keyword
MENU ▼
Read by QxMD icon Read
search

Mitochondrial AND cerebral

keyword
https://www.readbyqxmd.com/read/29223124/activation-of-mitochondrial-katp-channels-mediates-neuroprotection-induced-by-chronic-morphine-preconditioning-in-hippocampal-ca-1-neurons-following-cerebral-ischemia
#1
Maedeh Arabian, Nahid Aboutaleb, Mansoureh Soleimani, Marjan Ajami, Rouhollah Habibey, Hamidreza Pazoki-Toroudi
PURPOSE: Pharmacologic preconditioning, through activating several mechanisms and mediators, can increase the tolerance of different tissues against ischemia/reperfusion (I/R) injury. Recent studies have shown that morphine preconditioning has protective effects in different organs, especially in the heart. Nevertheless, its mechanisms are not well elucidated in the brain. The present study aimed to clarify whether the activation of mitochondrial KATP (mKATP) channels in chronic morphine (CM) preconditioning could decrease hippocampus damage following I/R injury...
December 6, 2017: Advances in Medical Sciences
https://www.readbyqxmd.com/read/29218106/extracorporeal-shock-wave-therapy-effectively-protects-brain-against-chronic-cerebral-hypo-perfusion-induced-neuropathological-changes
#2
Han-Tan Chai, Kuan-Hung Chen, Christopher Glenn Wallace, Chih-Hung Chen, Pei-Hsun Sung, Yung-Lung Chen, Chun-Man Yuen, Pei-Lin Shao, Cheuk-Kwan Sun, Hsueh-Wen Chang, Ching-Jen Wang, Mel S Lee, Hon-Kan Yip, Sheung-Fat Ko
This study tested the hypothesis that extracorporeal shock wave (ECSW) therapy could protect mouse brain from chronic cerebral hypoperfusion (CHP)-induced neuropathological changes in a bilateral carotid arterial stenosis (CAS) model. Adult-male C57BL/6 (B6) mice (n=36) were randomized into group 1 (sham-control), group 2 (CHP) and group 3 [CHP+ECSW (100 impulses at 0.15 mJ/mm2) on day 5, 10 and 15 after CHP induction]. By day 60 after CHP induction, the white matter lesion, protein expressions of inflammatory (TNF-α/NF-κB/iNOS), oxidative-stress (NOX-1/NOX-2/NOX-4/nitrotyrosine), angiogenesis (eNOS/CD31), apoptotic (Bax/caspase-3/PARP), fibrotic (Smad3/TGF-ß) and mitochondrial-damaged (cytosolic cytochrome-C) biomarkers were significantly higher in group 2 than in groups 1 and 3, and significantly higher in group 3 than in group 1, whereas the protein expressions of anti-apoptotic (Bcl-2), anti-fibrotic (BMP-2/Smad1/5), and mitochondrial-integrity (mitochondrial cytochrome-C) biomarkers showed an opposite pattern to inflammation among the three groups (all P<0...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/29215305/cerebrovascular-function-and-mitochondrial-bioenergetics-after-ischemia-reperfusion-in-male-rats
#3
Ibolya Rutkai, Ivan Merdzo, Sanjay V Wunnava, Genevieve T Curtin, Prasad Vg Katakam, David W Busija
The underlying factors promoting increased mitochondrial proteins, mtDNA, and dilation to mitochondrial-specific agents in male rats following tMCAO are not fully elucidated. Our goal was to determine the morphological and functional effects of ischemia/reperfusion (I/R) on mitochondria using electron microscopy, Western blot, mitochondrial oxygen consumption rate (OCR), and Ca2+ sparks activity measurements in middle cerebral arteries (MCAs) from male Sprague Dawley rats (Naïve, tMCAO, Sham). We found a greatly increased OCR in ipsilateral MCAs (IPSI) compared with contralateral (CONTRA), Sham, and Naïve MCAs...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29211056/krebs-cycle-metabolites-and-preferential-succinate-oxidation-following-neonatal-hypoxic-ischemic-brain-injury-in-mice
#4
Prateek V Sahni, Jimmy Zhang, Sergey Sosunov, Alexander Galkin, Zoya Niatsetskaya, Anatoly Starkov, Paul S Brookes, Vadim S Ten
BackgroundReverse electron transport (RET) driven by the oxidation of succinate has been proposed as the mechanism of accelerated production of reactive oxygen species (ROS) in post-ischemic mitochondria. However, it remains unclear whether upon reperfusion, mitochondria preferentially oxidase succinate.MethodsNeonatal mice were subjected to Rice-Vannucci model of hypoxic-ischemic brain injury (HI) followed by assessment of Krebs cycle metabolites, mitochondrial substrate preference, and H2O2 generation rate in the ischemic brain...
December 6, 2017: Pediatric Research
https://www.readbyqxmd.com/read/29206066/magnesium-induces-preconditioning-of-the-neonatal-brain-via-profound-mitochondrial-protection
#5
Gabriella Koning, Anna-Lena Leverin, Syam Nair, Leslie Schwendimann, Joakim Ek, Ylva Carlsson, Pierre Gressens, Claire Thornton, Xiaoyang Wang, Carina Mallard, Henrik Hagberg
Magnesium sulphate (MgSO4) given to women in preterm labor reduces cerebral palsy in their offspring but the mechanism behind this protection is unclear, limiting its effective, safe clinical implementation. Previous studies suggest that MgSO4 is not neuroprotective if administered during or after the insult, so we hypothesised that MgSO4 induces preconditioning in the immature brain. Therefore, we administered MgSO4 at various time-points before/after unilateral hypoxia-ischemia (HI) in seven-day-old rats...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29205598/an-auditory-brainstem-nucleus-as-a-model-system-for-neuronal-metabolic-demands
#6
Sonja Brosel, Benedikt Grothe, Lars Kunz
The correlation between neuronal activity and metabolism is essential for coding, plasticity, neurological disorders and the interpretation of functional neuroimaging data. Most likely, metabolic requirements depend upon neuron type and macroscopic energy demands vary with brain region. However, specific needs of individual neuron types are enigmatic. Therefore, we monitored metabolic activity in the lateral superior olive (LSO), an auditory brainstem nucleus containing only one neuron type. LSO neurons exhibit extreme but well described biophysics with firing rates of several hundred hertz and low input resistances of a few megaohms...
December 4, 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/29200367/anesthetic-management-in-mitochondrial-encephalomyopathy-a-case-report
#7
Toru Yamamoto, Noriko Miyazawa, Shinichi Yamamoto, Hiroshi Kawahara
We report on a morbidly obese 16-year-old boy (weight, 116 kg; height, 176 cm; body mass index, 35.5 kg/m2) with mitochondrial encephalomyopathy and a history of cerebral infarction, epilepsy, and severe mental retardation. The patient was scheduled for elective surgery under general anesthesia for multiple dental caries and entropion of the left eye. Preoperative examination results, including an electrocardiogram, were normal. No obvious cardiac function abnormalities were observed on echocardiography. Midazolam (10 mg) was administered orally as premedication 30 minutes before transfer to the operating room; however, the patient was uncooperative, and his body movements were difficult to control upon entering the operating room...
2017: Anesthesia Progress
https://www.readbyqxmd.com/read/29194538/mitochondrial-abnormalities-and-disruption-of-the-neuromuscular-junction-precede-the-clinical-phenotype-and-motor-neuron-loss-in-hfuswt-transgenic-mice
#8
Eva So, Jacqueline C Mitchell, Caroline Memmi, George Chennell, Gema Vizcay-Barrena, Leanne Allison, Christopher E Shaw, Caroline Vance
FUS mislocalisation and cytoplasmic aggregation are hallmark pathologies in FUS-related amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Many of the mechanistic hypotheses have focused on a loss of nuclear function in the FUS-opathies, implicating dysregulated RNA transcription and splicing in driving neurodegeneration. Recent studies describe an additional somato-dendritic localisation for FUS in the cerebral cortex implying a regulatory role in mRNA transport and local translation at the synapse...
November 28, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/29192254/effect-of-src-kinase-inhibition-on-cytochrome-c-smac-diablo-and-apoptosis-inducing-factor-aif-following-cerebral-hypoxia-ischemia-in-newborn-piglets
#9
Panagiotis Kratimenos, Ioannis Koutroulis, Beamon Agarwal, Stamatios Theocharis, Maria Delivoria-Papadopoulos
We have previously shown that cerebral Hypoxia-ischemia (HI) results in activation of Src kinase in the newborn piglet brain. We investigated the regulatory mechanism by which the pre-apoptotic proteins translocate from mitochondria to the cytosol during HI through the Src kinase. Newborn piglets were divided into 3 groups (n = 5/group): normoxic (Nx), HI and HI pre-treated with Src kinase inhibitor PP2 (PP2 + HI). Brain tissue HI was verified by neuropathological analysis and by Adenosine Triphosphate (ATP) and Phosphocreatine (PCr) levels...
November 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29186969/neuronal-and-astrocytic-involvement-in-striped-dolphins-stenella-coeruleoalba-with-morbilliviral-encephalitis
#10
R Lucá, R Giacominelli-Stuffler, S Mazzariol, S Roperto, C Cocumelli, G DI Guardo
Dolphin morbillivirus (DMV), a highly pathogenic agent, may cause peculiar, "brain-only" forms of infection (BOFDI), in which viral antigen and/or genome is found exclusively in the brain from striped dolphins (Stenella coeruleoalba). These BOFDIs show morphopathological similarities with subacute sclerosing panencephalitis and old dog encephalitis (ODE) in measles virus-infected patients and in canine distemper virus-infected dogs, respectively. The brain tissue from 3 BOFDI-affected striped dolphins was investigated by means of double labelling-indirect immunofluorescence (DL-IIF) and ultrastructurally, in order to characterize the DMV-targeted neuronal and non-neuronal cell populations, along with the associated submicroscopic findings...
2017: Acta Virologica
https://www.readbyqxmd.com/read/29183767/diabetes-induces-mitochondrial-dysfunction-and-alters-cholesterol-homeostasis-and-neurosteroidogenesis-in-the-rat-cerebral-cortex
#11
Simone Romano, Nico Mitro, Silvia Giatti, Silvia Diviccaro, Marzia Pesaresi, Roberto Spezzano, Matteo Audano, Luis Miguel Garcia-Segura, Donatella Caruso, Roberto Cosimo Melcangi
The nervous system synthesizes and metabolizes steroids (i.e., neurosteroidogenesis). Recent observations indicate that neurosteroidogenesis is affected by different nervous pathologies. Among these, long-term type 1 diabetes, together with other functional and biochemical changes, has been shown to alter neuroactive steroid levels in the nervous system. Using an experimental model of type 1 diabetes (i.e., streptozotocin injection) we here show that the levels of these molecules are already decreased in the rat cerebral cortex after one month of the initiation of the pathology...
November 25, 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/29177109/exome-sequencing-of-extended-families-with-alzheimer-s-disease-identifies-novel-genes-implicated-in-cell-immunity-and-neuronal-function
#12
H N Cukier, B K Kunkle, K L Hamilton, S Rolati, M A Kohli, P L Whitehead, J Jaworski, J M Vance, M L Cuccaro, R M Carney, J R Gilbert, L A Farrer, E R Martin, G W Beecham, J L Haines, M A Pericak-Vance
Objective: Alzheimer's disease (AD) is a neurodegenerative disorder for which more than 20 genetic loci have been implicated to date. However, studies demonstrate not all genetic factors have been identified. Therefore, in this study we seek to identify additional rare variants and novel genes potentially contributing to AD. Methods: Whole exome sequencing was performed on 23 multi-generational families with an average of eight affected subjects. Exome sequencing was filtered for rare, nonsynonymous and loss-of-function variants...
August 2017: Journal of Alzheimer's Disease and Parkinsonism
https://www.readbyqxmd.com/read/29168092/propofol-prevents-oxidative-stress-by-decreasing-the-ischemic-accumulation-of-succinate-in-focal-cerebral-ischemia-reperfusion-injury
#13
Wei Yu, Dapeng Gao, Wen Jin, Siliang Liu, Sihua Qi
Oxidative stress caused by mitochondrial dysfunction during reperfusion is a key pathogenic mechanism in cerebral ischemia-reperfusion (IR) injury. Propofol (2,6-diisopropylphenol) has been proven to attenuate mitochondrial dysfunction and reperfusion injury. The current study reveals that propofol decreases oxidative stress injury by preventing succinate accumulation in focal cerebral IR injury. We evaluated whether propofol could attenuate ischemic accumulation of succinate in transient middle cerebral artery occlusion in vivo...
November 22, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/29155300/mitochondrial-dysfunction-in-obesity
#14
REVIEW
Aline Haas de Mello, Ana Beatriz Costa, Jéssica Della Giustina Engel, Gislaine Tezza Rezin
Obesity leads to various changes in the body. Among them, the existing inflammatory process may lead to an increase in the production of reactive oxygen species (ROS) and cause oxidative stress. Oxidative stress, in turn, can trigger mitochondrial changes, which is called mitochondrial dysfunction. Moreover, excess nutrients supply (as it commonly is the case with obesity) can overwhelm the Krebs cycle and the mitochondrial respiratory chain, causing a mitochondrial dysfunction, and lead to a higher ROS formation...
November 16, 2017: Life Sciences
https://www.readbyqxmd.com/read/29151273/post-treatment-with-methylene-blue-is-effective-against-delayed-encephalopathy-after-acute-carbon-monoxide-poisoning
#15
Ningjun Zhao, Pengchong Liang, Xiaoying Zhuo, Chenglei Su, Xuemei Zong, Bingnan Guo, Han Dong, Xianliang Yan, Shuqun Hu, Quanguang Zhang, Xu Tie
Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) is the most severe and clinically intractable complication that occurs following acute carbon monoxide poisoning. Unfortunately, the mechanism of DEACMP is still vague. Growing evidence indicates that delayed cerebral damage following CO poisoning is related to oxidative stress, abnormal neuro-inflammation, apoptosis and immune-mediated injury. Our recent report indicated that methylene blue (MB) may be a promising therapeutic agent in the prevention of neuronal cell death and cognitive deficits following transient global cerebral ischaemia (GCI)...
November 19, 2017: Basic & Clinical Pharmacology & Toxicology
https://www.readbyqxmd.com/read/29146879/2-cl-mgv-1-ameliorates-apoptosis-in-the-thalamus-and-hippocampus-and-cognitive-deficits-after-cortical-infarct-in-rats
#16
Yicong Chen, Leo Veenman, Sukhdev Singh, Fubing Ouyang, Jiahui Liang, Weixian Huang, Ilan Marek, Jinsheng Zeng, Moshe Gavish
BACKGROUND AND PURPOSE: Focal cortical infarction causes neuronal apoptosis in the ipsilateral nonischemic thalamus and hippocampus, which is potentially associated with poststroke cognitive deficits. TSPO (translocator protein) is critical in regulating mitochondrial apoptosis pathways. We examined the effects of the novel TSPO ligand 2-(2-chlorophenyl) quinazolin-4-yl dimethylcarbamate (2-Cl-MGV-1) on poststroke cognitive deficits, neuronal mitochondrial apoptosis, and secondary damage in the ipsilateral thalamus and hippocampus after cortical infarction...
December 2017: Stroke; a Journal of Cerebral Circulation
https://www.readbyqxmd.com/read/29138968/mitochondrial-dysfunctions-contribute-to-energy-deficits-in-rodent-model-of-hepatic-encephalopathy
#17
Saurabh Dhanda, Aditya Sunkaria, Avishek Halder, Rajat Sandhir
Perturbations in the cerebral energy metabolism are anticipated to be an important factor by which ammonia may exert its toxic effects on the central nervous system. The present study was designed to investigate the role of impaired mitochondrial functions and cerebral energy metabolism in the development hepatic encephalopathy (HE) induced by of bile duct ligation (BDL). After four weeks of BDL, a significant increase in hepatic hydroxyproline and collagen content was observed which confirmed biliary fibrosis...
November 14, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/29131369/photobiomodulation-for-traumatic-brain-injury-and-stroke
#18
REVIEW
Michael R Hamblin
There is a notable lack of therapeutic alternatives for what is fast becoming a global epidemic of traumatic brain injury (TBI). Photobiomodulation (PBM) employs red or near-infrared (NIR) light (600-1100nm) to stimulate healing, protect tissue from dying, increase mitochondrial function, improve blood flow, and tissue oxygenation. PBM can also act to reduce swelling, increase antioxidants, decrease inflammation, protect against apoptosis, and modulate microglial activation state. All these mechanisms of action strongly suggest that PBM delivered to the head should be beneficial in cases of both acute and chronic TBI...
November 13, 2017: Journal of Neuroscience Research
https://www.readbyqxmd.com/read/29130578/sirt3-deregulation-is-linked-to-mitochondrial-dysfunction-in-alzheimer-s-disease
#19
Junghee Lee, Yunha Kim, Tian Liu, Yu Jin Hwang, Seung Jae Hyeon, Hyeonjoo Im, Kyungeun Lee, Victor E Alvarez, Ann C McKee, Soo-Jong Um, Manwook Hur, Inhee Mook-Jung, Neil W Kowall, Hoon Ryu
Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Sirtuins (SIRT, silent mating type information regulation 2 homolog in yeast) are NAD-dependent histone deacetylases involved in aging and longevity. The objective of this study was to investigate the relationship between SIRT3 and mitochondrial function and neuronal activity in AD...
November 11, 2017: Aging Cell
https://www.readbyqxmd.com/read/29129468/inhibition-of-rac1-ameliorates-neuronal-oxidative-stress-damage-via-reducing-bcl-2-rac1-complex-formation-in-mitochondria-through-pi3k-akt-mtor-pathway
#20
Yundan Pan, Na Wang, Pingping Xia, E Wang, Qulian Guo, Zhi Ye
Although the neuroprotective effects of Rac1 inhibition have been reported in various cerebral ischemic models, the molecular mechanisms of action have not yet been fully elucidated. In this study, we investigated whether the inhibition of Rac1 provided neuroprotection in a diabetic rat model of focal cerebral ischemia and hyperglycemia-exposed PC-12 cells. Intracerebroventricular administration of lentivirus expressing the Rac1 small hairpin RNA (shRNA) and specific Rac1 inhibitor NSC23766 not only decreased the infarct volumes and improved neurologic deficits with a correlated significant activation of mitochondrial DNA specific proteins, such as OGG1 and POLG, but also elevated Bcl-2 S70 phosphorylation in mitochondria...
November 10, 2017: Experimental Neurology
keyword
keyword
52589
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"