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Hypoxia-ischemia

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https://www.readbyqxmd.com/read/28548285/neonatal-hypoxia-ischemia-in-rat-increases-doublecortin-concentration-in-the-cerebrospinal-fluid
#1
Catherine Brégère, Urs Fisch, Martin H Sailer, Wolfgang S Lieb, Laurie Chicha, Fabienne Goepfert, Thomas Kremer, Raphael Guzman
Doublecortin (DCX) is a microtubule-associated protein widely used as an indicator of neurogenesis in immunohistochemical analyses of the postmortem adult brain. A recent study reported that DCX can be quantified in the cerebrospinal fluid (CSF) from healthy rats between postnatal day 0 (P0) and P30. However, it is currently unclear whether the concentration of DCX in the CSF (CSF-DCX) may represent a measure of endogenous neurogenesis. To address this question, the present study examined the impact of a neonatal hypoxic-ischemic (HI) brain injury, known to induce neurogenesis, on CSF-DCX...
May 26, 2017: European Journal of Neuroscience
https://www.readbyqxmd.com/read/28527815/neuroimaging-and-neuropathological-characteristics-of-cerebellar-injury-in-extremely-low-birth-weight-infants
#2
Mayumi Matsufuji, Nozomi Sano, Hisashi Tsuru, Sachio Takashima
OBJECTIVE: To determine the morphological characteristics and pathogenic factors of cerebellar injury in extremely low birth weight infants (ELBWI). SUBJECTS AND METHODS: Neuroimaging examination was performed on 17 eligible surviving ELBWI. Their MR images were assessed and classified its pattern of cerebellar injuries. Brain pathology was examined on 15 patients, who isolated this neuroimaging subjects. The trend of brain pathologies was revealed. RESULTS: Four types of morphological pattern were recognized: (i) the absence of major portions in the cerebellum (6/17 cases); (ii) focal cerebellar tissue loss (2/17); (iii) unilateral cerebellar atrophy/hypoplasia (3/17); (iv) small cerebellum with entrapped fourth ventricle (6/17)...
May 17, 2017: Brain & Development
https://www.readbyqxmd.com/read/28523564/prenatal-and-early-postnatal-environmental-enrichment-reduce-acute-cell-death-and-prevent-neurodevelopment-and-memory-impairments-in-rats-submitted-to-neonatal-hypoxia-ischemia
#3
L E Durán-Carabali, D M Arcego, F K Odorcyk, L Reichert, J L Cordeiro, E F Sanches, L D Freitas, C Dalmaz, A Pagnussat, C A Netto
Environmental enrichment (EE) is an experimental strategy to attenuate the negative effects of different neurological conditions including neonatal hypoxia ischemia encephalopathy (HIE). The aim of the present study was to investigate the influence of prenatal and early postnatal EE in animals submitted to neonatal HIE model at postnatal day (PND) 3. Wistar rats were housed in EE or standard conditions (SC) during pregnancy and lactation periods. Pups of both sexes were assigned to one of four experimental groups, considering the early environmental conditions and the injury: SC-Sham, SC-HIE, EE-sham, and EE-HIE...
May 18, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28512386/oxidative-stress-biomarkers-establishment-of-reference-values-for-isoprostanes-aopp-and-npbi-in-cord-blood
#4
Mariangela Longini, Elisa Belvisi, Fabrizio Proietti, Francesco Bazzini, Giuseppe Buonocore, Serafina Perrone
Oxidative stress (OS) is a common pathogenic factor involved in the onset of several diseases in humans, from immunologic disorders to malignancy, being a serious public health problem. In perinatal period, OS has been associated with adverse outcome of pregnancy and neonatal diseases. Dangerous effects of OS are mediated by increased production of free radicals (FRs) following various mechanisms, such as hypoxia, ischemia reperfusion, hyperoxia, inflammation, mitochondrial dysfunction, Fenton chemistry, and prostaglandin metabolism...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/28508995/l-carnitine-and-acetyl-l-carnitine-roles-and-neuroprotection-in-developing-brain
#5
Gustavo C Ferreira, Mary C McKenna
L-Carnitine functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation. Treatment with L-carnitine can ameliorate metabolic imbalances in many inborn errors of metabolism. In recent years there has been considerable interest in the therapeutic potential of L-carnitine and its acetylated derivative acetyl-L-carnitine (ALCAR) for neuroprotection in a number of disorders including hypoxia-ischemia, traumatic brain injury, Alzheimer's disease and in conditions leading to central or peripheral nervous system injury...
May 16, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28502584/up-regulation-of-mir-325-3p-suppresses-pineal-aralkylamine-n-acetyltransferase-aanat-after-neonatal-hypoxia-ischemia-brain-injury-in-rats
#6
Yuanyuan Yang, Bin Sun, Jian Huang, Lixiao Xu, Jian Pan, Chen Fang, Mei Li, Gen Li, Yanfang Tao, Xiaofeng Yang, Ying Wu, Po Miao, Ying Wang, Hong Li, Jing Ren, Meiqin Zhan, Yiping Fang, Xing Feng, Xin Ding
Survivors of hypoxic-ischemic brain damage (HIBD), besides impairment of psychomotor development, often develop circadian rhythm disorders, although the underlying mechanisms are largely unknown. Here, we first verified that mRNA and protein expression of pineal aralkylamine N-acetyltransferase (Aanat), a key regulator for melatonin (MT) synthesis, along with MT, were severely impaired after HIBD. In addition, we demonstrated that neonatal HIBD disrupted the circadian rhythmicity of locomotor activities in juvenile rats...
May 11, 2017: Brain Research
https://www.readbyqxmd.com/read/28499802/ampk-activates-foxo3a-and-promotes-neuronal-apoptosis-in-the-developing-rat-brain-during-the-early-phase-after-hypoxia-ischemia
#7
Deyuan Li, Lili Luo, Min Xu, Jinlin Wu, Lina Chen, Jinhui Li, Zhongqiang Liu, Guoyan Lu, Yang Wang, Lina Qiao
AMP-activated protein kinase (AMPK) is a key metabolic and stress sensor/effector. Few investigations have been performed to study the role of AMPK in developing rat brain with hypoxia-ischemia (HI). Forkhead transcriptional factor (FOXO3a) has been revealed to be a critical effector of AMPK-mediated celluar apoptosis. However, it is not clear whether AMPK/FOXO3a pathway is involved in neuronal apoptosis in the developing rat brain after HI. In this study, we generated hypoxia-ischemia brain damage (HIBD) model using postnatal day 7 rats...
May 10, 2017: Brain Research Bulletin
https://www.readbyqxmd.com/read/28495306/long-term-effects-of-enriched-environment-following-neonatal-hypoxia-ischemia-on-behavior-bdnf-and-synaptophysin-levels-in-rat-hippocampus-effect-of-combined-treatment-with-g-csf
#8
Myrsini Griva, Rosa Lagoudaki, Olga Touloumi, Evangelia Nousiopoulou, Filippos Karalis, Thomas Georgiou, Georgia Kokaraki, Constantina Simeonidou, Despina A Tata, Evangelia Spandou
Increasing evidence shows that exposure to an enriched environment (EE) is neuroprotective in adult and neonatal animal models of brain ischemia. However, the mechanisms underlying this effect remain unclear. The aim of the current study was to investigate whether post-weaning EE would be effective in preventing functional deficits and brain damage by affecting markers of synaptic plasticity in a neonatal rat model of hypoxia-ischemia (HI). We also examined the possibility that granulocyte-colony stimulating factor (G-CSF), a growth factor with known neuroprotective effects in a variety of experimental brain injury models, combined with EE stimulation could enhance the potential beneficial effect of EE...
May 8, 2017: Brain Research
https://www.readbyqxmd.com/read/28492551/haploinsufficiency-in-the-mitochondrial-protein-chchd4-reduces-brain-injury-in-a-mouse-model-of-neonatal-hypoxia-ischemia
#9
Yanyan Sun, Tao Li, Cuicui Xie, Yiran Xu, Kai Zhou, Juan Rodriguez, Wei Han, Xiaoyang Wang, Guido Kroemer, Nazanine Modjtahedi, Klas Blomgren, Changlian Zhu
Mitochondria contribute to neonatal hypoxic-ischemic brain injury by releasing potentially toxic proteins into the cytosol. CHCHD4 is a mitochondrial intermembrane space protein that plays a major role in the import of intermembrane proteins and physically interacts with apoptosis-inducing factor (AIF). The purpose of this study was to investigate the impact of CHCHD4 haploinsufficiency on mitochondrial function and brain injury after cerebral hypoxia-ischemia (HI) in neonatal mice. CHCHD4(+/-) and wild-type littermate mouse pups were subjected to unilateral cerebral HI on postnatal day 9...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28487967/comparative-analysis-of-the-beneficial-effects-of-treadmill-training-and-electroacupuncture-in-a-rat-model-of-neonatal-hypoxia-ischemia
#10
Ha Neui Kim, Malk Eun Pak, Myung Jun Shin, Soo Yeon Kim, Yong Beom Shin, Young Ju Yun, Hwa Kyoung Shin, Byung Tae Choi
In the present study, we investigated whether treadmill training and electroacupuncture (EA) have autonomous or synergistic beneficial effects on deficits caused by neonatal hypoxia‑ischemia in Sprague-Dawley rats. For this purpose, rats subjected to hypoxia-ischemia underwent treadmill training and EA stimulation from 4 to 8 weeks of age. Conventional EA (CEA) and scalp EA (SEA) were delivered by electrical stimulation (2 Hz, 1 mA) at traditional acupoints and at the scalp to the primary motor area, respectively...
June 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28487658/early-changes-in-glutamate-metabolism-and-perfusion-in-basal-ganglia-following-hypoxia-ischemia-in-neonatal-piglets-a-multi-sequence-3-0t-mr-study
#11
Yu-Xue Dang, Kai-Ning Shi, Xiao-Ming Wang
The excitotoxicity of glutamate metabolism as well as hemodynamic disorders of the brain are both risk factors for neonatal hypoxic-ischemic brain damage (HIBD). In the present study, changes in glutamate metabolism in the basal ganglia were detected by proton magnetic resonance spectroscopy ((1)H-MRS) at 0-6, 8-12, 24-30, and 48-60 h after the induction of hypoxia-ischemia (HI) in newborn piglets. Meanwhile, correlation analysis was performed by combining the microcirculatory perfusion informations acquired by intravoxel incoherent motion (IVIM) scan to explore their possible interaction mechanism...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28469656/neuroprotective-effects-of-autophagy-inhibition-on-hippocampal-glutamate-receptor-subunits-after-hypoxia-ischemia-induced-brain-damage-in-newborn-rats
#12
Li-Xiao Xu, Xiao-Juan Tang, Yuan-Yuan Yang, Mei Li, Mei-Fang Jin, Po Miao, Xin Ding, Ying Wang, Yan-Hong Li, Bin Sun, Xing Feng
Autophagy has been suggested to participate in the pathology of hypoxic-ischemic brain damage (HIBD). However, its regulatory role in HIBD remains unclear and was thus examined here using a rat model. To induce HIBD, the left common carotid artery was ligated in neonatal rats, and the rats were subjected to hypoxia for 2 hours. Some of these rats were intraperitoneally pretreated with the autophagy inhibitor 3-methyladenine (10 mM in 10 μL) or the autophagy stimulator rapamycin (1 g/kg) 1 hour before artery ligation...
March 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28448965/neuroprotective-treatments-after-perinatal-hypoxic-ischemic-brain-injury-evaluated-with-magnetic-resonance-spectroscopy
#13
Hester Rijkje Berger, Eva Brekke, Marius Widerøe, Tora Sund Morken
Perinatal hypoxic-ischemic brain injury is a major health problem. Adjuvant treatments that improve the neuroprotective effect of the current treatment, therapeutic hypothermia, are urgently needed. The growing knowledge about the complex pathophysiology of hypoxia-ischemia (HI) has led to the discovery of several important targets for neuroprotection. Early interventions should focus on the preservation of energy metabolism, the reduction of glutamate excitotoxicity and oxidative stress, the maintenance of calcium homeostasis, and the prevention of apoptosis...
April 28, 2017: Developmental Neuroscience
https://www.readbyqxmd.com/read/28445874/erythropoietin-treatment-exacerbates-moderate-injury-after-hypoxia-ischemia-in-neonatal-superoxide-dismutase-transgenic-mice
#14
R Ann Sheldon, Christine Windsor, Byong Sop Lee, Olatz Arteaga Cabeza, Donna M Ferriero
The neonatal brain is highly susceptible to oxidative stress as developing endogenous antioxidant mechanisms are overwhelmed. In the neonate, superoxide dismutase (SOD) overexpression worsens hypoxic-ischemic injury due to H2O2 accumulation in the brain. Erythropoietin (EPO) is upregulated in 2 phases after HI, early (4 h) and late (7 days), and exogenous EPO has been effective in reducing the injury, possibly through reducing oxidative stress. We hypothesized that exogenous EPO would limit injury from excess H2O2 seen in SOD1-overexpressing mice, and thus enhance recovery after HI...
April 27, 2017: Developmental Neuroscience
https://www.readbyqxmd.com/read/28442737/structural-and-biochemical-insights-of-cypa-and-aif-interaction
#15
Biancamaria Farina, Gianluigi Di Sorbo, Angela Chambery, Andrea Caporale, Guido Leoni, Rosita Russo, Fabiola Mascanzoni, Domenico Raimondo, Roberto Fattorusso, Menotti Ruvo, Nunzianna Doti
The Cyclophilin A (CypA)/Apoptosis Inducing Factor (AIF) complex is implicated in the DNA degradation in response to various cellular stress conditions, such as oxidative stress, cerebral hypoxia-ischemia and traumatic brain injury. The pro-apoptotic form of AIF (AIF(Δ1-121)) mainly interacts with CypA through the amino acid region 370-394. The AIF(370-394) synthetic peptide inhibits complex formation in vitro by binding to CypA and exerts neuroprotection in a model of glutamate-mediated oxidative stress. Here, the binding site of AIF(Δ1-121) and AIF(370-394) on CypA has been mapped by NMR spectroscopy and biochemical studies, and a molecular model of the complex has been proposed...
April 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28435981/-iron-metabolism-and-neonatal-hypoxic-ischemic-brain-damage
#16
Kai-Yu Xu, Fan Li
Iron is an essential element for nervous system development, and maintaining a normal iron level in nervous system is controlled by multiple factors. Recent studies reported that iron dysregulation and the following iron metabolic pathways played an important role in hypoxic ischemic brain damage (HIBD) in neonates. Circulatory iron level is altered after hypoxia-ischemia exposure, which may cause abnormal iron deposition in the nervous system followed by neuronal injury. Finding the causing factors for abnormal iron metabolism after hypoxia-ischemia exposure, as well as understanding the mechanisms how iron metabolism contributes to HIBD, will shed lights on HIBD prevention and treatment...
April 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/28434006/unbiased-quantification-of-subplate-neuron-loss-following-neonatal-hypoxia-ischemia-in-a-rat-model
#17
Alexandra Mikhailova, Naveena Sunkara, Patrick S McQuillen
BACKGROUND: Cellular targets of neonatal hypoxia-ischemia (HI) include both oligodendrocyte and neuronal lineages with differences in the patterns of vulnerable cells depending upon the developmental stage at which the injury occurs. Injury to the developing white matter is a characteristic feature of human preterm brain injury. Data are accumulating, however, for neuronal injury in the developing cerebral cortex. In the most widely used rodent model of preterm HI brain injury, conflicting data have been reported regarding the sensitivity of subplate neurons to early neonatal HI, with some reports of selective vulnerability and others that find no increased loss of subplate neurons in comparison with other cortical layers...
April 22, 2017: Developmental Neuroscience
https://www.readbyqxmd.com/read/28433663/mitochondrial-mechanisms-of-neuronal-rescue-by-f-68-a-hydrophilic-pluronic-block-co-polymer-following-acute-substrate-deprivation
#18
REVIEW
Janice C Wang, Vytautas P Bindokas, Matthew Skinner, Todd Emrick, Jeremy D Marks
Global brain ischemia can lead to widespread neuronal death and poor neurologic outcomes in patients. Despite detailed understanding of the cellular and molecular mechanisms mediating neuronal death following focal and global brain hypoxia-ischemia, treatments to reduce ischemia-induced brain injury remain elusive. One pathway central to neuronal death following global brain ischemia is mitochondrial dysfunction, one consequence of which is the cascade of intracellular events leading to mitochondrial outer membrane permeabilization...
April 19, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28426648/pregnancy-swimming-causes-short-and-long-term-neuroprotection-against-hypoxia-ischemia-in-very-immature-rats
#19
Eduardo Farias Sanches, Luz Elena Duran Carabali, Andrea Tosta, Fabrício Nicola, Felipe Schmitz, André Rodrigues, Cassiana Siebert, Angela Wyse, Carlos Alexandre Netto
BACKGROUND: Hypoxia-ischemia (HI) is a major cause of neurological damage in preterm. Pregnancy swimming alters the pup's brain development. We tested the effects of swimming during pregnancy in the very immature rat brain. METHODS: Female Wistar rats (n=12) were assigned to sedentary (SE, n=6) or swimming groups (SW, n=6). From the gestational day 0 (DG0) to GD21 they performed 20 min/daily swimming sessions. HI on postnatal day 3 rat cause sensorimotor and cognitive impairments...
April 20, 2017: Pediatric Research
https://www.readbyqxmd.com/read/28423529/pif-promotes-brain-re-myelination-locally-while-regulating-systemic-inflammation-clinically-relevant-multiple-sclerosis-m-smegmatis-model
#20
Giuseppe Migliara, Martin Mueller, Alessia Piermattei, Chaya Brodie, Michael J Paidas, Eytan R Barnea, Francesco Ria
Neurologic disease diagnosis and treatment is challenging. Multiple Sclerosis (MS) is a demyelinating autoimmune disease with few clinical forms and uncertain etiology. Current studies suggest that it is likely caused by infection(s) triggering a systemic immune response resulting in antigen/non-antigen-related autoimmune response in central nervous system (CNS). New therapeutic approaches are needed. Secreted by viable embryos, PreImplantation Factor (PIF) possesses a local and systemic immunity regulatory role...
March 28, 2017: Oncotarget
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