PubMed Health⌕ Search

Biomedical subjects

Torleiv Ole Rognum

Publications and source records attributed to Torleiv Ole Rognum.

12 recordsLinked to original sources
PubMed2006

The G protein beta3 subunit 825C allele is associated with sudden infant death due to infection.

AIM: To investigate the Gbeta3 subunit C825T polymorphism with regard to sudden unexpected infant death. The reported association between the Gbeta3s protein and increased immune cell function in humans makes this polymorphism highly interesting both with regard to sudden infant death syndrome (SIDS) and deleterious infectious disease. METHODS: The cases investigated in the present study consist of 250 SIDS cases, 38 cases of sudden unexpected infant death due to infection and 99 living infant controls. Typing of the C825T polymorphism was performed by real-time PCR with allele-specific probes and melting curve analyses. RESULTS: The cases of infectious death have a higher percentage of both the C allele (p=0.037 compared to the SIDS cases, p=0.022 compared to the controls) and the CC genotype (p=0.05 compared to the SIDS cases, p=0.016 compared to the controls). There were no differences between SIDS cases and controls. CONCLUSION: The observed association between the 825C allele and infectious death may indicate that the presence of the 825T allele exerts a protective effect towards serious infection, possibly through enhanced G protein signalling. The C allele, on the other hand, appears to represent a disadvantage in this regard.

Alleles↗
PubMed2005

[Bed sharing and sudden infant death].

BACKGROUND: The aim of the study was to investigate bed sharing as a risk factor for sudden infant death syndrome (SIDS). MATERIAL AND METHODS: Firstly, SIDS cases examined at our institute in two six-year periods before and after the back-to-sleep campaign (1984-89 and 1998-2003) were investigated. Secondly, a case-control study was performed, an investigation of variables such as bed sharing, parental smoking and breast-feeding in the SIDS group from the latter period versus 244 live control infants. RESULTS: The age distribution of the SIDS victims in the two periods with high and low SIDS rates differed significantly (p = 0.004). In the latter period, fewer SIDS cases were seen in the classical distributional peak between the third and the fourth month of life, and a larger proportion of SIDS cases were seen within the first month of life. Furthermore, a smaller proportion of SIDS victims were found dead in the prone position (decrease from 89% to 49%, p < 0.001); and bed sharing at time of death occurred more frequently (increase from 7% to 35%, p < 0.001). In the case-control study, bed sharing was a significant risk factor for SIDS in infants aged 0-2 months (multivariate OR 5.3; 95 % CI 1.3-22, p = 0.02). Bed sharing with a smoking mother was associated with a 16-fold increased risk of SIDS (OR 16; 95% CI 2.1 - 118, p = 0.007). No relationship between bed sharing and SIDS was evident for age >2 months. Only 12% of the bed sharing SIDS victims aged <2 months where found in the prone position. INTERPRETATION: Bed sharing is associated with an increased risk of SIDS for infants <2 months of age. Particularly hazardous is bed sharing with a smoking parent.

Breast Feeding↗
PubMed2005

Mitochondrial microsatellite instability in colorectal carcinomas--frequency and association with nuclear microsatellite instability.

The D310 mononucleotide repeat in the D-loop region in mitochondrial DNA has been identified as a hotspot for alterations in primary tumours. We examined D310 alterations as well as repeats in the ND1 and ND5 genes, in 95 colorectal carcinomas and in 95 controls without known gastrointestinal malignancy. D310 alterations were found in 32 (34%) of the carcinomas, in contrast to two persons (2%) in the control group. Thus, when frequency is concerned, D310 seems to be a hotspot for alterations in colorectal cancer. No mutations were found in the ND1 and ND5 genes. D310 instability was not associated with nuclear microsatellite instability, indicating different mechanisms of occurrence.

Adolescent↗
PubMed2004

Sudden infant death syndrome, infection and inflammatory responses.

Sudden infant death syndrome (SIDS) is sudden unexpected death in infancy for which there is no explanation after review of the history, a death scene investigation and a thorough autopsy. The use of common diagnostic criteria is a prerequisite for discussing the importance of infection, inflammatory responses and trigger mechanism in SIDS. Several observations of immune stimulation in the periphery and of interleukin-6 elevation in the cerebrospinal fluid of SIDS victims explain how infections can play a role in precipitating these deaths. Finally, these findings and important risk factors for SIDS are integrated in the concept of a vicious circle for understanding the death mechanism. The vicious circle is a concept to elucidate the interactions between unfavourable factors, including deficient auto-resuscitation, and how this could result in death.

Humans↗
PubMed2004

Telomere instability detected in sporadic colon cancers, some showing mutations in a mismatch repair gene.

Human telomeres are essential for genome stability and are composed of long simple tandem repeat arrays (STRs), comprising the consensus TTAGGG repeat interspersed, at the proximal end, with sequence-variant repeats. While the dynamics of telomere attrition through incomplete replication has been studied extensively, the effects on telomeres of error-prone DNA repair processes, known to affect other STRs, are poorly understood. We have compared the TTAGGG and sequence-variant interspersion patterns in the proximal 720 bp of telomeres in colon cancer and normal DNA samples. The frequency of telomere mutations was 5.8% per allele in a randomly collected panel of sporadic colon cancers, showing that telomere mutations occur in vivo. The mutation frequency rose to 18.6% per allele in sporadic tumours that exhibit instability at the polyA tract in the TGFbetaRII gene and to 35% per allele in tumours with somatic mutations in the hMSH2 gene. The majority of the characterized mutations resulted in the loss of one or a few repeats. If the mutation spectrum and frequency described here is reiterated in the rest of the array, there is the potential for extensive telomere destabilization especially in mismatch repair-defective cells. This may in turn lead to a greater requirement for telomere length maintenance earlier in tumourigenesis.

Base Pair Mismatch↗
PubMed2004

[Of what significance are diseases, intoxication and suicide in fatal traffic accidents?].

BACKGROUND: A large proportion of fatal car accidents cannot be explained by traffic environment, technical defects or risk-taking behaviour. Driver impairment from disease, alcohol, drugs or suicidal impulses may be involved. MATERIAL AND METHOD: Autopsy protocols from 167 car drivers involved in traffic accidents in Southeast Norway 1994-99 were reviewed retrospectively. RESULTS: In 89 of 135 deaths caused by trauma, there were no apparent explanations for the accident prior to autopsy. No differences were found with regard to signs of disease between drivers involved in unexplained and explained accidents. Drivers dead from trauma compared to drivers dead from natural causes had less often ischemic heart disease (p < 0.01). Blood alcohol level was above the statutory limit in 20% of drivers in both unexplained and explained accidents, and drugs were found in the blood in 27% of such cases. Only 13% of drivers in explained accidents collided with large motor vehicles, compared to 44% of the unexplained accidents. INTERPRETATION: Drivers with fatal injuries sustained in unexplained accidents seldom show signs of cardiac disease that could have contributed to the accident. It seems that such unexplained accidents are more often due to driving under the influence of alcohol or drugs, or to possible suicidal impulses.

Accidents, Traffic↗
PubMed2002

Evaluation of diagnostic tools applied in the examination of sudden unexpected deaths in infancy and early childhood.

During the period between 1984 and 1999, 309 cases of sudden unexpected death in infancy and early childhood (0-3 years) were investigated at the Institute of Forensic Medicine in Oslo. In 73 cases, an explainable cause of death was found. In this non-sudden infant death syndrome (SIDS) group, 42 cases were due to disease, 14 to accidents, 7 to neglect/abuse and 10 cases were due to homicide. In 43 cases, there were pathological findings at the autopsy or suspect features in the history and/or circumstances, which were, however, insufficient to explain death ("borderline" SIDS). In the remaining 193 cases, nothing of significance was detected ("pure" SIDS). The purpose of the present study was to evaluate the importance of the different diagnostic tools used in diagnosing non-SIDS and borderline SIDS cases. The definition of SIDS requires a negative history as well as a negative autopsy result. Thus, the following variables were analysed: circumstances, medical history and autopsy, which included a gross pathological investigation, histology, neuropathology, microbiology, radiology and toxicology. In diagnosing deaths due to disease, histology, neuropathology and microbiology were the most important diagnostic tools. In contrast, information about the circumstances of death and the gross pathological findings at autopsy most often revealed the cause of death in accidents and cases of neglect/abuse and homicide. Following the drop in SIDS rate in Norway after 1989, the share of pure SIDS in proportion to the total population of sudden unexpected deaths in infancy and early childhood has decreased. The increasing proportion of non-SIDS and borderline SIDS cases presents a challenge to improve the quality of the investigation in cases of sudden death in infancy and early childhood.

Age Distribution↗