| 1. |
- Lund, Sören, et al.
(författare)
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The dynamics of the LPS triggered inflammatory response of murine microglia under different culture and in vivo conditions
- 2006
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Ingår i: J Neuroimmunol. ; 180:1-2, s. 71-87
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Tidskriftsartikel (refereegranskat)abstract
- Overall, the inflammatory potential of lipopolysaccharide (LPS) in vitro and in vivo was investigated using different omics technologies. We investigated the hippocampal response to intracerebroventricular (i.c.v) LPS in vivo, at both the transcriptional and protein level. Here, a time course analysis of interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) showed a sharp peak at 4 h and a return to baseline at 16 h. The expression of inflammatory mediators was not temporally correlated with expression of the microglia marker F4/80, which did not peak until 2 days after LPS injection. Of 480 inflammation-related genes present on a microarray, 29 transcripts were robustly up-regulated and 90% of them were also detected in LPS stimulated primary microglia (PM) cultures. Further in vitro to in vivo comparison showed that the counter regulation response observed in vivo was less evident in vitro, as transcript levels in PM decreased relatively little over 16 h. This apparent deficiency of homeostatic control of the innate immune response in cultures may also explain why a group of genes comprising tnf receptor associated factor-1, endothelin-1 and schlafen-1 were regulated strongly in vitro, but not in vivo. When the overall LPS-induced transcriptional response of PM was examined on a large Affymetrix chip, chemokines and cytokines constituted the most strongly regulated and largest groups. Interesting new microglia markers included interferon-induced protein with tetratricopeptide repeat (ifit), immune responsive gene-1 (irg-1) and thymidylate kinase family LPS-inducible member (tyki). The regulation of the former two was confirmed on the protein level in a proteomics study. Furthermore, conspicuous regulation of several gene clusters was identified, for instance that of genes pertaining to the extra-cellular matrix and enzymatic regulation thereof. Although most inflammatory genes induced in vitro were transferable to our in vivo model, the observed discrepancy for some genes potentially represents regulatory factors present in the central nervous system (CNS) but not in vitro.
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| 2. |
- Rüetschi, Ulla, 1962, et al.
(författare)
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Proteomic analysis using protein chips to detect biomarkers in cervical and amniotic fluid in women with intra-amniotic inflammation
- 2005
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Ingår i: J Proteome Res. ; 4:6, s. 2236-42
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Tidskriftsartikel (refereegranskat)abstract
- Intra-amniotic inflammation (IAI) may cause preterm birth with poor neonatal out-come. To identify novel biomarkers for IAI, we analyzed amniotic and cervical fluid samples from 27 patients with signs of threatening preterm birth with or without IAI by surface-enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF-MS). Seventeen proteins were significantly overexpressed in amniotic fluid from IAI cases and more often in women with preterm labor than those with rupture of membranes. Five of these were identified as human neutrophil protein 1-3, calgranulin A and B.
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| 3. |
- Amer-Wåhlin, Isis, et al.
(författare)
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Fetal electrocardiogram: ST waveform analysis in intrapartum surveillance
- 2007
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Ingår i: Bjog. - : Wiley. ; 114:10, s. 1191-1193
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Tidskriftsartikel (refereegranskat)abstract
- ST waveform analysis of fetal electrocardiogram (ECG) for intrapartum surveillance (STAN) is a newly introduced method for fetal surveillance. The purpose of this commentary is to assist in the proper use of fetal ECG in combination with cardiotocography (CTG) during labour. Guidelines and recommendations concerning CTG and ST waveform interpretation and classification are stated that were agreed on by the European experts on ST waveform analysis for intrapartum surveillance during a meeting in Utretcht, The Netherlands in January 2007.
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| 4. |
- Amu, Sylvie, 1978, et al.
(författare)
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Cytokines in the placenta of Pakistani newborns with and without intrauterine growth retardation
- 2006
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Ingår i: Pediatr Res. ; 59:2, s. 254-8
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Tidskriftsartikel (refereegranskat)abstract
- Although intrauterine growth retardation (IUGR) is a major risk factor for increased neonatal mortality and morbidity, the mechanisms behind it are not clear. We analyzed cytokine gene expression and gene polymorphisms in infants with and without IUGR in Pakistan, where IUGR is very common. 45 IUGR and 55 control mother/infant pairs were studied. mRNA for IL-10, IL-8, TNF-alpha, TGF-beta, IL-6, IL-4, IL-1beta, IL-12, IFN-gamma and GAPDH was quantified with RT-PCR from placenta. Cytokine and cytokine receptor gene polymorphisms for -1087IL10, -308TNFA, -174IL6, +915TGFB1, intron 2 IL1RN, +36TNFR1, 150V IL4RA and -159CD14 were determined from genomic DNA. The serum levels of IL-1beta, IL-6, IL-8, IL-10, IL-12, TNF-alpha and TGF-beta were measured. There was a significant decrease of IL-10 and IL-12, but increase of TGF-beta in the decidua and similarly decrease of IL-10, but increase of TGF-beta in the trophoblasts of the IUGR placentas compared with the non-IUGR placentas. We found significantly lower levels of IL-1beta in serum from the mothers of the IUGR infants and of TGF-beta in serum of the infants with IUGR compared with the non-IUGR infants. We note that the IL-10 mRNA expression in the decidua was down-regulated, but the TGF-beta mRNA up-regulated in IUGR placentas of mothers from a population with multiple risk factors for IUGR. We propose that the low IL-10 in the placenta may be involved in the pathogenesis of IUGR and might possibly be treatable.
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| 5. |
- Babcock, M. A., et al.
(författare)
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Injury to the preterm brain and cerebral palsy: clinical aspects, molecular mechanisms, unanswered questions, and future research directions
- 2009
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Ingår i: J Child Neurol. - : SAGE Publications. - 0883-0738 .- 1708-8283. ; 24:9, s. 1064-84
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Tidskriftsartikel (refereegranskat)abstract
- Cerebral palsy will affect nearly 10% of the 60,000 very low-birth-weight infants born in the United States in the next year, and an even greater percentage will display some form of permanent neurological impairment resulting from injury to the preterm brain. The 2008 Neurobiology of Disease in Children Symposium, held in conjunction with the 37th annual meeting of the Child Neurology Society, aimed to define current knowledge and to develop specific aims for future clinical, translational, and fundamental science. A complex interplay of both destructive and developmental forces is responsible for injury to the preterm brain. Advances in imaging and histology have implicated a variety of cell types, though preoligodendrocyte injury remains the focus. Research into different mechanisms of injury is facilitating new neuroprotective and rehabilitative interventions. A cooperative effort is necessary to translate basic research findings into clinically effective therapies and better care for these children.
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| 6. |
- Blennow, Mats, et al.
(författare)
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Fosterasfyxi
- 2008
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Ingår i: Lärobok i obstetrik. Redaktörer: Marsal, Karel, Hagberg, Henrik, Westgren, Magnus. - : Studentlitteratur. - 9789144007311 ; , s. 235-242
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 7. |
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| 8. |
- Blennow, Mats, et al.
(författare)
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Omhändertagande av det asfyktiska barnet
- 2008
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Ingår i: Lärobok i neonatologi. Redaktörer: Lagercrantz, H; Hellström-Vestas, L; Norrman, M. - : Studentlitteratur. - 9789144046433 ; , s. 57-76
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 9. |
- Blomgren, Klas, 1963, et al.
(författare)
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Free radicals, mitochondria, and hypoxia-ischemia in the developing brain
- 2006
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Ingår i: Free Radic Biol Med. ; 40:3, s. 388-97
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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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| 10. |
- Carlsson, Ylva, 1975, et al.
(författare)
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Role of mixed lineage kinase inhibition in neonatal hypoxia-ischemia.
- 2009
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Ingår i: Developmental neuroscience. - : S. Karger AG. - 1421-9859 .- 0378-5866. ; 31:5, s. 420-6
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Tidskriftsartikel (refereegranskat)abstract
- Hypoxic-ischemic brain injury is often delayed and involves both apoptotic and immunoregulatory mechanisms. In this study, we used a neonatal model of hypoxia-ischemia to examine the effect of the mixed lineage kinase (MLK) inhibitor CEP-1347 on brain damage, apoptosis and inflammation. The tissue volume loss was reduced by 28% (p = 0.019) in CEP-1347-treated versus vehicle-treated rats and CEP-1347 significantly attenuated microgliosis at 7 days (p = 0.038). CEP-1347 decreased TUNEL-positive staining as well as cleaved caspase 3 immunoreactivity. CEP-1347 did not affect the expression of pro-inflammatory cytokines IL-1 beta, IL-6 and MCP-1, nor did it affect the expression of OX-42 (CR3) and OX-18 (MHC I) 24 h after the insult. In conclusion, the MLK inhibitor CEP-1347 has protective effects in a neonatal rat model of hypoxia-ischemia, which is mainly related to reduced apoptosis.
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