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Biomedical subjects

L B Andersen

Publications and source records attributed to L B Andersen.

At least 55 records · Page 3Linked to original sources
PubMed1994

Dietary factors related to fitness in young men and women.

BACKGROUND: In a previous paper we reported an inverse relationship between fitness and serum lipids in this group of young subjects. The present study investigates whether a higher fitness level was associated with a more prudent diet and whether this contributed to the observed relationship between fitness and serum lipids. METHODS: The study sample, comprising 70 women and 49 men ages 23-27 years, was a subgroup of a large random sample. Aerobic fitness was measured directly as maximal oxygen uptake (ml O2 min-1 kg-1) and dietary intake as 7-day food records. RESULTS: The highest fitness tertile had an intake of dietary fiber higher than that of the lowest tertile (25.2 g/10 MJ vs 21.9 g/10 MJ, P < 0.05) and a lower intake of sucrose (7.2 E% vs 9.8 E%, P < 0.01), whereas total fat intake and the ratio between polyunsaturated and saturated fatty acids were similar (35.4 E% vs 36.5 E%, P > 0.05, 0.39 vs 0.34, P > 0.05, respectively). No differences were observed in intake of alcohol, protein, and total carbohydrate. Multiple regression analyses showed no impact of dietary variables upon the relationship between serum lipids and fitness. CONCLUSIONS: Better fitness was associated with a better dietary composition with respect to dietary fiber and sucrose, but not to fat. The observed inverse relationship between fitness and serum lipids was not related to diet.

Adult↗
PubMed1994

Blood pressure, physical fitness and physical activity in 17-year-old Danish adolescents.

OBJECTIVE: To test the relationship between physical activity and physical fitness, and the relationship between these variables and the primordial risk factor blood pressure (BP). DESIGN: A cross-sectional study of all Danish pupils in the same grade at 'gymnasium' (the Danish upper secondary school). SETTING: Tests and questionnaires were administered by physical education and biology teachers according to a prescribed scheme. SUBJECTS: Study subjects were 13810 adolescents with a mean age of 17.1 years. Physical activity, smoking habits, and physical performance were measured in 4862 boys and 6573 girls. Blood pressure was measured in 2474 boys and 3535 girls. No difference was found in BP, physical activity and fitness variables between this group and a representative group of Danish school children at the same age. MAIN OUTCOME: Blood pressure and health-related physical performance such as strength, muscle endurance, flexibility and maximal oxygen uptake (VO2max) estimated from heart rate at submaximal workload were measured. Sports activity, other physical activity and smoking habits were assessed by questionnaires. RESULTS: There was a negative relationship between BP and VO2max up to the 50% percentile (50 ml min-1 kg-1) in boys and up to the upper 80-90% percentile (45 ml min-1 kg-1) in girls. In a multiple regression model with BP as dependent variable, VO2max related highly significant, also after adjustment for body weight and physical activity (P < 0.001). Other performance variables only explained a small part of the variance in BP. No relationship was found between BP and total physical activity or sports activity. CONCLUSION: In the adolescent population VO2max related negatively to BP after adjustment for body weight, physical activity, other fitness measures and sex, but physical activity or other fitness measures did not relate. Lower blood pressure was found with higher VO2max until levels of 50 and 45 ml min-1 kg-1 in boys and girls, respectively.

Adolescent↗
PubMed1994

Changes in physical activity are reflected in changes in fitness during late adolescence. A 2-year follow-up study.

The study describe changes over 2 years in different physical fitness measures and the relationship between these changes and changes in physical activity. Maximal aerobic work capacity (Wattmax), functional strength, muscle endurance, agility and flexibility were measured in 259 randomly selected high school boys and girls 16.5 years of age and followed-up 2 years later, while they still attended school. Most physical fitness measures increased over time in boys, and in girls an increase was found in arm extensor strength and trunk extensor endurance, but Wattmax per kg body mass decreased. Changes in physical performance between 16 and 18 years of age seem to be very similar in different countries, despite differences in physical activity patterns and absolute level of performance. No change was found in time of participation in physical activity or sports activity in either gender, but fewer girls participated in leisure-time sports at the 2nd test (p < 0.001). Change in physical activity or sports activity did not relate to change in physical fitness level. The relationships between level of sports participation (competition, for health or none) and physical fitness measures at baseline and at the 2nd test were weak or non-significant. Three explanations for the weak relationship between physical activity and fitness are suggested: (A) part of the variability in fitness is explained by genetics, (B) growth and hormonal changes, especially in boys, override the stimulus of training, and (C) the physical fitness level in adolescents is so high that only physical activity at high relative intensity is supposed to have an effect on the fitness level.

Adolescent↗
PubMed1994

Changes in CHD risk factors with age: a comparison of Danish adolescents and adults.

In 1983 a representative sample of Danish adolescents 16-19 yr of age were selected to participate in a study to determine risk profile for coronary heart disease. Eight years later (1991), we performed a follow-up study of the same participants 23-27 yr of age to compare risk factors. In the young adults power was generally high, 48.0 (SD +/- 7.8) and 39.6 (SD +/- 6.5) ml.min-1.kg-1 for men and women, respectively. Only 30% of the men and 26% of the women did not regularly participate in sport activities. Seventy-five percent of both genders bicycled daily, 50% of the men and 42% of the women as their daily transportation year round. Twenty percent, more men than women, were considered to be inactive. Women had a higher ratio of HDL-C/C than men (0.32 for women vs 0.26 for men). Mean values for blood pressure were 134/83 mm Hg and 122/78 mm Hg for men and women, respectively. Thirty-eight percent of the men and 10% of the women had an elevation above 140/90 mm Hg in either systolic blood pressure (SBP) or diastolic blood pressure (DBP). Cholesterol levels were high (10%) when compared with the U.S. population, but triglyceride levels were substantially lower (40%). Comparing the 1991 adults with the 1983 adolescents, the ranges were wider. In conclusion, the risk factor profile changes in men were less favorable than the profile for women; the changes in high risk groups were larger than changes in mean values.

Adolescent↗
PubMed1993

Maximal oxygen uptake, maximal voluntary isometric contraction and physical activity in young Danish adults.

In a randomly selected sample of 88 men and 115 women, aged 23-27 years from Denmark, maximal oxygen uptake (VO2max), maximal voluntary isometric contraction (MVC) in four muscle groups and physical activity were studied. The VO2max was 48.0 ml.min-1.kg-1 and 39.6 ml.min-1.kg-1 for the men and the women, respectively. The MVC was 10% lower than in a comparable group of Danes of the same age and height studied 35 years ago. Only in men was sports activity directly related to VO2max (ml.min-1.kg-1; r = 0.31, P < 0.01). The MVC of the knee extensors was related to VO2max in the men (r = 0.31, P < 0.01), but there was no relationship between the other measurements of MVC and VO2max. In the women VO2max (ml.min-1.kg-1) was only related to body size, i.e. body mass index, percentage body fat and body mass [(r = -0.47, -0.48 (both P < 0.001) and -0.34 (P < 0.01), respectively)]. There were differences in VO2max in the men, according to education and occupation. Blue collar workers and subjects attending vocational or trade schools in 1983 had lower VO2max, and more of them were physically inactive. In the women differences were also found, but there was no clear pattern among the groups. More of the women participated regularly in sports activity, but more of the men were very active compared to the women.

Adult↗
PubMed1993

An EcoRI RFLP in the 5' region of the human NF1 gene.

Von Recklinghausen neurofibromatosis or type 1 neurofibromatosis (NF1), is one of the most common autosomal dominant disorders. NF1 is characterized by neurofibromas, café-au-lait spots and Lisch nodules of the iris. The NF1 gene is located in 17q11.2. The restriction fragment length polymorphism reported here will be useful in linkage analysis in NF1 families.

Alleles↗
PubMed1993

Mutations in the neurofibromatosis 1 gene in sporadic malignant melanoma cell lines.

Neurofibromatosis type 1 (NF1) is a common autosomal dominant disorder characterized by progressive and variable involvement of tissues predominantly derived from the neural crest and a predisposition toward malignancies. The NF1 gene encodes neurofibromin, a GTPase-activating protein containing a GAP-related domain (NF1-GRD) that is capable of down-regulating ras by stimulating its intrinsic GTPase activity. We report a homozygous deletion of most of NF1 in one of eight malignant melanoma cell lines leading to loss of detectable mRNA and protein, as well as the apparent absence of protein and mRNA in another melanoma. This data suggests that NF1 can function as a tumour suppressor gene in the development or progression of malignant melanoma.

Chromosome Mapping↗
PubMed1993

An alternatively-spliced mRNA in the carboxy terminus of the neurofibromatosis type 1 (NF1) gene is expressed in muscle.

The gene for neurofibromatosis type 1 (NF1) was identified by positional cloning and found to contain two alternatively spliced exons. The first described alternatively spliced exon (exon 23a) is located within the GAP-related domain of the gene and inserts an additional 63 nucleotides into the NF1 mRNA. The second alternatively spliced exon (exon 48a) is located near the extreme carboxy terminus of the gene and inserts an additional 54 nucleotides into the mRNA. This second isoform, termed 3'ALT, was originally detected while screening a fetal brain cDNA library. Examination of its expression by reverse-transcribed RNA PCR demonstrates high level of expression in cardiac muscle, skeletal muscle and smooth muscle. Trace levels of expression are detected in brain and nerve. The 3'ALT isoform is expressed in fetal cardiac muscle, adult left ventricle and cardiac Purkinje cells. Further confirmation of the existence of this isoform was obtained by blotting the PCR products with a radiolabeled oligonucleotide entirely derived from sequences contained within exon 48a and by direct sequencing of the PCR products. Additionally, this isoform is expressed in muscle tissues from other vertebrate species. The expression of this isoform in muscle suggests that the NF1 gene may play additional tissue-specific roles in muscle development and signal transduction.

Alternative Splicing↗
PubMed1993

Tracking of cardiovascular disease risk factors including maximal oxygen uptake and physical activity from late teenage to adulthood. An 8-year follow-up study.

OBJECTIVES: The aim of the study was to analyse changes in coronary heart disease (CHD) risk factors from adolescence to young adulthood, and how changes in risk factors relate to changes in lifestyle. DESIGN: A randomized sample of school children was tested in 1983 and followed-up 8 years later. In 1983 a dropout of 0.7% was found and the sample was representative of 16-19-year-old Danes. SUBJECTS: Subjects followed-up 8 years later (two-thirds of the original sample) were 88 male and 115 female 15-19-year-old school children attending 18 high schools, nine vocational and nine trade schools, throughout Denmark. MAIN OUTCOME MEASURES: Height, body weight, body fat, occupation and coronary heart disease risk factors including physical activity (PA), fitness, blood pressure (BP), serum cholesterol, HDL cholesterol, triglyceride (TG) and smoking habits were assessed. RESULTS: In males all risk factors increased: the increases in total cholesterol level and systolic and diastolic BP were large, 0.85 mmol l-1 and 11 mmHg, respectively. In females, the risk for some factors increased (total cholesterol and BP), others decreased (higher HDL cholesterol), and triglyceride did not change. Significant tracking was found in both sexes, with the highest correlation coefficients in men. A total risk score was calculated by categorizing risk factors into six groups--1 to 6--and then adding the scores. Pearson correlation between the total risk scores in 1983 and 1991 in men was r = 0.67 (P < 0.001). Only a weak association was found for the total risk score in women. Nearly 50% of the boys, who were initially in the upper quintile of risk, were still in the upper quintile 8 years later for most risk factors. In men, the changes in risk factors were related to social factors. Blue-collar workers and the unemployed had the highest increase in risk factors, and the largest decrease in VO2max (ml min-1 kg-1) when analysed together. In both sexes the best relationship between 1983 and 1991 values was found in body mass index (BMI). Leisure time physical activity (PA) and triglyceride (TG) had a low correlation between 1983 and 1991 values. Physical activity had a non-significant correlation over time for women, indicating that PA in 1983 did not predict PA in 1991 at all. CONCLUSION: Coronary heart disease risk factors tracked in both males and females, but only in males was a strong relationship found for total risk from adolescence to young adulthood, indicating the influence of a poor lifestyle in high-risk men. Lower social status related to higher risk.

Adolescent↗
PubMed1993

A conserved alternative splice in the von Recklinghausen neurofibromatosis (NF1) gene produces two neurofibromin isoforms, both of which have GTPase-activating protein activity.

Sequence analysis has shown significant homology between the catalytic regions of the mammalian ras GTPase-activating protein (GAP), yeast Ira1p and Ira2p (inhibitory regulators of the RAS-cyclic AMP pathway), and neurofibromin, the protein encoded by the NF1 gene. Yeast expression experiments have confirmed that a 381-amino-acid segment of neurofibromin, dubbed the GAP-related domain (GRD), can function as a GAP. Using the RNA polymerase chain reaction with primers flanking the NF1-GRD, we have identified evidence for alternative splicing in this region of the NF1 gene. In addition to the already published sequence (type I), an alternative RNA carrying a 63-nucleotide insertion (type II) is present in all tissues examined, although the relative amounts of types I and II vary. The insertion is conserved across species but is not present in GAP, IRA1, or IRA2. GenBank searches have failed to identify significant similarity between the inserted sequence and known DNA or protein sequences, although the basic amino acid composition of the insertion shares features with nuclear targeting sequences. Expression studies in yeasts show that despite the partial disruption of the neurofibromin-IRA-GAP homology by this insertion, both forms of the NF1-GRD can complement loss of IRA function. In vivo assays designed to compare the GAP activity of the two alternatively spliced forms of the NF1-GRD show that both can increase the conversion of GTP-bound ras to its GDP-bound form, although the insertion of the 21 amino acids weakens this effect. The strong conservation of this alternative splicing suggests that both type I and II isoforms mediate important biological functions of neurofibromin.

Amino Acid Sequence↗
PubMed1992

NF1-related locus on chromosome 15.

A neurofibromatosis type I (NF1)-related locus has been identified on chromosome 15. It contains a partial copy of the NF1 GAP-related domain, which is known to interact with the ras protooncogenes. However, the chromosome 15 sequence contains multiple deletions resulting in frameshift mutations and stop codons in several highly conserved sequence blocks. The locus on chromosome 15 therefore represents an NF1 pseudogene. This nonprocessed NF1 pseudogene may produce additional fragments in Southern blotting, pulsed-field gel, and PCR experiments with some NF1 cDNA probes or oligonucleotides. In addition, certain regions of the NF1 gene also cross-hybridize with a locus on chromosome 14. These loci must be considered in mutation analysis of patients with NF1 since aberrant findings may not always reflect changes in the NF1 gene.

Base Sequence↗
PubMed1992

A yeast artificial chromosome contig encompassing the type 1 neurofibromatosis gene.

The yeast artificial chromosome (YAC) system (Burke et al., 1987, Science 236: 806-812) allows the direct cloning of large regions of the genome. A YAC contig map of approximately 700 kb encompassing the region surrounding the type 1 neurofibromatosis (NF1) locus on 17q11.2 has been constructed. A single YAC containing the entire NF1 locus has been constructed by homologous recombination in yeast. In the process of contig construction a novel method of YAC end rescue has been developed by YAC circularization in yeast and plasmid rescue in bacteria. YACs containing homology to the NF1 region but mapping to another chromosome have also been discovered. Sequences of portions of the homologous locus indicate that this other locus is a nonprocessed pseudogene.

Base Sequence↗
PubMed1992

Neurofibromatosis in infantile autism and other types of childhood psychoses.

Recent findings have suggested that the simultaneous occurrence of neurofibromatosis and childhood psychosis might be more than a coincidence. In this study of 341 children with infantile autism and other types of childhood psychosis seen as inpatients in two university clinics of child psychiatry in a 25-year period, only one case (0.3%) of concomitant occurrence of the disorders was found, which is a frequency no higher than expected by chance.

Autistic Disorder↗
PubMed1991

A de novo Alu insertion results in neurofibromatosis type 1.

Neurofibromatosis type 1 (NF1) is a common autosomal dominant disorder with a high mutation rate and variable expression, characterized by neurofibromas, café-au-lait spots, Lisch nodules of the iris, and less frequent features including bone deformities and learning disabilities. The recently cloned NF1 gene encodes a transcript of 13 kilobases from a ubiquitously expressed locus on chromosome 17. Most NF1 patients are expected to have unique mutations, but only a few have so far been characterized, restricting genetic and functional information and the design of DNA diagnostics. We report an unusual NF1 mutation, that of a de novo Alu repetitive element insertion into an intron, which results in deletion of the downstream exon during splicing and consequently shifts the reading frame. This previously undescribed mechanism of mutation indicates that Alu retrotransposition is an ongoing process in the human germ line.

Adult↗
PubMed1991

Molecular and cytogenetic analysis of tumors in von Recklinghausen neurofibromatosis.

Von Recklinghausen neurofibromatosis (NF1) is a common autosomal dominant disorder mapped to 17q11.2 and typically characterized by the occurrence of neural crest-derived tumors. The gene has recently been cloned using reverse genetics or "positional cloning" approaches. Its function, however, remains unknown. We have performed cytogenetic and molecular analyses on 9 malignant tumors from NF1 patients to look for loss of alleles or chromosome rearrangements involving chromosome 17 to test the hypothesis that the NF1 gene acts as a recessive "tumor suppressor" gene. Loss of alleles on this chromosome was detected for 3 of 9 malignant tumors. Two peripheral nerve sheath tumors showed allele loss at informative loci on both the long and short arms of chromosome 17. In contrast, a glioblastoma with focal gliosarcoma showed loss of heterozygosity on the short arm of chromosome 17 only, and not at loci on the long arm. One nerve sheath tumor was previously shown by direct sequence analysis to have a point mutation at the TP53 locus at 17p13. These data support a role for the TP53 gene or other genes on the short arm of chromosome 17 in at least some malignancies in NF1. Six other neurofibrosarcomas showed no allele loss at informative loci on chromosome 17. Cytogenetic analysis was performed on 7 tumors, including 2 with allele loss. The two tumors with allele loss showed abnormal karyotypes while all others were normal. Southern blot and pulsed-field gel analysis using probes within or closely linked to the NF1 locus detected no gross deletions or rearrangements in the tumors studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗