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PubMed2002

Hunting for electrophiles that harm human DNA: Frits Sobels Award Lecture.

This lecture is dedicated to Frits Sobels and his farsighted vision on research directions in genetic toxicology. Some accomplishments by the author's research group in the area of cancer etiology research and pre-clinical drug safety evaluation are presented. Praziquantel, an antischistosomal drug, was found to be devoid of any genetic effects which determined the drug companies to proceed with further safety evaluation and marketing. This highly efficient life-saving drug is now in use world wide. Biomonitoring methods have been developed to quantitate carcinogens, their metabolites or DNA adducts in humans exposed environmentally and endogenously to genotoxic agents. The methods were applied in ecological and case-control studies aimed at establishing causal relationships between exposure and disease. Results from both field studies in Iran and laboratory investigations supported the hypothesis that opium use, in particular ingestion of its pyrolysates, may be a risk factor for esophageal cancer in this region, probably acting together with nutritional deficiencies and thermal injury. By applying the nitrosoproline (NPRO) test in ecological studies on esophageal cancer causation in China some support was obtained for the involvement of N-nitroso compounds. In inhabitants of high risk areas endogenous nitrosamine synthesis could be markedly reduced by ingestion of vitamin C. Ultrasensitive detection methods for etheno-DNA adducts, which are formed by lipid peroxidation products resulting from increased oxidative stress, have been developed. Known cancer risk factors such as metal storage, chronic inflammatory processes and a high omega-6 PUFA fat diet increased the background level of these miscoding DNA adducts many times. They were found to increase progressively in premalignant lesions of cancer-prone tissues of humans and rodents, probably contributing to the genetic instability that drives cells to malignancy. Etheno-DNA adducts are thus promising markers to verify the efficiency of chemopreventive measures in humans.

Animals↗
PubMed2002

The hunt for coeliac disease in primary care.

BACKGROUND: Serological screening suggests that most coeliac disease goes undetected. AIM: To determine how often coeliac disease is found in patients referred for gastroscopy by general practitioners. DESIGN: Testing of 9971 consecutive patients referred to a single health centre for their first open-access gastroscopy over a 10-year period, without previously-diagnosed coeliac disease or dermatitis herpetiformis. METHODS: Endoscopy and routine duodenal biopsy were in use throughout the study period. The occurrence of coeliac disease was evaluated in patients with dyspepsia, in those with regurgitation, and in those with symptoms suggestive of coeliac disease. RESULTS: Altogether, 147 (1.47%) patients had coeliac disease: 18/2974 (0.61%) with regurgitation, 41/5347 (0.77%) with dyspepsia, and 88/1650 (5.33%) with suspected coeliac disease. Increasing age reduced the risk very slightly (OR 0.98; 95%CI 0.97-0.99). Risk was significantly increased when there was a suspicion of coeliac disease (OR 9.085; 95%CI 5.371-15.369), while no difference was found between patients with dyspepsia and those with reflux disease (OR 1.33; 95%CI 0.75-2.34). The risk in women was not increased (OR 0.97; 95%CI 0.69-1.38). DISCUSSION: In this primary-care setting, <1% of patients with upper abdominal symptoms suffered from coeliac disease; population-based serological screening is expected to yield a corresponding prevalence. When physicians had suspected coeliac disease, the condition was nine times more common.

Adolescent↗
PubMed2006

Mice, humans and haplotypes--the hunt for disease genes in SLE.

Defining the polymorphisms that contribute to the development of complex genetic disease traits is a challenging, although increasingly tractable problem. Historically, the technical difficulties in conducting association studies across the entire human genome are such that murine models have been used to generate candidate genes for analysis in human complex diseases, such as SLE. In this article we discuss the advantages and disadvantages of this approach and specifically address some assumptions made in the transition from studying one species to another, using lupus as an example. These issues include differences in genetic structure and genetic organisation which are a reflection on the population history. Clearly there are major differences in the histories of the human population and inbred laboratory strains of mice. Both human and murine genomes do exhibit structure at the genetic level. That is to say, they comprise haplotypes which are genomic regions that carry runs of polymorphisms that are not independently inherited. Haplotypes therefore reduce the number of combinations of the polymorphisms in the DNA in that region and facilitate the identification of disease susceptibility genes in both mice and humans. There are now novel means of generating candidate genes in SLE using mutagenesis (with ENU) in mice and identifying mice that generate antinuclear autoimmunity. In addition, murine models still provide a valuable means of exploring the functional consequences of genetic variation. However, advances in technology are such that human geneticists can now screen large fractions of the human genome for disease associations using microchip technologies that provide information on upwards of 100,000 different polymorphisms. These approaches are aimed at identifying haplotypes that carry disease susceptibility mutations and rely less on the generation of candidate genes.

Animals↗
PubMed2004

Hunting for the mutation in inherited thrombophilia.

Mutation detection in inherited thrombophilia remains largely confined to the research laboratory. However, there are specific situations when investigating the genetic defect causing thrombophilia can provide additional useful clinical information. This review discusses the value of genetic analysis in the common inherited thrombophilias.

Antithrombins↗
PubMedDate not supplied

Yes, an Easter egg hunt!

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Education, Nursing, Baccalaureate↗
PubMed2002

Chickenpox and the geniculate ganglion: facial nerve palsy, Ramsay Hunt syndrome and acyclovir treatment.

Facial nerve palsy has long been considered to have an infectious etiology. Recent diagnostic analyses in children and adults have provided convincing evidence that reactivation of varicella-zoster virus (VZV), sometimes during infectious mononucleosis, can lead to cranial nerve VII palsy. The site of reactivation from latency is the geniculate ganglion. Virus most likely enters the ganglion during chickenpox, via the sensory branches of the facial nerve located on the ear and tongue. Retrospective reviews suggest that patients with VZV-related facial nerve palsy have poorer outcomes than other cases of Bell's palsy. Therefore treatment with acyclovir is suggested when VZV reactivation i slikely.

Adult↗
PubMed1991

Hunting accidents.

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Accident Prevention↗
PubMed2002

Treasure hunting in a new era: genotyping of single nucleotide polymorphisms and the search for complex disease genes by association scans.

Genotyping single nucleotide polymorphisms by technologies like those described in this issue are propelling us towards a new era in the study of human genetics. This new era promises improved prospects for mapping genes responsible for complex human diseases and other complex traits. In this article, I sketch empirical results and statistical theory that together form the scientific rationale for anticipating enhanced success in gene mapping in the new era that is now approaching.

Genetic Diseases, Inborn↗
PubMed2004

Inflammatory bowel disease gene hunting by linkage analysis: rationale, methodology, and present status of the field.

Observed inflammatory bowel disease (IBD) familial clustering and increased monozygotic twin concordance has led to the hypothesis that genetic loci containing IBD susceptibility genes can be identified by whole genome linkage mapping approaches. Methodology including collecting carefully phenotyped multiplex pedigrees, genotyping using highly informative microsatellite markers and linkage analysis by non-parametric allele sharing methods has been established. Eleven published genome wide screens (GWS) have studied more than 1,200 multiplex IBD pedigrees. Two-thirds of affected relative pairs were Crohn's disease (CD), 20% ulcerative colitis (UC) and the remaining were mixed. Seven loci (IBDI-7) on chromosomes 16q, 12, 6p, 14q, 5q, 19, and 1p have been identified with genome wide significant and independently replicated linkage. Risk alleles/haplotypes have been defined for the IBD1 (CARD15/NOD2), IBD3 (HLA) and IBD5 (5q cytokine cluster) loci. There has been evidence for a second chromosome 16 locus (IBD8) independent of NOD2 that overlaps IBD1 on the pericentromeric p-arm. Several other regions show great promise for containing additional IBD loci, particularly chromosome 3p with genome wide evidence in one study at 3p26 and more centromeric evidence in several other studies, and chromosomes 2q, 3q, 4q, 7, 11p, and Xp each with suggestive evidence of linkage in one and additional evidence in two or more studies. Single GWSs and fine mapping studies containing very large sets of pedigrees and in particular, more UC pedigrees, and the use of creative analytic and disease stratification schemes are required to identify, establish and refine weaker IBD loci.

Colitis, Ulcerative↗
PubMed2004

New approaches to gene hunting in IBD.

Without a doubt, one of the greatest promises of the human genome project has been the expectation that its completion will rapidly accelerate the discovery of the heritable components of complex disease. Such discoveries will educate us as to the underlying causes of disease and hold out great promise for medicine in the future by potentially enabling the prediction of individual risk, the selection of therapy based on genetic profile, and a more rational approach to designing drugs. Unfortunately, discovering these genetic components of complex disease has been much more difficult than initially hoped and, to date, very few positive results have been conclusively confirmed. We review here approaches to tackling the problem of gene finding in complex disease with an emphasis on new approaches that may complement and supplement existing methods that have been making only slow progress toward the elucidation of the genetic architecture of disease. Along the way we highlight the successful work by many groups in studying the genetics of IBD, where significant successes have arrived earlier than in most other complex human diseases.

Chromosome Mapping↗
PubMed2006

Incidence of musculoskeletal complaints in a large adult Norwegian county population. The HUNT Study.

STUDY DESIGN: Cross-sectional study. Between 1995 and 1997, all inhabitants aged 20 years and older in the Nord-Trøndelag county in Norway were invited to fill in 2 different questionnaires at different times concerning musculoskeletal complaints. OBJECTIVE: To estimate the incidence of musculoskeletal complaints lasting at least 15 days during the past month at 9 different anatomic sites in relation to age and gender. SUMMARY OF BACKGROUND DATA: Incidence data of musculoskeletal complaints are scarce. METHODS: Individuals who reported no musculoskeletal complaints lasting for at least 3 months during the past year were defined as a population at risk and were subjects for the incidence estimates. RESULTS: Of 49,720 individuals (response rate 53.5%), the overall age-adjusted incidence of musculoskeletal complaints was 7.9% (95% confidence interval 7.5% to 8.2%) (women: 7.1%, men: 8.7%). The highest incidence rate was found for the lower back (women: 2.3%, men: 2.8%). The incidence of spinal complaints declined after age 60 years, whereas the incidence of complaints in lower limbs and distal upper limbs tended to be stable or increase in the older age groups. CONCLUSIONS: In this, to our knowledge, first large-scale population-based study evaluating the incidence of musculoskeletal complaints, nearly 1 in 12 individuals reported musculoskeletal complaints lasting at least 15 days during the past month.

Adult↗
PubMed2006

A single weekly bout of exercise may reduce cardiovascular mortality: how little pain for cardiac gain? 'The HUNT study, Norway'.

BACKGROUND: The observation that exercise training reduces cardiovascular mortality is robust and consistent, but the amount and intensity of exercise that is required for risk reduction is not yet resolved. METHODS: We studied the association between the amount and intensity of exercise and cardiovascular mortality in 27 143 men and 28 929 women who were free from known cardiovascular disease at the beginning of follow-up between 1984 and 1986. The relative risk of death was calculated as the rate of death among participants within a given physical activity category compared with the rate of death in the reference category (no physical activity). We used Cox regression analysis to adjust for age and other potentially confounding factors. RESULTS: After 16 years (SD 4 years) of follow-up, 2946 men (10.8%) and 2486 women (8.6%) had died from ischaemic heart disease or stroke. A single weekly bout of exercise of high intensity reduced the risk of cardiovascular death, both in men [relative risk (RR) 0.61, 95% confidence interval (CI) 0.49-0.75], and women (RR 0.49, 95% CI 0.27-0.89), compared with those who reported no activity. There was no additional benefit from increasing the duration or the number of exercise sessions per week. The risk reduction related to exercise increased with increasing age in men, but not in women. CONCLUSION: These results challenge the current recommendation that expenditure of at least 1000 kcal per week is required to achieve exercise-induced protection against premature cardiovascular mortality.

Adult↗