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https://www.readbyqxmd.com/read/28206988/inhibition-of-autophagy-blocks-cathepsins-tbid-mitochondrial-apoptotic-signaling-pathway-via-stabilization-of-lysosomal-membrane-in-ischemic-astrocytes
#1
Xian-Yong Zhou, Yu Luo, Yong-Ming Zhu, Zhi-He Liu, Thomas A Kent, Jia-Guo Rong, Wei Li, Shi-Gang Qiao, Min Li, Yong Ni, Kazumi Ishidoh, Hui-Ling Zhang
Our previous study and others have demonstrated that autophagy is activated in ischemic astrocytes and contributes to astrocytic cell death. However, the mechanisms of ischemia-induced autophagy remain largely unknown. In this study, we established a rat's model of permanent middle cerebral artery occlusion (pMCAO) and an in vitro oxygen and glucose deprivation (OGD) model. Autophagy was inhibited by either pharmacological treatment with 3-methyladenine (3-MA) and wortmannin (Wort) or genetic treatment with knockdown of Atg5 in primary cultured astrocytes and knockout of Atg5 in mouse embryonic fibroblast (MEF) cells, respectively...
February 16, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28202127/-role-of-mitophagy-in-neonatal-rats-with-hypoxic-ischemic-brain-damage
#2
Ming-Xi Li, Yi Qu, De-Zhi Mu
OBJECTIVE: To investigate mitophagy in an animal model of hypoxic-ischemic brain damage (HIBD) and its role in HIBD. METHODS: A total of 120 neonatal Sprague-Dawley rats aged 7 days were divided into three groups: sham-operation, HIBD, and autophagy inhibitor intervention (3MA group). The rats in the HIBD group were treated with right common carotid artery ligation and then put in a hypoxic chamber (8% oxygen and 92% nitrogen) for 2.5 hours. Those in the 3MA group were given ligation and hypoxic treatment at 30 minutes after intraperitoneal injection of 2 μL 3MA...
February 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28186868/effects-of-near-infrared-light-on-cerebral-bioenergetics-measured-with-phosphorus-magnetic-resonance-spectroscopy
#3
Dionyssios Mintzopoulos, Timothy E Gillis, Clark E Tedford, Marc J Kaufman
OBJECTIVE: Cerebral photobiomodulation (PBM) improves mood and cognition. Cerebral metabolic enhancement is a mechanism proposed to underlie PBM effects. No PBM studies to date have applied phosphorus magnetic resonance spectroscopy ((31)P MRS), which can be used to assess metabolic intermediates such as phosphocreatine (PCr) and adenosine triphosphate, the latter of which is elevated by PBM. Accordingly, we used 9.4 Tesla (31)P MRS to characterize effects of single and repeat cerebral PBM treatments on metabolism...
February 9, 2017: Photomedicine and Laser Surgery
https://www.readbyqxmd.com/read/28178891/up-regulation-of-cerebral-cytochrome-c-oxidase-and-hemodynamics-by-transcranial-infrared-laser-stimulation-a-broadband-near-infrared-spectroscopy-study
#4
Xinlong Wang, Fenghua Tian, Divya D Reddy, Sahil S Nalawade, Douglas W Barrett, Francisco Gonzalez-Lima, Hanli Liu
Transcranial infrared laser stimulation (TILS) is a noninvasive form of brain photobiomulation. Cytochrome-c-oxidase (CCO), the terminal enzyme in the mitochondrial electron transport chain, is hypothesized to be the primary intracellular photoacceptor. We hypothesized that TILS up-regulates cerebral CCO and causes hemodynamic changes. We delivered 1064-nm laser stimulation to the forehead of healthy participants ( n = 11), while broadband near-infrared spectroscopy was utilized to acquire light reflectance from the TILS-treated cortical region before, during, and after TILS...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28177040/clinical-pathological-and-molecular-evaluations-and-ct-scan-screening-of-coenurosis-coenurus-cerebralis-in-sheep-and-calves
#5
Abdullah Gazioglu, Sami Simsek, Omer Kizil, Ali Osman Ceribasi, Harun Kaya Kesik, Haroon Ahmed
The aims of this study were to diagnose coenurosis by means of computerized tomography (CT) scan imaging and molecular characterization of the CO1 gene using the polymerase chain reaction (PCR). Sheep and calves were necropsied, and CT scans on the cephalic region were performed on the animals. Sections of brain tissue infected with parasites were then stained with hematoxylin and eosin for microscopic examination. Material collected from brain cysts was fixed in 70% ethanol. PCR amplification was carried out using the CO1 mitochondrial gene...
February 6, 2017: Revista Brasileira de Parasitologia Veterinária, Brazilian Journal of Veterinary Parasitology
https://www.readbyqxmd.com/read/28176051/piracetam-attenuates-lps-induced-neuroinflammation-and-cognitive-impairment-in-rats
#6
Alok Tripathi, Pankaj Paliwal, Sairam Krishnamurthy
The present study was performed to investigate the effect of piracetam on neuroinflammation induced by lipopolysaccharide (LPS) and resulting changes in cognitive behavior. Neuroinflammation was induced by a single dose of LPS solution infused into each of the lateral cerebral ventricles in concentrations of 1 μg/μl, at a rate of 1 μl/min over a 5-min period, with a 5-min waiting period between the two infusions. Piracetam in doses of 50, 100, and 200 mg/kg i.p. was administered 30 min before LPS infusion and continued for 9 days...
February 7, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28150130/three-year-follow-up-of-high-dose-ubiquinol-supplementation-in-a-case-of-familial-multiple-system-atrophy-with-compound-heterozygous-coq2-mutations
#7
Jun Mitsui, Ken Koguchi, Toshimitsu Momose, Miwako Takahashi, Takashi Matsukawa, Tsutomu Yasuda, Shin-Ichi Tokushige, Hiroyuki Ishiura, Jun Goto, Shigeaki Nakazaki, Tomoyoshi Kondo, Hidefumi Ito, Yorihiro Yamamoto, Shoji Tsuji
We report a 3-year follow-up of high-dose ubiquinol supplementation in a case of familial multiple system atrophy (MSA) with compound heterozygous nonsense (R387X) and missense (V393A) mutations in COQ2. A high-dose ubiquinol supplementation substantially increased total coenzyme Q10 levels in cerebrospinal fluid as well as in plasma. The patient was at the advanced stage of MSA, and the various scores of clinical rating scales remained stable without changes during the 3 years. The cerebral metabolic ratio of oxygen measured by (15)O2 PET, however, increased by approximately 30% after administration of ubiquinol, suggesting that ubiquinol can improve mitochondrial oxidative metabolism in the brain...
February 1, 2017: Cerebellum
https://www.readbyqxmd.com/read/28149158/effect-of-propofol-on-mitochondrial-atp-content-and-atpase-activity-in-hippocampus-of-rats-with-cerebral-ischemia-reperfusion-injury
#8
Dan-Juan Yu, Hui-Yang Gao
OBJECTIVE: Study on the influence of the cerebral Ischemia-reperfusion Injury (IRI) on mitochondrial adenosine triphosphate (ATP) content and ATPase activity in hippocampus of rats, as well as the protective effect of propofol on IRI in rats. METHODS: A total of 40 male SD rats were randomly divided into 5 groups: sham operation group (Group A), ischemia reperfusion control group (Group B) and ischemic reperfusion with propofol pretreatment group (C group). Group C was further divided into three sub groups according to the different doses of propofol: Group C1 (50 mg/kg), Group C2 (100 mg/kg) and Group C3 (150 mg/kg)...
February 2017: Saudi Journal of Biological Sciences
https://www.readbyqxmd.com/read/28144826/neuroprotective-effects-and-mechanisms-of-action-of-multifunctional-agents-targeting-free-radicals-monoamine-oxidase-b-and-cholinesterase-in-parkinson-s-disease-model
#9
Zheng Liu, Wei Cai, Ming Lang, Ruizuo Yan, Zhenshen Li, Gaoxiao Zhang, Pei Yu, Yuqiang Wang, Yewei Sun, Zaijun Zhang
Parkinson's disease (PD) is a complex neurodegenerative disorder with multifactorial pathologies, including progressive loss of dopaminergic (DA) neurons, oxidative stress, mitochondrial dysfunction, and increased monoamine oxidase (MAO) enzyme activity. There are currently only a few agents approved to ameliorate the symptoms of PD; however, no agent is able to reverse the progression of the disease. Due to the multifactorial pathologies, it is necessary to develop multifunctional agents that can affect more than one target involved in the disease pathology...
January 31, 2017: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/28142208/intravenously-transplanted-human-bone-marrow-endothelial-progenitor-cells-engraft-within-brain-capillaries-preserve-mitochondrial-morphology-and-display-pinocytotic-activity-towards-bbb-repair-in-ischemic-stroke-rats
#10
Svitlana Garbuzova-Davis, Edward Haller, Roger Lin, Cesario V Borlongan
Stroke is a life threatening disease with limited therapeutic options. Cell therapy has emerged as an experimental stroke treatment. Blood-brain barrier (BBB) impairment is a key pathological manifestation of ischemic stroke, and barrier repair is an innovative target for neurorestoration in stroke. Here, we evaluated via electron microscopy the ability of transplanted human bone marrow endothelial progenitor cells (hBMEPCs) to repair the BBB in adult Sprague-Dawley rats subjected to transient middle cerebral artery occlusion (tMCAO)...
January 31, 2017: Stem Cells
https://www.readbyqxmd.com/read/28134843/role-of-antioxidants-in-neonatal-hypoxic-ischemic-brain-injury-new-therapeutic-approaches
#11
REVIEW
Olatz Arteaga, Antonia Álvarez, Miren Revuelta, Francisco Santaolalla, Andoni Urtasun, Enrique Hilario
Hypoxic-ischemic brain damage is an alarming health and economic problem in spite of the advances in neonatal care. It can cause mortality or detrimental neurological disorders such as cerebral palsy, motor impairment and cognitive deficits in neonates. When hypoxia-ischemia occurs, a multi-faceted cascade of events starts out, which can eventually cause cell death. Lower levels of oxygen due to reduced blood supply increase the production of reactive oxygen species, which leads to oxidative stress, a higher concentration of free cytosolic calcium and impaired mitochondrial function, triggering the activation of apoptotic pathways, DNA fragmentation and cell death...
January 28, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28130053/vascular-protective-effects-of-klf2-on-a%C3%AE-induced-toxicity-implications-for-alzheimer-s-disease
#12
Xuejun Fang, Xiaoli Zhong, Gang Yu, Si Shao, Qidong Yang
Alzheimer's disease (AD) is characterized by excessive amounts of senile plaques and neurofibrillary tangles in the brain, and cerebrovascular pathologies in AD are attracting increasingly more attention. Krüppel-like factor (KLF) 2, a transcription regulator expressed in the mouse embryonic vasculature and involved in the regulation of vascular gene expression, serves as a protective factor in endothelial cells. However, whether KLF2 is involved in neurodegenerative disease, and especially in AD, remains unknown...
January 24, 2017: Brain Research
https://www.readbyqxmd.com/read/28129719/differences-in-reperfusion-induced-mitochondrial-oxidative-stress-and-cell-death-between-hippocampal-ca1-and-ca3-subfields-is-due-to-the-mitochondrial-thioredoxin-system
#13
Bocheng Yin, German Barrionuevo, Ines Batinic-Haberle, Mats Sandberg, Stephen Weber
AIMS: The susceptibility of CA1 over CA3 to damage from cerebral ischemia may be related to the differences in reactive oxygen species (ROS) production/removal between the two hippocampal subfields. We aimed to measure CA1/CA3 differences in net ROS production in real time in the first thirty minutes of reperfusion in pyramidal cells. We aimed to determine the underlying cause of the differential vulnerability of CA1 and CA3. RESULTS: Real-time determinations of mitochondrial H2O2 and, independently, glutathione (GSH) redox status from roGFP-based probes in individual pyramidal cells in organotypic hippocampal cultures during oxygen-glucose deprivation (OGD)-reperfusion (RP) demonstrate a significantly more oxidizing environment during reperfusion in CA1 than CA3 mitochondria...
January 27, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28125731/correlated-5-hydroxymethylcytosine-5hmc-and-gene-expression-profiles-underpin-gene-and-organ-specific-epigenetic-regulation-in-adult-mouse-brain-and-liver
#14
I-Hsuan Lin, Yi-Fan Chen, Ming-Ta Hsu
BACKGROUND: DNA methylation is an epigenetic mechanism essential for gene regulation and vital for mammalian development. 5-hydroxymethylcytosine (5hmC) is the first oxidative product of the TET-mediated 5-methylcytosine (5mC) demethylation pathway. Aside from being a key intermediate in cytosine demethylation, 5hmC may have potential regulatory functions with emerging importance in mammalian biology. METHODS: Here, we investigate the global 5hmC enrichment in five brain structures, including cerebellum, cerebral cortex, hippocampus, hypothalamus and thalamus, as well as liver tissues from female and male adult mice by using chemical capture-based technique coupled with next-generation sequencing...
2017: PloS One
https://www.readbyqxmd.com/read/28112032/spermidine-preconditioning-ameliorates-laurate-induced-brain-injury-by-maintaining-mitochondrial-stability
#15
Yi Zhang, Jie Yin, Lang Zhang, Chu-Chu Qi, Ze-Lin Ma, Li-Ping Gao, De-Gui Wang, Yu-Hong Jing
Ischemic precondition plays a protective effect during cerebral ischemia. This effect partly depends on the autophagic activity. However, whether the activity of autophagy can exert the protective effects after cerebral ischemia is unclear. In this study, rats were treated with spermidine, an activator of autophagy, and injected with sodium laurate via the internal carotid artery to stimulate cerebral small vessel disease (CSVD). The effects of the spermidine precondition on brain injury were evaluated by behavioural test, histology assay, ultrastructure observation, and autophagic-related signals...
March 2017: Neurological Research
https://www.readbyqxmd.com/read/28110213/cannabidiol-attenuates-ogd-r-induced-damage-by-enhancing-mitochondrial-bioenergetics-and-modulating-glucose-metabolism-via-pentose-phosphate-pathway-in-hippocampal-neurons
#16
Shanshan Sun, Fangyuan Hu, Jihong Wu, Shenghai Zhang
Deficient bioenergetics and diminished redox conservation have been implicated in the development of cerebral ischemia/reperfusion injury. In this study, the mechanisms underlying the neuroprotective effects of cannabidiol (CBD), a nonpsychotropic compound derived from Cannabis sativa with FDA-approved antiepilepsy properties, were studied in vitro using an oxygen-glucose-deprivation/reperfusion (OGD/R) model in a mouse hippocampal neuronal cell line. CBD supplementation during reperfusion rescued OGD/R-induced cell death, attenuated intracellular ROS generation and lipid peroxidation, and simultaneously reversed the abnormal changes in antioxidant biomarkers...
December 31, 2016: Redox Biology
https://www.readbyqxmd.com/read/28101749/twenty-seven-years-of-cerebral-pyruvate-recycling
#17
Sebastián Cerdán
Cerebral pyruvate recycling is a metabolic pathway deriving carbon skeletons and reducing equivalents from mitochondrial oxaloacetate and malate, to the synthesis of mitochondrial and cytosolic pyruvate, lactate and alanine. The pathway allows both, to provide the tricarboxylic acid cycle with pyruvate molecules produced from alternative substrates to glucose and, to generate reducing equivalents necessary for the operation of NADPH requiring processes. At the cellular level, pyruvate recycling involves the activity of malic enzyme, or the combined activities of phosphoenolpyruvate carboxykinase and pyruvate kinase, as well as of those transporters of the inner mitochondrial membrane exchanging the corresponding intermediates...
January 18, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28100843/pathophysiology-and-molecular-basis-of-selected-metabolic-abnormalities-in-huntington-s-disease
#18
Jolanta Krzysztoń-Russjan
Huntington's disease (HD) is an incurable, devastating neurodegenerative disease with a known genetic background and autosomally dominant inheritance pattern. HTT gene mutation (mHTT) is associated with polymorphic fragment elongation above 35 repeats of the CAG triplet. The mHTT product is an altered protein with a poly-Q elongated fragment, with the highest expression determined in the central nervous system (CNS) and with differentiated expression outside the CNS. A drastic loss of striatal and deeper layers of the cerebral cortex neurons was determined in the CNS, but muscle and body weight mass loss with dysfunction of many organs was also observed...
December 30, 2016: Postȩpy Higieny i Medycyny Doświadczalnej
https://www.readbyqxmd.com/read/28095372/impaired-mitochondrial-respiration-in-large-cerebral-arteries-of-rats-with-type-2-diabetes
#19
Ivan Merdzo, Ibolya Rutkai, Venkata N L R Sure, Catherine A McNulty, Prasad V G Katakam, David W Busija
Mitochondrial dysfunction has been suggested as a potential underlying cause of pathological conditions associated with type 2 diabetes (T2DM). We have previously shown that mitochondrial respiration and mitochondrial protein levels were similar in the large cerebral arteries of insulin-resistant Zucker obese rats and their lean controls. In this study, we extend our investigations into the mitochondrial dynamics of the cerebral vasculature of 14-week-old Zucker diabetic fatty obese (ZDFO) rats with early T2DM...
January 18, 2017: Journal of Vascular Research
https://www.readbyqxmd.com/read/28091829/inhibition-of-dpp-4-activity-and-neuronal-atrophy-with-genistein-attenuates-neurological-deficits-induced-by-transient-global-cerebral-ischemia-and-reperfusion-in-streptozotocin-induced-diabetic-mice
#20
Mithun Singh Rajput, Purnima Dey Sarkar, Nilesh Prakash Nirmal
Genistein, an isoflavonoid phytoestrogen, has been known for its potential pharmacological properties especially for neuroprotection and treating diabetes. The present study aims to determine the neuroprotective efficacy of genistein against global cerebral ischemia-reperfusion-induced neuronal injury in streptozotocin-induced diabetic mice and explore the underlying mechanisms. Streptozotocin-induced diabetic mice were subjected to transient cerebral ischemia by occluding both common carotid arteries for 30 min followed by 24 h reperfusion to induce neuronal injury...
January 16, 2017: Inflammation
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