scholarly journals Metagenomics Analysis of Thrombus Samples Retrieved from Mechanical Thrombectomy

2021 ◽  
Vol 16 (1) ◽  
pp. 39-45
Author(s):  
Atulabh Vajpeyee ◽  
Puneet Singh Chauhan ◽  
Swapnil Pandey ◽  
Shivam Tiwari ◽  
Lokendra Bahadur Yadav ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Carotid Plaque ◽  
Mechanical Thrombectomy ◽  
Artery Occlusion ◽  
Symptomatic Carotid ◽  
Symptomatic Carotid Stenosis ◽  
Biofilm Dispersion ◽  
Tandem Lesions

Purpose: The purpose of this study was to assess the microbiota in middle cerebral artery thrombi retrieved in mechanical thrombectomy arising out of symptomatic carotid plaque within 6 hours of acute ischemic stroke. Thrombi were subjected to next-generation sequencing for a bacterial signature to determine their role in atherosclerosis.Materials and Methods: We included 4 human middle cerebral artery thrombus samples (all patients were male). The median age for the patients was 51±13.6 years. Patients enrolled in the study from Pacific Medical University and Hospital underwent mechanical thrombectomy in the stroke window period. All patients underwent brain magnetic resonance angiography (MRA) and circle of Willis and neck vessel MRA along with the standard stroke workup to establish stroke etiology. Only patients with symptomatic carotid stenosis and tandem lesions with ipsilateral middle cerebral artery occlusion were included in the study. Thrombus samples were collected, stored at –80 degrees, and subjected to metagenomics analysis.Results: Of the 4 patients undergoing thrombectomy for diagnosis with ischemic stroke, all thrombi recovered for bacterial DNA in qPCR were positive. More than 27 bacteria were present in the 4 thrombus samples. The majority of bacteria were <i>Lactobacillus, Stenotrophomonas, Pseudomonas, Staphylococcus</i>, and <i>Finegoldia</i>.Conclusion: Genesis of symptomatic atherosclerotic carotid plaque leading to thromboembolism could be either due to direct mechanisms like acidification and local inflammation of plaque milieu with lactobacillus, biofilm dispersion leading to inflammation like with pseudomonas fluorescence, or enterococci or indirect mechanisms like Toll 2 like signaling by gut microbiota.

Abstract 166: Endothelial Overexpression of LOX-1 Increases Stroke Size in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Oxidized Ldl ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
The Brain

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.

scholarly journals A Novel Model for Encephalomyosynangiosis Surgery after Middle Cerebral Artery Occlusion-Induced Stroke in Mice

2021 ◽  
Author(s):  
Mitch Paro ◽  
Daylin Gamiotea Turro ◽  
Leslie Blumenfeld ◽  
Ketan R Bulsara ◽  
Rajkumar Verma
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Therapeutic Option ◽  
Treatment Options ◽  
Artery Occlusion ◽  
Novel Treatment ◽  
Graft Tissue ◽  
Cerebral Artery Occlusion

Background and Purpose: No effective treatment is available for most patients who suffer ischemic stroke. Development of novel treatment options is imperative. The brain attempts to self-heal after ischemic stroke via various mechanism mediated by restored blood circulation in affected region of brain but this process is limited by inadequate angiogenesis or neoangiogenesis. Encephalomyosynangiosis (EMS) is a neurosurgical procedure that achieves angiogenesis with low morbidity in patients with moyamoya disease, reducing risk of stroke. However, EMS, surgery has never been studied as an therapeutic option after ischemic stroke. Here we described a novel procedure and feasibility data for EMS after ischemic stroke in mice. Methods: A 60 mins of middle cerebral artery occlusion (MCAo) was used to induce ischemic stroke in mice. After 3-4 hours of MCAo onset/sham, EMS was performed. Mortality of EMS, MCAo and. MCAo+EMS mice was recorded up to 21 days after surgery. Graft tissue viability was measured using a nicotinamide adenine dinucleotide reduced tetrazolium reductase assay. Results: EMS surgery after ischemic stroke does not increase mortality compared to stroke alone. Graft muscle tissue remained viable 21 days after surgery. Conclusions: This novel protocol is effective and well-tolerated, may serve as novel platform for new angiogenesis and thus recovery after ischemic stroke. If successful in mice, EMS can a very feasible and novel treatment option for ischemic stroke in humans.

Abstract TP106: Automated Assessment of Behavioral Function After Experimental Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Terrance Chiang ◽  
Sean Harvey ◽  
Arjun V Pendharkar ◽  
Michelle Y Cheng ◽  
Gary K Steinberg
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Motor Deficit ◽  
Motor Deficits ◽  
Stroke Models ◽  
Cerebral Artery Occlusion ◽  
Significant Motor

Introduction: Manual scoring of behavior tests is commonly used for assessing motor deficits after stroke, however, it is labor intensive and subject to bias. These limitations lead to inconsistent assessment between research groups and non-reproducible data. In this study, we investigated the feasibility of an automated motor deficit assessment system, Erasmus ladder, in two ischemic stroke models. Methods: Distal middle cerebral artery occlusion (dMCAO n=10) or transient middle cerebral artery occlusion (tMCAO 30 minutes, n=15) were performed on male C57BL6J mice (11-13 weeks) to generate cortical ischemic stroke, with. Naïve mice (n=10) were used as controls. Immunohistochemistry was performed on brains collected at post-stroke day (PD) 30 to assess for infarct size (MAP2) and inflammation (CD68). Mice without infarct in both cortex and striatum were excluded from the study. Behavior was assessed using Erasmus ladder at pre-stroke baseline (4 unperturbed and 4 perturbed sessions) and on PD 7, 14, 21, and 28 (all perturbed sessions). Results: Erasmus ladder detected significant motor deficits in the tMCAO model, specifically in the pre- and post- perturbed times as well as several key step types (HH long). Analyses in the tMCAO model reveal changes in various step patterns and their capability to react to the perturbation (obstacle). These significant motor deficits after tMCAO were detectable until PD28. We also observed a sustained decline in the use of affected limb compared to unaffected limb until PD28. While this trend is also present in dMCAO model, motor deficits were detected in the dMCAO only at early timepoints (PD7) and the difference subsided by PD28. Conclusion: We have assessed the data collected by Erasmus ladder on mice that underwent two commonly used stroke models (tMCAO and dMCAO). Our data showed that Erasmus ladder can detect long term motor deficit including reduced use of affected limb, step pattern, and motor reaction to obstacle. This automated instrument is effective in detecting motor deficits in the tMCAO model and thus, can be used to evaluate treatments for enhancing recovery after stroke.

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