Publications by authors named "Ashild Vege"

Sudden Infant Death Syndrome (SIDS) is the sudden and unexpected death of an otherwise healthy infant less than 1 year of age where the cause of death remains unexplained after a thorough post-mortem investigation and evaluation of the circumstances. Epidemiological, clinical, biochemical, immunological and pathological evidence indicates that three factors must coincide for SIDS to occur: a vulnerable developmental stage of the immune system and central nervous system in the infant, predisposing factors, and external trigger events. This model is referred to as the fatal triangle or triple risk hypothesis.

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Humans are daily exposed to mineral oil saturated hydrocarbons (MOSH) from the diet. We exposed female Fischer 344 rats to a broad mixture and sub-fractions of MOSH. Chemical characterization of the MOSH mixture used and material accumulated in rat tissues were previously reported (Barp et al.

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Article Synopsis
  • Researchers examined mRNA gene expression in 14 cases of sudden infant deaths attributed to infection, comparing them to a control group of 12 cases from various causes using advanced genetic technology.
  • The study found that 19 genes showed altered expression in the infected infants, with 15 of those genes notably changed in heart tissue.
  • A key finding was the downregulation of the KCNE5 gene in heart tissue, which is linked to Brugada syndrome and sudden death, suggesting it may play a role in the fatal outcomes during infectious illnesses in infants.
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Aim: This study reviewed cases of sudden unexpected child deaths in Norway to determine the significance of death-scene investigations (DSIs) in establishing cause and manner of death, and thereby it is relevance to legal protection.

Methods: Data from forensic autopsy reports and DSIs were collected and analysed for cases of unexpected deaths in children below 4 years of age in Norway during 2010-2016.

Results: Out of 141 cases, the death scene was investigated as a voluntary procedure in 75 cases and by the police in 41 cases.

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Humans are daily exposed to mineral oil saturated hydrocarbons (MOSH) from the diet. We exposed female Fischer 344 rats to a broad mixture and sub-fractions of MOSH. Chemical characterization of the MOSH mixture used and material accumulated in rat tissues were previously reported.

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Background: The pathophysiology and outcome of meningococcal septic shock is closely associated with the plasma level of lipopolysaccharides (LPS, endotoxin) and the circulating level of meningococcal DNA. The aim of the present study was to quantify the number of in different formalin-fixed, paraffin-embedded (FFPE) tissue samples and fresh frozen (FF) tissue samples from patients with systemic meningococcal disease (SMD), to explore the distribution of in the body.

Methods: DNA in FFPE and FF tissue samples from heart, lungs, liver, kidneys, spleen and brain from patients with meningococcal shock and controls (lethal pneumococcal infection) stored at variable times, were isolated.

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Aim: Disturbances in brain function and development may play a role in sudden infant death syndrome (SIDS). This Norwegian study aimed to test the hypothesis that specific variants of genes involved in water transport and potassium homeostasis would be predisposing factors for SIDS.

Methods: Genetic variation in the genes encoding aquaporin-4 (AQP4), Kir4.

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Background: A large number of studies have tried to uncover a genetic predisposition for sudden infant death syndrome (SIDS), but there is still uncertainty concerning the pathogenesis of these deaths. The purpose of this study was to investigate mRNA gene expression in SIDS cases and controls, in order to uncover genes that are differentially expressed in the two groups.

Methods: Tissue from brain, heart, and liver from 15 SIDS cases and 15 controls were included in the study, and mRNA expression was determined using the Illumina whole genome gene expression DASL HT assay.

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Fulminant meningococcal sepsis is characterized by a massive growth of bacteria in the circulation, regarded as the primary inflammatory site, with no specific solid organ focus. Here we aimed to study the local inflammatory response in organs using a porcine model of fulminant meningococcal septic shock challenged with exponentially increasing doses of heat inactivated Neisseria meningitidis. The results were compared with those obtained in organs post mortem from three patients with lethal meningococcal septic shock.

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Article Synopsis
  • The study aimed to explore the genetic factors, specifically polymorphisms in the MAOA and 5-HTT genes, related to sudden infant death syndrome (SIDS) in Norway.
  • The researchers analyzed samples from 193 SIDS cases and 335 control subjects, using techniques like polymerase chain reaction and gel electrophoresis, but found no significant differences in the genetic variations between the two groups.
  • The conclusion suggests that the specific genetic variations studied are not linked to SIDS, but further investigation into other genes involved in serotonin pathways is recommended, as they may still play a role in some cases.
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  • The study investigates the link between cytokine gene polymorphisms and immune activation in infants who experienced sudden infant death syndrome (SIDS).
  • Researchers evaluated the expression of HLA-DR in the laryngeal mucosal of 97 SIDS victims and correlated it with cytokine levels and gene variants.
  • Findings suggest that specific cytokine polymorphisms and higher levels of IL-6 are associated with risk factors in SIDS, highlighting genetic factors that may disrupt immune balance in these cases.
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Autopsies can give valuable information about the cause of death, and represent an important tool for obtaining valid cause of death statistics. In particular, they may shed light on the circumstances of death in ambiguous and criminal cases. To address the need for information on current autopsy practices, forensic autopsy rates in two counties in Central Norway over the period 2007-2009 were assessed.

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The purpose of this study was to investigate the aquaporin-4 (AQP4) gene in cases of sudden infant death syndrome (SIDS) and controls and to elucidate the hypothesis that a genetically determined disturbed water homeostasis in the brain is involved as a predisposing factor in SIDS. The single nucleotide polymorphisms (SNPs) rs2075575, rs4800773, rs162004, and rs3763043 in the AQP4 gene were investigated in 141 SIDS cases and 179 controls. For each SIDS case, a brain/body weight ratio was calculated.

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Several studies indicate that interleukin gene polymorphisms are of importance to sudden infant death syndrome (SIDS), and so far it has been reported that associations between SIDS and polymorphism in the genes encoding tumor necrosis factor alpha, IL (interleukin)-6, and IL-10. IL-1 are important for the synthesis of acute phase proteins, and it is a pyrogen cytokine that may cause fever. The purpose of the present study was to investigate two polymorphisms in the IL-1alpha gene; a variable number of tandem repeat (VNTR) in intron 6 and a single nucleotide polymorphism in +4845G/T, as well as the -511C/T polymorphism in the gene encoding IL-1beta, and a VNTR in intron 2 of the competitive antagonist IL-1Ra, in SIDS cases, cases of infectious death, and controls.

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Mild infection may trigger sudden death in the vulnerable infant by cytokine interactions with a compromised medullary serotonergic (5-HT) system, leading to disrupted cardiorespiratory regulation and sleep-related sudden death. The cytokine interleukin (IL)-6 is elevated in the cerebrospinal fluid in SIDS. We tested the hypothesis that the expression of IL-6 receptors (IL-6R) and/or gp130 (involved in IL-6R signaling) is altered in the medullary 5-HT system in SIDS.

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Aim: To investigate the innate immune components surfactant protein A (SP-A) and D (SP-D) in victims of sudden infant death syndrome (SIDS).

Methods: Ten common single nucleotide polymorphisms (SNPs) in the exons of SP-A1, SP-A2 and SP-D genes were analysed in 42 cases of SIDS and 46 explained sudden infant deaths. SP-A and SP-D protein expression in tissue from the aerodigestive tract was semi-quantitatively evaluated by immunohistochemistry.

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Several studies indicate that the immune system is stimulated in sudden infant death syndrome (SIDS). Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that strongly affects the cytokine cascade. A genetic variant associated with high production of TNF-alpha may thus be of significance in the pathogenesis of SIDS.

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Infection with Helicobacter pylori has been proposed to be a common cause of Sudden Infant Death Syndrome (SIDS). We investigated the frequency of H. pylori infection in 160 infant deaths and 156 live controls by means of the Helicobacter pylori stool antigen (HpSA) immunoassay.

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Aim: To investigate polymorphisms in the serotonin transporter (5-HTT) gene in cases of sudden infant death syndrome (SIDS) and controls, and further to elucidate a possible relationship between 5-HTT genotypes and external risk factors for SIDS.

Method: The subjects investigated consist of 163 SIDS cases and 243 controls. Polymorphisms in both the promoter and intron 2 of the 5-HTT gene were investigated, and the genotypes were determined using polymerase chain reaction (PCR) and gel electrophoresis.

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Life-threatening arrhythmias have been suspected as one cause of the sudden infant death syndrome (SIDS), and this hypothesis is supported by the observation that mutations in arrhythmia susceptibility genes occur in 5-10% of cases. However, the functional consequences of cardiac potassium channel gene mutations associated with SIDS and how these alleles might mechanistically predispose to sudden death are unknown. To address these questions, we studied four missense KCNH2 (encoding HERG) variants, one compound KCNH2 genotype, and a missense KCNQ1 mutation all previously identified in Norwegian SIDS cases.

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Background: Surfactant protein A (SP-A) is synthesized in the lung and is a part of the innate immune system. The aim of this study was to evaluate the expression of SP-A in lung tissue from fetuses, infants, children and adults with special regard to sudden infant death syndrome (SIDS).

Methods: A total of 160 cases were studied; 19 fetuses and neonates, 59 SIDS and 49 explained infant deaths below 1 year of age, 19 toddlers and 14 adults.

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Article Synopsis
  • The study aimed to explore the link between mitochondrial DNA mutations and sudden infant death syndrome (SIDS) by analyzing tRNA genes in affected infants and controls.* -
  • Researchers sequenced mitochondrial genes in 24 SIDS cases and 10 controls, along with checking a specific ND3 gene mutation in a broader group, but found no significant differences.* -
  • The findings suggest that there is no clear association between mitochondrial tRNA gene mutations and SIDS, implying these mutations may not be a risk factor for the syndrome.*
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Aim: Long QT syndrome (LQTS) has been shown to be the cause of death in some cases originally diagnosed as sudden infant death syndrome (SIDS). Such cardiac arrhythmias have also been noted in families with mitochondrial disease, and studies indicate that mitochondrial disease could be involved in SIDS. This makes the mtDNA polymorphism T3394C interesting, as a previous study has shown it to be associated with electrocardiographic (ECG) changes after exercise in a family with LQTS, where some members harboured a KCNH2 mutation.

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Background: Mutations in genes responsible for the congenital long-QT syndrome, especially SCN5A, have been identified in some cases of sudden infant death syndrome. In a large-scale collaborative genetic screen, several SCN5A variants were identified in a Norwegian sudden infant death syndrome cohort (n=201). We present functional characterization of 7 missense variants (S216L, R680H, T1304M, F1486L, V1951L, F2004L, and P2006A) and 1 in-frame deletion allele (delAL586-587) identified by these efforts.

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