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| 2. |
- Eklind, Saskia, et al.
(författare)
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The role of glucose in brain injury following the combination of lipopolysaccharide or lipoteichoic acid and hypoxia-ischemia in neonatal rats
- 2004
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Ingår i: Dev Neurosci. ; 26:1, s. 61-7
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Tidskriftsartikel (refereegranskat)abstract
- We have previously shown that lipopolysaccharide (LPS) sensitizes the immature rat brain to subsequent hypoxic-ischemic (HI) injury; however, the underlying mechanisms remain unclear. In this study, we examined the role of glucose in the sensitizing effects of LPS and lipoteichoic acid (LTA) in combination with HI in 7-day-old rats. LPS/HI resulted in hypoglycemia which lasted 24 h and lactate levels were increased from 6 to 10 h after LPS administration. LPS/HI induced severe brain injury, which persisted 2 weeks after LPS/HI. Administration of glucose to LPS-treated animals with HI reduced brain injury in the cerebral cortex and hippocampus, while striatal damage remained. LTA/HI did not affect blood glucose, lactate or brain injury. In conclusion, enhanced blood glucose levels during HI after LPS administration conferred protection in some brain regions but not in the striatum, suggesting that alterations in glucose can only partly explain the sensitizing effect of LPS.
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| 3. |
- Elden, Helen, 1959, et al.
(författare)
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Effects of acupuncture and stabilising exercises as adjunct to standard treatment in pregnant women with pelvic girdle pain: randomised single blind controlled trial
- 2004
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Ingår i: The 5th Interdisciplinary World Congress on Low Back Pain & Pelvic Pain”, 2004, Melbourne.. - 9080255149
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Konferensbidrag (refereegranskat)abstract
- OBJECTIVES: To compare the efficacy of standard treatment, standard treatment plus acupuncture, and standard treatment plus stabilising exercises for pelvic girdle pain during pregnancy. DESIGN: Randomised single blind controlled trial. Settings East Hospital, Gothenburg, and 27 maternity care centres in Sweden. PARTICIPANTS: 386 pregnant women with pelvic girdle pain. INTERVENTIONS: Treatment for six weeks with standard treatment (n = 130), standard treatment plus acupuncture (n = 125), or standard treatment plus stabilising exercises (n = 131). MAIN OUTCOME MEASURES: Primary outcome measure was pain (visual analogue scale); secondary outcome measure was assessment of severity of pelvic girdle pain by an independent examiner before and after treatment. RESULTS: After treatment the stabilising exercise group had less pain than the standard group in the morning (median difference = 9, 95% confidence interval 1.7 to 12.8; P = 0.0312) and in the evening (13, 2.7 to 17.5; P = 0.0245). The acupuncture group, in turn, had less pain in the evening than the stabilising exercise group (-14, -18.1 to -3.3; P = 0.0130). Furthermore, the acupuncture group had less pain than the standard treatment group in the morning (12, 5.9 to 17.3; P < 0.001) and in the evening (27, 13.3 to 29.5; P < 0.001). Attenuation of pelvic girdle pain as assessed by the independent examiner was greatest in the acupuncture group. CONCLUSION: Acupuncture and stabilising exercises constitute efficient complements to standard treatment for the management of pelvic girdle pain during pregnancy. Acupuncture was superior to stabilising exercises in this study.
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| 6. |
- Hagberg, Henrik, 1955
(författare)
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Mitochondrial impairment in the developing brain after hypoxia-ischemia
- 2004
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Ingår i: J Bioenerg Biomembr. ; 36:4, s. 369-73
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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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| 7. |
- Hagberg, Henrik, 1955, et al.
(författare)
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PARP-1 gene disruption in mice preferentially protects males from perinatal brain injury
- 2004
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Ingår i: J Neurochem. ; 90:5, s. 1068-75
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Tidskriftsartikel (refereegranskat)abstract
- Poly(ADP-ribose) polymerase-1 is over-activated in the adult brain in response to ischemia and contributes to neuronal death, but its role in perinatal brain injury remains uncertain. To address this issue, 7-day-old wild-type (wt) and PARP-1 gene deficient (parp+/- and parp-/-) Sv129/CD-1 hybrid mice were subjected to unilateral hypoxia-ischemia and histologic damage was assessed 10 days later by two evaluators. Poly(ADP-ribose) polymerase-1 knockout produced moderate but significant (p < 0.05) protection in the total group of animals, but analysis by sex revealed that males were strongly protected (p < 0.05) in contrast to females in which there was no significant effect. Separate experiments demonstrated that PARP-1 was activated over 1-24 h in both females and males after the insult in neonatal wt mice and rats using immnocytochemistry and western blotting for poly(ADP-ribose). Brain levels of NAD+ were also significantly reduced, but the decrease of NAD+ during the early post-hypoxia-ischemia (HI) phase was only seen in males. The results indicate that hypoxia-ischemia activates Poly(ADP-ribose) polymerase-1 in the neonatal brain and that the sex of the animal strongly influences its role in the pathogenesis of brain injury.
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| 8. |
- Hagberg, Henrik, 1955, et al.
(författare)
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Preconditioning and the developing brain
- 2004
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Ingår i: Semin Perinatol. - : Elsevier BV. - 0146-0005. ; 28:6, s. 389-95
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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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| 9. |
- Hedtjärn, Maj, 1973, et al.
(författare)
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Global gene expression in the immature brain after hypoxia-ischemia
- 2004
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Ingår i: J Cereb Blood Flow Metab. ; 24:12, s. 1317-32
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Tidskriftsartikel (refereegranskat)abstract
- Ischemia induces a complex response of differentially expressed genes in the brain. In order to understand the specific mechanisms of injury in the developing brain, it is important to obtain information on global changes in the transcriptome after neonatal hypoxia-ischemia. In this study, oligonucleotide arrays were used to investigate genomic changes at 2, 8, 24, and 72 hours after neonatal hypoxia-ischemia, which was induced in 9-day-old mice by left carotid artery ligation followed by hypoxia (10% O2). In total, 343 genes were differentially expressed in cortex, hippocampus, thalamus, and striatum 2 to 72 hours after hypoxia-ischemia, when comparing ipsilateral with contralateral hemispheres and with controls, using the significance analysis for microarrays. A total of 283 genes were upregulated and 60 were downregulated, and 94% of the genes had not previously been shown after neonatal hypoxia-ischemia. Genes related to transcription factors and metabolism had mostly upregulated transcripts, whereas most downregulated genes belonged to the categories of ion and vesicular transport and signal transduction. Genes involved in transcription, stress, and apoptosis were induced early after the insult, and many new genes that may play important roles in the pathophysiology of neonatal hypoxia-ischemia were identified.
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| 10. |
- Hedtjärn, Maj, 1973, et al.
(författare)
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Inflammatory gene profiling in the developing mouse brain after hypoxia-ischemia
- 2004
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Ingår i: J Cereb Blood Flow Metab. ; 24:12, s. 1333-51
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Tidskriftsartikel (refereegranskat)abstract
- Brain ischemia triggers an inflammatory reaction that progresses for days to weeks and seems to have a role in secondary progression of injury. Inflammation induces a complex pattern of signaling molecules with partly contradictory actions, and the responses may be different in the immature and adult brain. The authors characterized the global inflammatory gene expression in the developing brain as a first step toward understanding the protective and deleterious effects of inflammation after hypoxia-ischemia. Oligonucleotide arrays were used to investigate inflammatory genes in cortex, hippocampus, thalamus, and striatum at 2, 8, 24, and 72 hours after hypoxia-ischemia, which was induced in 9-day-old mice by left carotid artery ligation followed by hypoxia. After hypoxia-ischemia, 148 inflammatory genes were differentially expressed. More than 97% of the genes were upregulated and 93% had not previously been reported after hypoxia-ischemia in the immature brain. The results indicate that microglia/macrophages, T- and B-cells, NK-cells, mast cells, dendritic cells, and polymorphonuclear leukocytes may participate in the response to hypoxia-ischemia. In addition, novel cytokines/chemokines, complement-related, interferon-regulated, components of the TIR/nuclear factor-kappaB pathway, and a number of immunomodulatory genes were induced. Several of these genes may of pathophysiologic significance after neonatal hypoxia-ischemia.
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