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Träfflista för sökning "LAR1:gu ;mspu:(researchreview);pers:(Hagberg Henrik 1955)"

Sökning: LAR1:gu > Forskningsöversikt > Hagberg Henrik 1955

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  • Blomgren, Klas, 1963, et al. (författare)
  • Free radicals, mitochondria, and hypoxia-ischemia in the developing brain
  • 2006
  • Ingår i: Free Radic Biol Med. ; 40:3, s. 388-97
  • Forskningsöversikt (refereegranskat)abstract
    • The immature brain is particularly susceptible to free radical injury because of its poorly developed scavenging systems and high availability of iron for the catalytic formation of free radicals. Neurons are more vulnerable to free radical damage than glial cells, but oligodendrocyte progenitors and immature oligodendrocytes in very prematurely born infants are selectively vulnerable to depletion of antioxidants and free radical attack. Reactive oxygen and nitrogen species play important roles in the initiation of apoptotic mechanisms and in mitochondrial permeability transition, and therefore constitute important targets for therapeutic intervention. Oxidative stress is an early feature after cerebral ischemia and experimental studies targeting the formation of free radicals demonstrate various degrees of protection after perinatal insults. Oxidative stress-regulated release of proapoptotic factors from mitochondria appears to play a much more important role in the immature brain. This review will summarize and compare with the adult brain some of the current knowledge of free radical formation in the developing brain and its roles in the pathophysiology after cerebral hypoxia-ischemia.
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3.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Apoptotic mechanisms in the immature brain: involvement of mitochondria.
  • 2009
  • Ingår i: Journal of child neurology. - : SAGE Publications. - 1708-8283 .- 0883-0738. ; 24:9, s. 1141-6
  • Forskningsöversikt (refereegranskat)abstract
    • Brain injury after hypoxic-ischemic encephalopathy often develops with delayed appearance, opening a therapeutic window. Clinical studies in newborns show that post-hypoxic-ischemic hypothermia improves outcome. This has generated renewed interest in the molecular mechanisms of hypoxic-ischemic brain injury. In this brief review, we propose that mitochondrial permeabilization is crucial for injury to advance beyond the point of no return. We suggest that excitatory amino acids, nitric oxide, inflammation, trophic factor withdrawal, and an increased pro- versus antiapoptotic Bcl-2 protein ratio will trigger Bax-dependent mitochondrial outer membrane permeabilization. Mitochondrial outer membrane permeabilization, in turn, elicits mitochondrial release of cytochrome C, apoptosis-inducing factor, second mitochondria-derived activator of caspase/Diablo, and HtrA2/Omi. Cytochrome C efflux activates caspase-9/-3, leading to DNA fragmentation. Apoptosis-inducing factor interacts with cyclophilin A and induces chromatinolysis. Blockage of mitochondrial outer membrane permeabilization holds promise as a strategy for perinatal brain protection.
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4.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Brain injury in preterm infants--what can the obstetrician do?
  • 2005
  • Ingår i: Early human development. - : Elsevier BV. - 0378-3782. ; 81:3, s. 231-5
  • Forskningsöversikt (refereegranskat)abstract
    • Mothers at increased risk of preterm birth often receive glucocorticoids (GC), antibiotics and tocolytics by the obstetrician but the question is whether such interventions affect the risk of brain injury and neurological outcome. We suggest that one single course of antenatal GC is the most important treatment that can be offered to patients at risk of preterm birth at 24-34 weeks of gestation to prevent brain injury. Betamethasone seems advantageous to dexamethasone and repeated courses of GC should probably be avoided. Antibiotics given to patients with preterm premature rupture of membranes reduce neonatal morbidity and decrease the risk of sonographic cerebral abnormalities even though the effect on long-term neurological outcome is uncertain. From the perspective of the immature CNS, there is no evidence for treatment with tocolytics even though it allows transfer of the patient to a tertiary center and increases the likelihood of administration of a complete course of corticosteroids which may affect outcome.
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5.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Effect of inflammation on central nervous system development and vulnerability
  • 2005
  • Ingår i: Curr Opin Neurol. - 1350-7540. ; 18:2, s. 117-23
  • Forskningsöversikt (refereegranskat)abstract
    • PURPOSE OF REVIEW: Preterm infants are at high risk for neurological sequelae and cognitive dysfunction. These problems have been attributed to a high occurrence of central nervous system (CNS) lesions, but suboptimal brain development appears to be just as important. In this brief review we present the hypothesis that systemic infection/inflammation can severely interfere with normal CNS function and development. RECENT FINDINGS: We focus on the effects of lipopolysaccharide because it is often used to model the systemic inflammatory response induced by infections. The inflammatory signals are propagated across the intact or ruptured blood-brain barrier to the CNS by proinflammatory cytokines, prostaglandins, or lipopolysaccharide. Subsequently, microglia are triggered to release cytokines, oxygen free radicals and trophic factors, which will influence the CNS in various ways. Cognition, dendritic length and spine density, dopaminergic cells, neurogenesis and glial proliferation will be affected. Furthermore, CNS vulnerability and, in some instances, cerebral anomalies and white matter damage are produced. SUMMARY: Hypothetically, all of these effects on the CNS triggered by inflammation may have severe consequences for the individual's ability to cope with environmental exposures during childhood and adulthood.
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7.
  • Hagberg, Henrik, 1955 (författare)
  • Mitochondrial impairment in the developing brain after hypoxia-ischemia
  • 2004
  • Ingår i: J Bioenerg Biomembr. ; 36:4, s. 369-73
  • Forskningsöversikt (refereegranskat)abstract
    • The pattern of cell death in the immature brain differs from that seen in the adult CNS. During normal development, more than half of the neurons are removed through apoptosis, and mediators like caspase-3 are highly upregulated. The contribution of apoptotic mechanisms in cell death appears also to be substantial in the developing brain, with a marked activation of downstream caspases and signs of DNA fragmentation. Mitochondria are important regulators of cell death through their role in energy metabolism and calcium homeostasis, and their ability to release apoptogenic proteins and to produce reactive oxygen species. We find that secondary brain injury is preceded by impairment of mitochondrial respiration, signs of membrane permeability transition, intramitochondrial accumulation of calcium, changes in the Bcl-2 family proteins, release of proapoptotic proteins (cytochrome C, apoptosis inducing factor) and downstream activation of caspase-9 and caspase-3 after hypoxia-ischemia. These data support the involvement of mitochondria-related mechanisms in perinatal brain injury.
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8.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Perinatal brain damage: The term infant.
  • 2016
  • Ingår i: Neurobiology of disease. - : Elsevier BV. - 1095-953X .- 0969-9961. ; 92 (Pt A), s. 102-12
  • Forskningsöversikt (refereegranskat)
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9.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Preconditioning and the developing brain
  • 2004
  • Ingår i: Semin Perinatol. - : Elsevier BV. - 0146-0005. ; 28:6, s. 389-95
  • Forskningsöversikt (refereegranskat)abstract
    • Preconditioning occurs when a subinjurious exposure renders the brain less vulnerable to a subsequent damaging exposure. In this essay, various models of preconditioning in the immature brain are discussed. Adenosine, excitatory amino acids, nitric oxide, hypoxia-inducible factor, ATP-sensitive K+ channels, caspases, heat shock proteins, inflammatory mediators and gene expression all seem to be involved in sensing, transducing and executing preconditioning resistance. Also reviewed in this essay is evidence that some subinjurious exposures render the brain more vulnerable to a subsequent damaging exposure. We believe that unraveling the mechanisms of how the developing brain becomes inherently resilient or vulnerable will offer important insights into the pathogenesis of injury. Preconditioning of the brain or induction of tolerance of the immune system might be utilized in the future to decrease CNS vulnerability and the occurrence of perinatal brain injury.
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10.
  • Hagberg, Henrik, 1955, et al. (författare)
  • Role of cytokines in preterm labour and brain injury.
  • 2005
  • Ingår i: BJOG : an international journal of obstetrics and gynaecology. - : Wiley. - 1470-0328. ; 112 Suppl 1, s. 16-8
  • Forskningsöversikt (refereegranskat)abstract
    • Intrauterine infection induces an intra-amniotic inflammatory response involving the activation of a number of cytokines and chemokines which, in turn, may trigger preterm contractions, cervical ripening and rupture of the membranes. Infection and cytokine-mediated inflammation appear to play a prominent role in preterm birth at early gestations (<30 weeks). The role of infection/inflammation in preterm birth in Europe has been incompletely characterised. The rate of preterm birth in Sweden is lower, and the rate of chorioamnionitis, bacterial vaginosis (BV), neonatal sepsis, and urinary tract infections during pregnancy is lower compared with the USA. In a Swedish population of women with preterm labour or preterm premature rupture of the membranes (PPROM) <34 weeks of gestation, microorganisms were detected in the amniotic fluid in 25% of women with PPROM and in 16% of those in preterm labour. Nearly half of these women had intra-amniotic inflammation defined as elevated interleukin-6 (IL-6) and IL-8, and there was a high degree of correlation between cytokine levels and preterm birth or the presence of microbial colonisation. These data do not support the hypothesis that infection-related preterm birth is less frequent in northern Europe than elsewhere. The intra-amniotic inflammatory response has also been associated with white matter injury and cerebral palsy. We find that in experimental models, induction of a systemic inflammatory response using lipopolysaccharide activates toll-like receptors (TLRs), which produce either white matter lesions or increase brain susceptibility to secondary insults. Recently, IL-18 in umbilical blood was shown to correlate with brain injury in preterm infants and IL-18 deficiency in mice decreases CNS vulnerability.
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