Design and control considerations for safe needle steering in brain tissue

CCCA12 ◽  
2012 ◽  
Author(s):  
Craig A. Lehocky ◽  
Xiao Li ◽  
Cameron N. Riviere
Keyword(s):  
Brain Tissue ◽  
Needle Steering ◽  
And Control

Acute and chronic synaptic pathology in multiple sclerosis gray matter

2021 ◽  
pp. 135245852110221
Author(s):  
Marco Vercellino ◽  
Stella Marasciulo ◽  
Silvia Grifoni ◽  
Elena Vallino-Costassa ◽  
Chiara Bosa ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Brain Tissue ◽  
Gray Matter ◽  
Axonal Loss ◽  
Strong Indication ◽  
Synaptic Loss ◽  
Synaptic Density ◽  
Synaptic Pathology ◽  
Gabaergic Synapses ◽  
And Control

Objectives: To investigate the extent of synaptic loss, and the contribution of gray matter (GM) inflammation and demyelination to synaptic loss, in multiple sclerosis (MS) brain tissue. Methods: This study was performed on two different post-mortem series of MS and control brains, including deep GM and cortical GM. MS brain samples had been specifically selected for the presence of active demyelinating GM lesions. Over 1,000,000 individual synapses were identified and counted using confocal microscopy, and further characterized as glutamatergic/GABAergic. Synaptic counts were also correlated with neuronal/axonal loss. Results: Important synaptic loss was observed in active demyelinating GM lesions (−58.9%), while in chronic inactive GM lesions, synaptic density was only mildly reduced compared to adjacent non-lesional gray matter (NLGM) (−12.6%). Synaptic loss equally affected glutamatergic and GABAergic synapses. Diffuse synaptic loss was observed in MS NLGM compared to control GM (−21.2% overall). Conclusion: This study provides evidence, in MS brain tissue, of acute synaptic damage/loss during active GM inflammatory demyelination and of synaptic reorganization in chronically demyelinated GM, affecting equally glutamatergic and GABAergic synapses. Furthermore, this study provides a strong indication of widespread synaptic loss in MS NLGM also independently from focal GM demyelination.

scholarly journals Metabolite differences in vascular dementia and control human brain tissue

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Tyler C. Hammond ◽  
Xin Xing ◽  
Peter T. Nelson ◽  
Stephanie Ham ◽  
Ai‐Ling Lin
Keyword(s):  
Human Brain ◽  
Vascular Dementia ◽  
Brain Tissue ◽  
Human Brain Tissue ◽  
And Control

scholarly journals Serum and Brain Metabolomic Variations Reveal Perturbation of Sleep Deprivation on Rats and Ameliorate Effect of Total Ginsenoside Treatment

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Xiao-jun Gou ◽  
Fang Cen ◽  
Zi-quan Fan ◽  
Ying Xu ◽  
Hong-yi Shen ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Brain Tissue ◽  
Panax Ginseng ◽  
Well Being ◽  
Metabolite Profile ◽  
Control Group ◽  
Protective Effects ◽  
Serum Samples ◽  
Tissue Samples ◽  
And Control

Sleep loss or sleep deprivation (SD) refers to shorter sleep than average baseline need, and SD has been a serious problem of modern societies which affects health and well-being.Panax ginsengis a well-known traditional Chinese medicine (TCM). Our previous study has demonstrated that total ginsenosides (GS), the extracts fromPanax ginseng, could effectively improve cognition and behavior on SD rats. However, little is known about its metabolomic study. In this study, serum and brain metabolomic method based on gas chromatography coupled with mass spectrometry (GC/MS) was employed to evaluate the efficacy and study the mechanism of GS on a rat model of SD. With pattern recognition analysis of serum and brain tissue metabolite profile, a clear separation of the model group and control group was acquired for serum and brain tissue samples; the MGS (model + GS) group showed a tendency of recovering when compared to control group, which was consistent with behavioral and biochemical parameters. 39 and 40 potential biomarkers of brain tissues and serum samples, respectively, were identified and employed to explore the possible mechanism. Our work revealed that GS has significant protective effects on SD, and metabolomics is a useful tool for evaluating efficacy and elucidating mechanism in TCM.

scholarly journals Heme Oxygenase-1 and Ferritin are Increased in Cerebral Arteries after Subarachnoid Hemorrhage in Monkeys

2000 ◽  
Vol 20 (7) ◽  
pp. 1066-1076 ◽  
Author(s):  
Shigeki Ono ◽  
Zhen-Du Zhang ◽  
Linda S. Marton ◽  
Baktiar Yamini ◽  
Emily Windmeyer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Heme Oxygenase ◽  
Cerebral Arteries ◽  
Heme Oxygenase 1 ◽  
Messenger Ribonucleic Acid ◽  
Control Side ◽  
Key Factor ◽  
Polymerase Chain ◽  
And Control

Hemoglobin is a key factor in the production of cerebral vasospasm. Metabolism of hemoglobin involves breakdown of heme by heme oxygenase (HO) and sequestration of the released iron in ferritin. We determined whether subarachnoid hemorrhage induces these proteins in cerebral arteries and, if so, in which cells they are produced. Whether the changes correlated with vasospasm also was investigated. Subarachnoid hemorrhage was created in monkeys, and vasospasm was assessed by angiography in cohorts of animals killed 3, 7, or 14 days after the hemorrhage. Ferritin and HO-1 messenger ribonucleic acid (mRNA) and protein were measured by competitive reverse transcription-polymerase chain reaction and Western blotting in hemorrhage-side and control-side cerebral arteries and brain tissue. The location of these proteins was determined by immunohistochemistry. There was significant vasospasm 3 and 7 days but not 14 days after subarachnoid hemorrhage. There were no significant changes in mRNA for HO-1 or ferritin in cerebral arteries or brain tissue at any time. There was a significant increase in HO-1 and ferritin protein in hemorrhage-side compared with control-side cerebral arteries at 3, 7, and 14 days. The increase in HO-1 protein was maximal at 3 days, whereas the increase in ferritin protein was maximal at 7 days. There was no detectable increase in HO-1 or ferritin protein in brain tissue at any time. Immunohistochemistry localized HO-1 protein and ferritin to cells in the adventitia of the arterial wall. We show that subarachnoid hemorrhage is associated with a significant increase in HO-1 and ferritin proteins in cerebral arteries that begins at least as early as 3 days after the hemorrhage and that persists for up to 14 days.

scholarly journals P3-174: QUANTITATION OF THE BACTERIAL PRODUCT LIPOPOLYSACCHARIDE (LPS) IN POSTMORTEM SERUM AND BRAIN TISSUE FROM AD, MCI, AND CONTROL PATIENTS

2019 ◽  
Vol 15 ◽  
pp. P997-P997
Author(s):  
Garilyn Jentarra ◽  
Ping Chu ◽  
Natalie Elliott ◽  
T. Bucky Jones ◽  
Jason Kaufman ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Bacterial Product ◽  
And Control
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