous scar with only small islands of necrotic tissue. In a large animal model, electrolysis is a safe method for creating areas of hepatic necrosis. The lesions heal with time and are associated with minimal morbidity. The results support a trial of electrolysis in patients with unresectable liver tumours.


Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Tito G M Vivas-Buitrago ◽  
Ignacio Jusue Torres ◽  
Gabriel D Pinilla-Monsalve ◽  
Armelle Lokossou ◽  
Jiadi Xu ◽  
...  

Abstract INTRODUCTION Early diagnosis of NPH during its initial stages is almost impossible, given the delayed onset of clinical symptoms, making the study and the understanding of the CSF dynamics very challenging in human subjects. In this study, we explore these dynamics in a novel animal model with induced chronic communicating hydrocephalus with the aim to better understand the pathophysiology of NPH to pursue earlier diagnostic tools that will ultimately translate into better treatment outcomes. METHODS Chronic communicating hydrocephalus was induced in 15 adult Sprague-Dawley rats using a technique developed by our group. Kaolin is injected into the subarachnoid space over the cerebral convexities. Additionally, 4 animals were used as controls and 3 as shams with saline injections. PCMRI was performed to calculate the aqueductal stroke volume (ASV) and T2-W images for ventricular size measurements on days 15, 60, 90, and 120 using a Bruker 11.7-TMR. Nonparametric tests were implemented to analyze the ASV and its correlation with the ventricular volumes after the hydrocephalus induction. RESULTS Kaolin-injected (KI) animals showed a significant ventricular enlargement at all time points. A significant difference in ASV was present between KI and controls at all times. There was a significant positive correlation between the ventricular volume expansion and the ASV between 15 and 60 d. CONCLUSION An initial active phase of rapid ventricular enlargement shows a strong correlation between the expansion of the ventricular volume and the increment in ASV during the first 60 d, followed by a second phase with a less ventricular enlargement and heterogeneous behavior in the ASV. Results may suggest an optimal window for CSF diversion treatment. This hypothesis will be explored in the following experiment by shunting groups of animals at all time points. Future studies will include an evaluation of the intracranial pressure and histological/microstructural analysis to better understand the ASV variations after 60 d.


Epilepsia ◽  
2016 ◽  
Vol 57 (9) ◽  
pp. 1406-1415 ◽  
Author(s):  
Jerome Niquet ◽  
Roger Baldwin ◽  
Keith Norman ◽  
Lucie Suchomelova ◽  
Lucille Lumley ◽  
...  

2005 ◽  
Vol 93 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Sang-Woon Choi ◽  
Simonetta Friso ◽  
Mary K. Keyes ◽  
Joel B. Mason

The availability of folate is implicated as a determinant of DNA methylation, a functionally important feature of DNA. Nevertheless, when this phenomenon has been examined in the rodent model, the effect has not always been observed. Several reasons have been postulated for the inconsistency between studies: the rodent is less dependent on folate as a methyl source than man; juvenile animals, which most studies use, are more resistant to folate depletion than old animals; methods to measure genomic DNA methylation might not be sensitive enough to detect differences. We therefore examined the relationship between folate and genomic DNA methylation in an elder rat model with a newly developed method that can measure genomic DNA methylation sensitively and precisely. Thirty-nine 1-year-old rats were divided into three groups and fed a diet containing 0, 4·5 or 18 μmol folate/kg (folate-deplete, -replete and -supplemented groups, respectively). Rats were killed at 8 and 20 weeks. At both time points, mean liver folate concentrations increased incrementally between the folate-deplete, -replete and -supplemented rats (Pfor trend <0·001) and by 20 weeks hepatic DNA methylation also increased incrementally between the folate-deplete, -replete and -supplemented rats (Pfor trend=0·025). At both time points folate-supplemented rats had significantly increased levels of DNA methylation compared with folate-deplete\ rats (P<0·05). There was a strong correlation between hepatic folate concentration and genomic DNA methylation in the liver (r0·48,P=0·004). In the liver of this animal model, dietary folate over a wide range of intakes modulates genomic DNA methylation.


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