scholarly journals Microglia and Stem-Cell Mediated Neuroprotection after Neonatal Hypoxia-Ischemia

2021 ◽  
Author(s):  
Catherine Brégère ◽  
Bernd Schwendele ◽  
Boris Radanovic ◽  
Raphael Guzman
Keyword(s):  
Stem Cell ◽  
Animal Studies ◽  
Treatment Options ◽  
Neurological Deficits ◽  
Potential Contribution ◽  
Term Infants ◽  
Brain Repair ◽  
Neonatal Hypoxia ◽  
Microglial Phenotype ◽  
Hypoxia Ischemia

AbstractNeonatal hypoxia-ischemia encephalopathy (HIE) refers to a brain injury in term infants that can lead to death or lifelong neurological deficits such as cerebral palsy (CP). The pathogenesis of this disease involves multiple cellular and molecular events, notably a neuroinflammatory response driven partly by microglia, the brain resident macrophages. Treatment options are currently very limited, but stem cell (SC) therapy holds promise, as beneficial outcomes are reported in animal studies and to a lesser degree in human trials. Among putative mechanisms of action, immunomodulation is considered a major contributor to SC associated benefits. The goal of this review is to examine whether microglia is a cellular target of SC-mediated immunomodulation and whether the recruitment of microglia is linked to brain repair. We will first provide an overview on microglial activation in the rodent model of neonatal HI, and highlight its sensitivity to developmental age. Two complementary questions are then addressed: (i) do immune-related treatments impact microglia and provide neuroprotection, (ii) does stem cell treatment modulates microglia? Finally, the immune-related findings in patients enrolled in SC based clinical trials are discussed. Our review points to an impact of SCs on the microglial phenotype, but heterogeneity in experimental designs and methodological limitations hamper our understanding of a potential contribution of microglia to SC associated benefits. Thorough analyses of the microglial phenotype are warranted to better address the relevance of the neuroimmune crosstalk in brain repair and improve or advance the development of SC protocols in humans. Graphical abstract

Sildenafil Improves Brain Injury Recovery following Term Neonatal Hypoxia-Ischemia in Male Rat Pups

2016 ◽  
Vol 38 (4) ◽  
pp. 251-263 ◽  
Author(s):  
Armin Yazdani ◽  
Zehra Khoja ◽  
Aaron Johnstone ◽  
Laura Dale ◽  
Emmanouil Rampakakis ◽  
...  
Keyword(s):  
Brain Injury ◽  
Gait Analysis ◽  
Left Hemisphere ◽  
Neurological Deficits ◽  
Male Rat ◽  
Boundary Zone ◽  
Neonatal Hypoxia ◽  
Rat Pups ◽  
Hypoxia Ischemia ◽  
Injury Recovery

Term asphyxiated newborns remain at risk of developing brain injury despite available neuropreventive therapies such as hypothermia. Neurorestorative treatments may be an alternative. This study investigated the effect of sildenafil on brain injury induced by neonatal hypoxia-ischemia (HI) at term-equivalent age. Neonatal HI was induced in male Long-Evans rat pups at postnatal day 10 (P10) by left common carotid ligation followed by a 2-hour exposure to 8% oxygen; sham-operated rat pups served as the control. Both groups were randomized to oral sildenafil or vehicle twice daily for 7 consecutive days. Gait analysis was performed on P27. At P30, the rats were sacrificed, and their brains were extracted. The surfaces of both hemispheres were measured on hematoxylin and eosin-stained brain sections. Mature neurons and endothelial cells were quantified near the infarct boundary zone using immunohistochemistry. HI caused significant gait impairment and a reduction in the size of the left hemisphere. Treatment with sildenafil led to an improvement in the neurological deficits as measured by gait analysis, as well as an improvement in the size of the left hemisphere. Sildenafil, especially at higher doses, also caused a significant increase in the number of neurons near the infarct boundary zone. In conclusion, sildenafil administered after neonatal HI may improve brain injury recovery by promoting neuronal populations.

scholarly journals Stem cells for brain repair in neonatal hypoxia–ischemia

2013 ◽  
Vol 30 (1) ◽  
pp. 37-46 ◽  
Author(s):  
L. Chicha ◽  
T. Smith ◽  
R. Guzman
Keyword(s):  
Stem Cells ◽  
Brain Repair ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Új lehetőségek a refrakter és relabált Hodgkin-lymphomás betegek kezelésében

2015 ◽  
Vol 156 (45) ◽  
pp. 1824-1833 ◽  
Author(s):  
Árpád Illés ◽  
Ádám Jóna ◽  
Zsófia Simon ◽  
Miklós Udvardy ◽  
Zsófia Miltényi
Keyword(s):  
Stem Cell ◽  
Hodgkin Lymphoma ◽  
Treatment Options ◽  
Survival Rates ◽  
Relapse Free Survival ◽  
Term Survival ◽  
Free Survival ◽  
Novel Treatment ◽  
Refractory Hodgkin Lymphoma

Introduction: Hodgkin lymphoma is a curable lymphoma with an 80–90% long-term survival, however, 30% of the patients develop relapse. Only half of relapsed patients can be cured with autologous stem cell transplantation. Aim: The aim of the authors was to analyze survival rates and incidence of relapses among Hodgkin lymphoma patients who were treated between January 1, 1980 and December 31, 2014. Novel therapeutic options are also summarized. Method: Retrospective analysis of data was performed. Results: A total of 715 patients were treated (382 men and 333 women; median age at the time of diagnosis was 38 years). During the studied period the frequency of relapsed patients was reduced from 24.87% to 8.04%. The numbers of autologous stem cell transplantations was increased among refracter/relapsed patients, and 75% of the patients underwent transplantation since 2000. The 5-year overall survival improved significantly (between 1980 and 1989 64.4%, between 1990 and 1999 82.4%, between 2000 and 2009 88.4%, and between 2010 and 2014 87.1%). Relapse-free survival did not change significantly. Conclusions: During the study period treatment outcomes improved. For relapsed/refractory Hodgkin lymphoma patients novel treatment options may offer better chance for cure. Orv. Hetil., 2015, 156(45), 1824–1833.

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

Posterior circulation stroke: an easily overlooked complication of catheter ablation of atrial fibrillation

2020 ◽  
Vol 13 (8) ◽  
pp. e234661
Author(s):  
Tahir Nazir ◽  
Mohiuddin Sharief ◽  
James Farthing ◽  
Irfan M Ahmed
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Treatment Options ◽  
Posterior Circulation ◽  
Diagnosis And Treatment ◽  
Neurological Deficits ◽  
Cerebellar Infarction ◽  
Af Ablation ◽  
Posterior Circulation Stroke ◽  
Ventricular Response

Catheter ablation of atrial fibrillation (AF) has established itself as a safe and proven rhythm control strategy for selected patients with AF over the past decade. Thromboembolic complications of catheter ablation are becoming rare in anticoagulated patients with a risk of stroke reported as 0.3%. A particular challenge is posed by clinical presentation due to ischaemic stroke involving the posterior circulation following catheter ablation because of its substantial differences from the carotid territory stroke, making the timely diagnosis and treatment very difficult. It is crucial to keep an index of clinical suspicion in patients presenting with neurological deficits related to vertebrobasilar circulation following ablation. We describe the case of a man who presented with dizziness and palpitations after radiofrequency catheter ablation of AF. He was found to be in AF with a rapid ventricular response. His dizziness was initially attributed to the cardiac dysrhythmia. As his symptoms continued despite heart rate control, he underwent further investigations and was eventually diagnosed with a posterior circulation stroke resulting in left cerebellar infarction. He was treated with antiplatelet therapy and improved significantly over the following few days. We review and present an up-to-date brief literature review on the complications of catheter ablation of AF and describe pathophysiology, clinical features, diagnosis and treatment options for posterior circulation stroke after AF ablation. This case aims to raise awareness among clinicians about posterior circulation stroke after AF ablation.

scholarly journals Oxidative Stress as a Possible Target in the Treatment of Toxoplasmosis: Perspectives and Ambiguities

2021 ◽  
Vol 22 (11) ◽  
pp. 5705
Author(s):  
Karolina Szewczyk-Golec ◽  
Marta Pawłowska ◽  
Roland Wesołowski ◽  
Marcin Wróblewski ◽  
Celestyna Mila-Kierzenkowska
Keyword(s):  
Oxidative Stress ◽  
Animal Studies ◽  
Treatment Options ◽  
Natural Antioxidants ◽  
Redox Status ◽  
Host Cells ◽  
Common Disease ◽  
Parasite Viability

Toxoplasma gondii is an apicomplexan parasite causing toxoplasmosis, a common disease, which is most typically asymptomatic. However, toxoplasmosis can be severe and even fatal in immunocompromised patients and fetuses. Available treatment options are limited, so there is a strong impetus to develop novel therapeutics. This review focuses on the role of oxidative stress in the pathophysiology and treatment of T. gondii infection. Chemical compounds that modify redox status can reduce the parasite viability and thus be potential anti-Toxoplasma drugs. On the other hand, oxidative stress caused by the activation of the inflammatory response may have some deleterious consequences in host cells. In this respect, the potential use of natural antioxidants is worth considering, including melatonin and some vitamins, as possible novel anti-Toxoplasma therapeutics. Results of in vitro and animal studies are promising. However, supplementation with some antioxidants was found to promote the increase in parasitemia, and the disease was then characterized by a milder course. Undoubtedly, research in this area may have a significant impact on the future prospects of toxoplasmosis therapy.

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