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Sökning: LAR1:gu > Forskningsöversikt > Blomgren Klas 1963

  • Resultat 1-8 av 8
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1.
  • 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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2.
  • Blomgren, Klas, 1963-, et al. (författare)
  • Pathological apoptosis in the developing brain
  • 2007
  • Ingår i: Apoptosis. - 1360-8185. ; 12:5, s. 993
  • Forskningsöversikt (refereegranskat)abstract
    • More than half of the initially-formed neurons are deleted in certain brain regions during normal development. This process, whereby cells are discretely removed without interfering with the further development of remaining cells, is called programmed cell death (PCD). The term apoptosis is used to describe certain morphological manifestations of PCD. Many of the effectors of this developmental cell death program are highly expressed in the developing brain, making it more susceptible to accidental activation of the death machinery, e.g. following hypoxia-ischemia or irradiation. Recent evidence suggests, however, that activation and regulation of cell death mechanisms under pathological conditions do not exactly mirror physiological, developmentally regulated PCD. It may be argued that the conditions after e.g. ischemia are not even compatible with the execution of PCD as we know it. Under pathological conditions cells are exposed to various stressors, including energy failure, oxidative stress and unbalanced ion fluxes. This results in parallel triggering and potential overshooting of several different cell death pathways, which then interact with one another and result in complex patterns of biochemical manifestations and cellular morphological features. These types of cell death are here called "pathological apoptosis," where classical hallmarks of PCD, like pyknosis, nuclear condensation and caspase-3 activation, are combined with non-PCD features of cell death. Here we review our current knowledge of the mechanisms involved, with special focus on the potential for therapeutic intervention tailored to the needs of the developing brain.
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3.
  • Blomgren, Klas, 1963- (författare)
  • Stamceller och hjärnskador.
  • 2012
  • Ingår i: Barnläkaren.. ; 1, s. 13-15
  • Forskningsöversikt (refereegranskat)
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4.
  • Galluzzi, L, et al. (författare)
  • Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes.
  • 2009
  • Ingår i: Cell death and differentiation. - 1476-5403. ; 16:8, s. 1093
  • Forskningsöversikt (refereegranskat)abstract
    • Cell death is essential for a plethora of physiological processes, and its deregulation characterizes numerous human diseases. Thus, the in-depth investigation of cell death and its mechanisms constitutes a formidable challenge for fundamental and applied biomedical research, and has tremendous implications for the development of novel therapeutic strategies. It is, therefore, of utmost importance to standardize the experimental procedures that identify dying and dead cells in cell cultures and/or in tissues, from model organisms and/or humans, in healthy and/or pathological scenarios. Thus far, dozens of methods have been proposed to quantify cell death-related parameters. However, no guidelines exist regarding their use and interpretation, and nobody has thoroughly annotated the experimental settings for which each of these techniques is most appropriate. Here, we provide a nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls. These guidelines are intended for investigators who study cell death, as well as for reviewers who need to constructively critique scientific reports that deal with cellular demise. Given the difficulties in determining the exact number of cells that have passed the point-of-no-return of the signaling cascades leading to cell death, we emphasize the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells.
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5.
  • Galluzzi, Lorenzo, et al. (författare)
  • Mitochondrial membrane permeabilization in neuronal injury.
  • 2009
  • Ingår i: Nature reviews. Neuroscience. - 1471-0048. ; 10:7, s. 481-94
  • Forskningsöversikt (refereegranskat)abstract
    • Acute neurological conditions such as cerebrovascular diseases and trauma are associated with irreversible loss of neurons and glial cells. Severe or prolonged injury results in uncontrollable cell death within the core of lesions. Conversely, cells that are less severely damaged succumb in a relatively slow fashion, frequently via the intrinsic pathway of cell death, through the deterioration of mitochondrial functions. The permeabilization of mitochondrial membranes determines whether cells will succumb to or survive the injury, and represents a 'point of no return' in mitochondrial cell death. It is therefore an attractive target for the development of new neuroprotective interventions.
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6.
  • Hangen, Emilie, et al. (författare)
  • Life with or without AIF.
  • 2010
  • Ingår i: Trends in biochemical sciences. - 0968-0004. ; 35:5, s. 278-87
  • Forskningsöversikt (refereegranskat)abstract
    • Apoptosis-inducing factor (AIF) was initially discovered as a caspase-independent death effector. AIF fulfills its lethal function after its release from mitochondria and its translocation to the nucleus of the dying cell. The contribution of AIF to programmed cell death is dependent upon the cell type and apoptotic insult. Recent in vivo data indicate that, in addition to its lethal activity, AIF plays a vital mitochondrial role in healthy cells. A segment of AIF which is dispensable for its apoptotic function carries an NADH-oxidase domain that regulates the respiratory chain complex I and is required for cell survival, proliferation and mitochondrial integrity. Mice that express reduced levels of AIF constitute a reliable model of complex I deficiency. Here we discuss recent reports on the survival-related function(s) of AIF.
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8.
  • Kuhn, Hans-Georg, 1961-, et al. (författare)
  • Developmental dysregulation of adult neurogenesis.
  • 2011
  • Ingår i: The European journal of neuroscience. - 1460-9568. ; 33:6, s. 1115-22
  • Forskningsöversikt (refereegranskat)abstract
    • Rather than a singular event that suddenly appears during adulthood, adult neurogenesis has long been recognized as the continuation of postnatal neurogenic activity. During the first postnatal weeks, significant cellular changes occur within and adjacent to germinal matrices of the subventricular zone and dentate gyrus. The majority of granule cells are generated during this period. In addition, radial glia are transformed into astrocyte-like stem cells, the ependymal layer is formed, and the highest rates of angiogenesis, gliogenesis and myelination are observed. The first postnatal weeks are critical as the brain growth rate is maximal, and changes during this period can have a great impact on neurogenesis levels and overall brain function later in life. This review chronicles cellular changes and some of the clinically relevant dysregulations that can occur during the postnatal period, and discusses the possible impact of these changes on neurogenesis and cognitive function later in life.
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