M. A. Estudillo-Guerra, I. Mesia-Toledo, Noga Rogel, N. Yaghoubi, Z. Ahmed, R. Black-Schaffer, L. Morales-Quezada
{"title":"Trans-Spinal Direct Current Stimulation in Spasticity: A Literature Mini-Review","authors":"M. A. Estudillo-Guerra, I. Mesia-Toledo, Noga Rogel, N. Yaghoubi, Z. Ahmed, R. Black-Schaffer, L. Morales-Quezada","doi":"10.3389/fstro.2022.921450","DOIUrl":"https://doi.org/10.3389/fstro.2022.921450","url":null,"abstract":"Spasticity is common after a stroke and has a negative impact on functional and quality-of-life measures. There is an unmet medical need to provide safe and effective treatment using non-pharmacological approaches. Trans-spinal direct current stimulation (tsDCS) is an emerging modality for non-invasive neuromodulation that induces reduction of spinal excitability leading to a decrease in spasticity. We describe current treatment options for spasticity, including a literature review about the use of tsDCS in patients with spasticity. We found four clinical studies that used tsDCS to treat spasticity for different neurological conditions including hereditary spastic paraplegia, upper extremity spasticity following stroke, multiple sclerosis, and incomplete chronic spinal cord injury. Spasticity was the primary outcome in three of the studies and a secondary outcome in the final study. The three studies that addressed spasticity as the primary outcome found that active tsDCS decreased spasticity compared to sham. These studies suggest that tsDCS can modulate spinal motor and sensory spinal pathways through the use of specific electrode montages and stimulation parameters. This therapy can improve motor functions and may represent a viable treatment option for spasticity.","PeriodicalId":73108,"journal":{"name":"Frontiers in stroke","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79582801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Compromised endothelial progenitor cell exosomal communication with endothelial cells in hypertension ischemia conditions","authors":"Shuzhen Chen, Venkata Polaki, J. Bihl, Jinju Wang","doi":"10.3389/fstro.2022.1015463","DOIUrl":"https://doi.org/10.3389/fstro.2022.1015463","url":null,"abstract":"We have previously demonstrated that endothelial progenitor cell (EPC) derived exosomes (EPC-EXs) can protect endothelial cells (ECs) against hypoxia injury. Given that EX function varies upon the cellular status and EPC function is declined in hypertension, we speculate the function of EPC-EXs is altered in hypertension-ischemia conditions. Here, we studied the EPC-EX mediated communications of EPCs with ECs in hypertension-ischemia conditions. EPC-EXs were prepared from the bone marrow EPCs of wild-type (WT) and hypertensive renin transgene (R+) mice (WT-EPC-EXs and R-EPC-EXs, respectively). To mimic hypertension-ischemia injury, ECs were challenged with angiotensin II (Ang II; 10−6 M) plus hypoxia (1% O2 for 6 h) and reoxygenation (21% O2 for 24 h). To determine the function of EPC-EXs, ECs were co-cultured with EXs during the reoxygenation period. EX uptake efficiency, EC viability, and angiogenic function were assessed. We found that: (1) The incorporation efficiency of R-EPC-EXs by ECs was significantly decreased compared to the WT-EPC-EXs. (2) Ang II plus hypoxia reoxygenation-injured ECs displayed decreased cell viability, increased cell apoptosis, and compromised angiogenic ability, which were alleviated by R-EPC-EXs. (3) WT-EPC-EXs elicited better effects than R-EPC-EXs on protecting ECs from hypertension plus hypoxia injury. In conclusion, our data have demonstrated that EPC-EXs mediated communication of EPCs and ECs is compromised in hypertension-ischemia conditions, suggesting that impairment of EPC exosomal communication might contribute to the exaggerated cerebral ischemia injury in hypertension-associated ischemic stroke.","PeriodicalId":73108,"journal":{"name":"Frontiers in stroke","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78852161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Frontiers in strokePub Date : 2022-01-01Epub Date: 2022-12-21DOI: 10.3389/fstro.2022.1026066
Tyler C Hammond, Sarah Messmer, Jacqueline A Frank, Doug Lukins, Rita Colwell, Ai-Ling Lin, Keith R Pennypacker
{"title":"Gut microbial dysbiosis correlates with stroke severity markers in aged rats.","authors":"Tyler C Hammond, Sarah Messmer, Jacqueline A Frank, Doug Lukins, Rita Colwell, Ai-Ling Lin, Keith R Pennypacker","doi":"10.3389/fstro.2022.1026066","DOIUrl":"10.3389/fstro.2022.1026066","url":null,"abstract":"<p><strong>Background: </strong>An imbalanced gut microbial community, or dysbiosis, has been shown to occur following stroke. It is possible that this dysbiosis negatively impacts stroke recovery and rehabilitation. Species level resolution measurements of the gut microbiome following stroke are needed to develop and test precision interventions such as probiotic or fecal microbiota transplant therapies that target the gut microbiome. Previous studies have used 16S rRNA amplicon sequencing in young male mice to obtain broad profiling of the gut microbiome at the genus level following stroke, but further investigations will be needed with whole genome shotgun sequencing in aged rats of both sexes to obtain species level resolution in a model which will better translate to the demographics of human stroke patients.</p><p><strong>Methods: </strong>Thirty-nine aged male and female rats underwent middle cerebral artery occlusion. Fecal samples were collected before stroke and 3 days post stroke to measure gut microbiome. Machine learning was used to identify the top ranked bacteria which were changed following stroke. MRI imaging was used to obtain infarct and edema size and cerebral blood flow (CBF). ELISA was used to obtain inflammatory markers.</p><p><strong>Results: </strong>Dysbiosis was demonstrated by an increase in pathogenic bacteria such as <i>Butyricimonas virosa</i> (15.52 fold change, <i>p</i> < 0.0001), <i>Bacteroides vulgatus</i> (7.36 fold change, <i>p</i> < 0.0001), and <i>Escherichia coli</i> (47.67 fold change, <i>p</i> < 0.0001). These bacteria were positively associated with infarct and edema size and with the inflammatory markers Ccl19, Ccl24, IL17a, IL3, and complement C5; they were negatively correlated with CBF. Conversely, beneficial bacteria such as <i>Ruminococcus flavefaciens</i> (0.14 fold change, <i>p</i> < 0.0001), <i>Akkermansia muciniphila</i> (0.78 fold change, <i>p</i> < 0.0001), and <i>Lactobacillus murinus</i> (0.40 fold change, <i>p</i> < 0.0001) were decreased following stroke and associated with all the previous parameters in the opposite direction of the pathogenic species. There were not significant microbiome differences between the sexes.</p><p><strong>Conclusion: </strong>The species level resolution measurements found here can be used as a foundation to develop and test precision interventions targeting the gut microbiome following stroke. Probiotics that include <i>Ruminococcus flavefaciens, Akkermansia muciniphila, and Lactobacillus murinus</i> should be developed to target the deficit following stroke to measure the impact on stroke severity.</p>","PeriodicalId":73108,"journal":{"name":"Frontiers in stroke","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9945937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10800047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}