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Hypoxia-ischemia

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https://www.readbyqxmd.com/read/29781223/delayed-injury-of-hippocampal-interneurons-after-neonatal-hypoxia-ischemia-and-therapeutic-hypothermia-in-a-murine-model
#1
Raul Chavez-Valdez, Paul Emerson, Janasha Goffigan-Holmes, Alfredo Kirkwood, Lee J Martin, Frances J Northington
Delayed hippocampal injury and memory impairments follow neonatal hypoxia-ischemia (HI) despite the use of therapeutic hypothermia (TH). Death of hippocampal pyramidal cells occurs acutely after HI, but characterization of delayed cell death and injury of interneurons (INs) is unknown. We hypothesize that injury of INs after HI is: i) asynchronous to that of pyramidal cells, ii) independent of injury severity, and iii) unresponsive to TH. HI was induced in C57BL6 mice at p10 with unilateral right carotid ligation and 45 min of hypoxia (FiO2 =0...
May 21, 2018: Hippocampus
https://www.readbyqxmd.com/read/29772556/perinatal-brain-injury-mechanisms-and-therapeutic-approaches
#2
Joanne O Davidson, Justin M Dean, Mhoyra Fraser, Guido Wassink, Ted C Andelius, Simerdeep K Dhillon, Laura Bennet, Alistair Jan Gunn
Brain damage resulting from perinatal hypoxia-ischemia evolves slowly over time. While a small number of brain cells may die during a sufficiently profound period of hypoxia-ischemia, many will show initial recovery during a "latent" phase characterized by actively suppressed neural metabolism and activity. Critically, this transient recovery may be followed after ~6 hours by a phase of secondary deterioration, with delayed seizures, failure of mitochondrial function, cytotoxic edema, and bulk cell death over ~72 hours...
June 1, 2018: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/29769005/adenosine-synthetic-methods-of-its-derivatives-and-antitumor-activity
#3
Margarita Gutierrez, Francisco Valdes, Victor Luna, Barbara Arevalo, Nelson Brown
Since 1929, several researchers have conducted studies in relation the nucleoside of adenosine (1) mainly distribution identifying, characterizing their biological importance and synthetic chemistry to which this type of molecule has been subjected to obtain multiple of its derivatives. The receptors that interact with adenosine and its derivatives, called purinergic receptors, are classified as A1, A2A, A2B and A3. In the presence of agonists and antagonists, these receptors are involved in various physiological processes and diseases...
May 16, 2018: Mini Reviews in Medicinal Chemistry
https://www.readbyqxmd.com/read/29768254/neuroprotection-against-hypoxic-ischemic-injury-%C3%AE-opioid-receptors-and-bdnf-trkb-pathway
#4
Shiying Sheng, Jingzhong Huang, Yi Ren, Feng Zhi, Xuansong Tian, Guoqiang Wen, Guanghong Ding, Terry C Xia, Fei Hua, Ying Xia
The delta-opioid receptor (DOR) is one of three classic opioid receptors in the opioid system. It was traditionally thought to be primarily involved in modulating the transmission of messages along pain signaling pathway. Although there were scattered studies on its other neural functions, inconsistent results and contradicting conclusions were found in past literatures, especially in terms of DOR's role in a hypoxic/ischemic brain. Taking inspiration from the finding that the turtle brain exhibits a higher DOR density and greater tolerance to hypoxic/ischemic insult than the mammalian brain, we clarified DOR's specific role in the brain against hypoxic/ischemic injury and reconciled previous controversies in this aspect...
May 11, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29765933/a-pilot-study-of-inhaled-co-therapy-in-neonatal-hypoxia-ischemia-carboxyhemoglobin-concentrations-and-brain-volumes
#5
Martha Douglas-Escobar, Monique Mendes, Candace Rossignol, Nikolay Bliznyuk, Ariana Faraji, Abdullah S Ahmad, Sylvain Doré, Michael D Weiss
Objective: The objective of this pilot study was to start evaluating the efficacy and the safety (i.e., carboxyhemoglobin concentration of carbon monoxide (CO)) as a putative neuroprotective therapy in neonates. Study Design: Neonatal C57BL/6 mice were exposed to CO at a concentration of either 200 or 250 ppm for a period of 1 h. The pups were then sacrificed at 0, 10, 20, 60, 120, 180, and 240 min after exposure to either concentration of CO, and blood was collected for analysis of carboxyhemoglobin. Following the safety study, 7-day-old pups underwent a unilateral carotid ligation...
2018: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/29761012/an-overview-of-protective-strategies-against-ischemia-reperfusion-injury-the-role-of-hyperbaric-oxygen-preconditioning
#6
Ciprian Hentia, Alex Rizzato, Enrico Camporesi, Zhongjin Yang, Danina M Muntean, Dorel Săndesc, Gerardo Bosco
Introduction: Ischemia/reperfusion (I/R) injury, such as myocardial infarction, stroke, and peripheral vascular disease, has been recognized as the most frequent causes of devastating disorders and death currently. Protective effect of various preconditioning stimuli, including hyperbaric oxygen (HBO), has been proposed in the management of I/R. Methods: In this study, we searched and reviewed up-to-date published papers to explore the pathophysiology of I/R injury and to understand the mechanisms underlying the protective effect of HBO as conditioning strategy...
May 2018: Brain and Behavior
https://www.readbyqxmd.com/read/29760953/hyperglycemia-potentiates-a-shift-from-apoptosis-to-rip1-dependent-necroptosis
#7
William D McCaig, Payal S Patel, Sergey A Sosunov, Nicole L Shakerley, Tori A Smiraglia, Miranda M Craft, Katharine M Walker, Matthew A Deragon, Vadim S Ten, Timothy J LaRocca
Apoptosis and necroptosis are the primary modes of eukaryotic cell death, with apoptosis being non-inflammatory while necroptosis is highly inflammatory. We previously demonstrated that, once activated, necroptosis is enhanced by hyperglycemia in several cell types. Here, we determine if hyperglycemia affects apoptosis similarly. We show that hyperglycemia does not enhance extrinsic apoptosis but potentiates a shift to RIP1-dependent necroptosis. This is due to increased levels and activity of RIP1, RIP3, and MLKL, as well as decreased levels and activity of executioner caspases under hyperglycemic conditions following stimulation of apoptosis...
2018: Cell Death Discovery
https://www.readbyqxmd.com/read/29752344/mir-4463-inhibits-the-migration-of-human-aortic-smooth-muscle-cells-by-amot
#8
Xueqin Wang, Chao Du, Xuemei He, Xian Deng, Yanzheng He, Xiangyu Zhou
Aberrant vascular smooth muscle cell (VSMC) migration has been implicated in a variety of vascular disorders, while the signal pathways governing this process remain unclear. Here, we investigated whether microRNAs (miRNAs), which are strong posttranscriptional regulators of gene expression, could alter VSMC migration. We detected the expression of miR-4463 in the plasma of patients with atherosclerosis and in human aortic smooth muscle cells (HASMCs) under hypoxia-ischemia condition, and investigated the migration effect and its downstream pathways...
May 11, 2018: Bioscience Reports
https://www.readbyqxmd.com/read/29751053/l-cysteine-suppresses-hypoxia-ischemia-injury-in-neonatal-mice-by-reducing-glial-activation-promoting-autophagic-flux-and-mediating-synaptic-modification-via-h-2-s-formation
#9
Danqing Xin, Xili Chu, Xuemei Bai, Weiwei Ma, Hongtao Yuan, Jie Qiu, Changxing Liu, Tong Li, Xin Zhou, Wenqiang Chen, Dexiang Liu, Zhen Wang
We previously reported that L-Cysteine, an H2 S donor, significantly alleviated brain injury after hypoxia-ischemic (HI) injury in neonatal mice. However, the mechanisms underlying this neuroprotective effect of L-Cysteine against HI insult remain unknown. In the present study, we tested the hypothesis that the protective effects of L-Cysteine are associated with glial responses and autophagy, and L-Cysteine attenuates synaptic injury as well as behavioral deficits resulting from HI. Consistent with our previous findings, we found that treatment with L-Cysteine after HI reduced early brain injury, improved behavioral deficits and synaptic damage, effects which were associated with an up-regulation of synaptophysin and postsynaptic density protein 95 expression in the lesioned cortex...
May 8, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29747893/perinatal-brain-injury-mechanisms-prevention-and-outcomes
#10
REVIEW
Christopher M Novak, Maide Ozen, Irina Burd
Perinatal brain injury may lead to long-term morbidity and neurodevelopmental impairment. Improvements in perinatal care have resulted in the survival of more infants with perinatal brain injury. The effects of hypoxia-ischemia, inflammation, and infection during critical periods of development can lead to a common pathway of perinatal brain injury marked by neuronal excitotoxicity, cellular apoptosis, and microglial activation. Various interventions can prevent or improve the outcomes of different types of perinatal brain injury...
June 2018: Clinics in Perinatology
https://www.readbyqxmd.com/read/29740570/influence-of-sex-on-gestational-complications-fetal-to-neonatal-transition-and-postnatal-adaptation
#11
REVIEW
Sheila Lorente-Pozo, Anna Parra-Llorca, Begoña Torres, Isabel Torres-Cuevas, Antonio Nuñez-Ramiro, María Cernada, Ana García-Robles, Maximo Vento
Fetal sex is associated with striking differences during in utero development, fetal-to-neonatal transition, and postnatal morbidity and mortality. Male sex fetuses are apparently protected while in utero resulting in a higher secondary sex rate for males than for females. However, during fetal-to-neonatal transition and thereafter in the newborn period, female exhibits a greater degree of maturation that translates into a better capacity to stabilize, less incidence of prematurity and prematurity-associated morbidities, and better long-term outcomes...
2018: Frontiers in Pediatrics
https://www.readbyqxmd.com/read/29729731/an-amperometric-glutamate-biosensor-for-monitoring-glutamate-release-from-brain-nerve-terminals-and-in-blood-plasma
#12
T Borisova, D Kucherenko, O Soldatkin, I Kucherenko, A Pastukhov, A Nazarova, M Galkin, A Borysov, N Krisanova, A Soldatkin, A El Skaya
An excess of the excitatory neurotransmitter, glutamate, in the synaptic cleft during hypoxia/ischemia provokes development of neurotoxicity and originates from the reversal of Na+ -dependent glutamate transporters located in the plasma membrane of presynaptic brain nerve terminals. Here, we have optimized an electrochemical glutamate biosensor using glutamate oxidase and developed a biosensor-based methodological approach for analysis of rates of tonic, exocytotic and transporter-mediated glutamate release from isolated rat brain nerve terminals (synaptosomes)...
August 31, 2018: Analytica Chimica Acta
https://www.readbyqxmd.com/read/29725299/octadecylpropyl-sulfamide-reduces-neurodegeneration-and-restores-the-memory-deficits-induced-by-hypoxia-ischemia-in-mice
#13
Elk Kossatz, Daniel Silva-Peña, Juan Suárez, Fernando R de Fonseca, Rafael Maldonado, Patricia Robledo
The PPAR-α agonist, oleoylethanolamide (OEA) has neuroprotective properties in stroke models. However, its rapid degradation represents a limitation for an effective therapeutic approach. In this study, we evaluated the effects of a stable OEA-modeled compound, octadecylpropyl sulfamide (SUL) on the cognitive, behavioral, cellular and molecular alterations associated with hypoxia-ischemia (HI) in mice. Mice subjected to HI were treated with the PPAR-α antagonist GW6471 (GW) (1 mg/kg) followed 15 min later by SUL (3 and 10 mg/kg)...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29724989/role-of-hypoxia-inducible-factors-1%C3%AE-hif1%C3%AE-in-sh-sy5y-cell-autophagy-induced-by-oxygen-glucose-deprivation
#14
Guohui Niu, Dengna Zhu, Xiaoli Zhang, Jun Wang, Yunxia Zhao, Xin Wang
BACKGROUND HIF-1α plays an important role in hypoxia-ischemia brain damage. Accumulating evidences demonstrates that HIF-1α can contribute to cell autophagy. Oxygen-glucose deprivation (OGD) is a commonly used ischemic model in vitro. Our study was performed to investigate the influences of HIF-1α on autophagy in SH-SY5Y cells under OGD treatment. MATERIAL AND METHODS An OGD model was constructed in SH-SY5Y cells. PI method and MTT assay were used to test cell death and viability, respectively. Western blot assay was used to estimate the protein levels of HIF-1α and LC3...
May 4, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/29720941/neonatal-seizure-models-to-study-epileptogenesis
#15
REVIEW
Yuka Kasahara, Yuji Ikegaya, Ryuta Koyama
Current therapeutic strategies for epilepsy include anti-epileptic drugs and surgical treatments that are mainly focused on the suppression of existing seizures rather than the occurrence of the first spontaneous seizure. These symptomatic treatments help a certain proportion of patients, but these strategies are not intended to clarify the cellular and molecular mechanisms underlying the primary process of epilepsy development, i.e., epileptogenesis. Epileptogenic changes include reorganization of neural and glial circuits, resulting in the formation of an epileptogenic focus...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29718007/upregulation-of-cholesterol-24-hydroxylase-following-hypoxia-ischemia-in-neonatal-mouse-brain
#16
Fuxin Lu, Jun Zhu, Selena Guo, Brandon J Wong, Farid F Chehab, Donna M Ferriero, Xiangning Jiang
BackgroundMaintenance of cholesterol homeostasis is crucial for brain development. Brain cholesterol relies on de novo synthesis and is cleared primarily by conversion to 24S-hydroxycholesterol (24S-HC) with brain-specific cholesterol 24-hydroxylase (CYP46A1). We aimed to investigate the impact of hypoxia-ischemia (HI) on brain cholesterol metabolism in the neonatal mice.MethodsPostnatal day 9 C57BL/6 pups were subjected to HI using the Vannucci model. CYP46A1 expression was assessed with western blotting and its cellular localization was determined using immunofluorescence staining...
May 2, 2018: Pediatric Research
https://www.readbyqxmd.com/read/29713307/fetal-neuroprotection-by-magnesium-sulfate-from-translational-research-to-clinical-application
#17
REVIEW
Clément Chollat, Loïc Sentilhes, Stéphane Marret
Despite improvements in perinatal care, preterm birth still occurs regularly and the associated brain injury and adverse neurological outcomes remain a persistent challenge. Antenatal magnesium sulfate administration is an intervention with demonstrated neuroprotective effects for preterm births before 32 weeks of gestation (WG). Owing to its biological properties, including its action as an N -methyl-d-aspartate receptor blocker and its anti-inflammatory effects, magnesium is a good candidate for neuroprotection...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29706928/repetitive-neonatal-erythropoietin-and-melatonin-combinatorial-treatment-provides-sustained-repair-of-functional-deficits-in-a-rat-model-of-cerebral-palsy
#18
Lauren L Jantzie, Akosua Y Oppong, Fatu S Conteh, Tracylyn R Yellowhair, Joshua Kim, Gabrielle Fink, Adam R Wolin, Frances J Northington, Shenandoah Robinson
Cerebral palsy (CP) is the leading cause of motor impairment for children worldwide and results from perinatal brain injury (PBI). To test novel therapeutics to mitigate deficits from PBI, we developed a rat model of extreme preterm birth (<28 weeks of gestation) that mimics dual intrauterine injury from placental underperfusion and chorioamnionitis. We hypothesized that a sustained postnatal treatment regimen that combines the endogenous neuroreparative agents erythropoietin (EPO) and melatonin (MLT) would mitigate molecular, sensorimotor, and cognitive abnormalities in adults rats following prenatal injury...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29706927/tweak-receptor-deficiency-has-opposite-effects-on-female-and-male-mice-subjected-to-neonatal-hypoxia-ischemia
#19
Anton Kichev, Ana A Baburamani, Regina Vontell, Pierre Gressens, Linda Burkly, Claire Thornton, Henrik Hagberg
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine member of the TNF family. TWEAK binds to its only known receptor, Fn14, enabling it to activate downstream signaling processes in response to tissue injury. The aim of this study was to investigate the role of TWEAK signaling in neonatal hypoxia-ischemia (HI). We found that after neonatal HI, both TWEAK and Fn14 expression were increased to a greater extent in male compared with female mice. To assess the role of TWEAK signaling after HI, the size of the injury was measured in neonatal mice genetically deficient in Fn14 and compared with their wild-type and heterozygote littermates...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29701785/mitochondrial-adaptations-to-variable-environments-and-their-role-in-animals-stress-tolerance
#20
Inna Sokolova
Mitochondria are the key organelles involved in energy and redox homeostasis, cellular signaling and survival. Animal mitochondria are exquisitely sensitive to environmental stress, and stress-induced changes in the mitochondrial integrity and function have major consequences for the organismal performance and fitness. Studies in the model organisms such as terrestrial mammals and insects showed that mitochondrial dysfunction is a major cause of injury during pathological conditions and environmental insults such as hypoxia, ischemia-reperfusion and exposure to toxins...
April 26, 2018: Integrative and Comparative Biology
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