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- Danielsson, C, et al.
(författare)
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Is Cardiac Arrhythmia in the Human Embryo a Possible Mechanism for Cardiovascular Defects by I-Kr Blocking Antidepressants? in BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, vol 91, issue 5, pp 345-345
- 2011
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Ingår i: BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY. - : WILEY-BLACKWELL, COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA. ; , s. 345-345
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Konferensbidrag (refereegranskat)abstract
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- Skold, A C, et al.
(författare)
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Translational Research: Electrophysiological Development in the Embryonic Heart of Rats, Rabbits, and Humans in BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY, vol 91, issue 5, pp 357-357
- 2011
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Ingår i: BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY. - : WILEY-BLACKWELL, COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA. ; , s. 357-357
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Konferensbidrag (refereegranskat)abstract
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- Esbjörnsson, M, et al.
(författare)
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Muscle fibre types and enzyme activities after training with local leg ischaemia in man.
- 1993
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Ingår i: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 148:3, s. 233-41
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Tidskriftsartikel (refereegranskat)abstract
- Eight healthy men performed supine one-legged training on a bicycle ergometer 45 min per leg four times per week for 4 week. The ergometer and lower body were inside a pressure chamber, the opening of which was sealed at the level of the crotch. One leg trained with impeded leg blood flow (I-leg), induced by an increased (50 mmHg) chamber pressure, at the highest tolerable intensity. The contralateral leg trained at the same power under normal pressure (N-leg). Before and after training biopsies were taken from the vastus lateralis of both legs and maximal one-legged exercise tests were executed with both legs. Biopsies were repeated when the subjects had been back to their habitual physical activity for 3 months. Training increased exercise time to exhaustion, but more in the I-leg than in the N-leg. After training, the I-leg had higher activity of citrate synthase (CS), a marker of oxidative capacity, and lower activity of the M-subunit of lactate dehydrogenase isoenzymes. It also had a higher percentage of type-I fibres and a lower percentage of IIB fibres, larger areas of all fibre types and a greater number of capillaries per fibre. It is concluded that ischaemic training changes the muscle metabolic profile in a direction facilitating aerobic metabolism. An altered fibre-type composition may contribute, but is not enough prerequisite for the change.
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- Kaijser, L., et al.
(författare)
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Muscle oxidative capacity and work performance after training under local leg ischemia
- 1990
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 69:2, s. 785-787
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Tidskriftsartikel (refereegranskat)abstract
- Healthy young men executed supine one-legged cycle training four times per week for 4 wk with legs and the cycle ergometer inside a pressure chamber, the opening of which was sealed by a rubber membrane at the level of the crotch. Each training session started by training one leg under ischemic conditions induced by increased chamber pressure (50 mmHg) at the highest intensity tolerable for 45 min. Then the other leg was trained with the same power profile but normal atmospheric chamber pressure. Before and after the training period, both legs executed one-legged exercise tests under both normal and increased chamber pressure and muscle biopsies were taken from the vastus lateralis. Ischemic training increased performance more than normal training, the difference being greater for exercise executed under ischemic conditions. The difference in performance increase between the legs was paralleled by a greater muscle citrate synthase activity in the ischemically than in the normally trained leg.
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- Andersson, Bert, 1952, et al.
(författare)
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Angiotensin-II type 1 receptor gene polymorphism and long-term survival in patients with idiopathic congestive heart failure.
- 1999
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Ingår i: European journal of heart failure. - 1388-9842. ; 1:4, s. 363-9
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Tidskriftsartikel (refereegranskat)abstract
- It has been suggested that a genetic polymorphism in the angiotensin II type 1 receptor gene (ATRG) and the ACE gene DD genotype might have a synergistic influence on the risk of developing cardiovascular disease.To study the possible interaction between polymorphisms in the ACE gene and the ATRG, regarding survival and left ventricular function.Polymorphism of the two genes was studied in a population-based cohort of 194 patients with idiopathic heart failure, recruited from the western part of Sweden 1985-1988. The patients were investigated by echocardiography. The survival status was checked during the 7-year follow-up period.Although there was no statistically significant additive risk of the ATRG polymorphism, patients carrying the ACE gene DD genotype in combination with a C allele of the ATRG tended to have a poorer prognosis. DD +AA, OR 1.24 (95% CI 0.67-2.32, P = 0.49); DD +AC, OR 1.64 (95% CI 0.95-2.83, P = 0.08); DD + CC, OR 3.54 95% CI 0.78-16.1, P = 0.10); DD +AC/CC, OR 1.84 (95% CI 1.10-3.08, P = 0.02). Patients with the DD +AC/CC genotypes tended to have lower ejection fraction and increased left ventricular mass.There was a trend toward a worse prognosis in patients with the combination of a C-allele in the ATRG and the ACE gene DD genotype, suggesting an interaction of these two genetic polymorphisms on disease severity.
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- Andersson, Bert, 1952, et al.
(författare)
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The DD genotype of the angiotensin-converting enzyme gene is associated with increased mortality in idiopathic heart failure.
- 1996
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Ingår i: Journal of the American College of Cardiology. - : Elsevier BV. - 0735-1097. ; 28:1, s. 162-7
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to investigate the association between the homozygous DD (deletion) genotype of the angiotensin-converting enzyme gene and survival and cardiac function in patients with idiopathic congestive heart failure.The DD genotype gene is a linkage marker for an etiologic mutation at or near the angiotensin-converting enzyme gene and has been associated with increased risk for the development of coronary artery disease, left ventricular hypertrophy and left ventricular dilation after myocardial infarction. We investigated the association between this angiotensin-converting enzyme genotype and mortality in a population-based cohort of patients with idiopathic congestive heart failure.The genotype was determined in 193 patients recruited from a large unselected population of patients with congestive heart failure (n = 2,711). The patients were studied with echocardiography, and survival data were obtained after 5 years of follow-up. A control group from the general population (n = 77) was studied by a similar procedure.The frequency of the D allele was not significantly different in the study and control groups (0.57 vs 0.56, p = NS). Long-term survival was significantly worse in the patients with the DD genotype than in the remaining patients (5-year survival rate 49% vs. 72%, p = 0.0011 as assessed by log rank test). The independent importance of the DD genotype for prognosis was verified by a multivariate Cox proportional hazards analysis, by which the odds ratio for mortality and the DD genotype was 1.69 (95% confidence interval 1.01 to 2.82). The only significant difference in cardiac function data between the two groups was an increase in left ventricular mass index in the DD group (153 +/- 57 vs 134 +/- 44 g/m2, p = 0.019).Angiotensin-converting enzyme gene DD polymorphism was associated with poorer survival and an increase in left ventricular mass in patients with idiopathic heart failure. The results suggest a possible pathophysiologic pathway between angiotensin-converting enzyme gene polymorphism, angiotensin-converting enzyme activity, myocardial hypertrophy and survival. Therefore, the DD genotype may be a marker of poor prognosis in patients with congestive heart failure.
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- Axfors, Cathrine, et al.
(författare)
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Cohort profile : the Biology, Affect, Stress, Imaging and Cognition (BASIC) study on perinatal depression in a population-based Swedish cohort
- 2019
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Ingår i: BMJ Open. - : BMJ. - 2044-6055. ; 9:10
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: With the population-based, prospective Biology, Affect, Stress, Imaging and Cognition (BASIC) cohort, we aim to investigate the biopsychosocial aetiological processes involved in perinatal depression (PND) and to pinpoint its predictors in order to improve early detection.PARTICIPANTS: From September 2009 to November 2018, the BASIC study at Uppsala University Hospital, Sweden, has enrolled 5492 women, in 6478 pregnancies, of which 46.3% first-time pregnancies and with an average age of 31.5 years. After inclusion around gestational week 16-18, participants are followed-up with data collection points around gestational week 32, at childbirth, as well as three times postpartum: after 6 weeks, 6 months and 1 year. At the last follow-up, 70.8% still remain in the cohort.FINDINGS TO DATE: In addition to internet-based surveys with self-report instruments, participants contribute with biological samples, for example, blood samples (maternal and from umbilical cord), biopsies (umbilical cord and placenta) and microbiota samples. A nested case-control subsample also takes part in cognitive and emotional tests, heart rate variability tests and bioimpedance tests. Subprojects have identified various correlates of PND of psychological and obstetric origin in addition to factors of the hypothalamic-pituitary-adrenal axis and immune system.FUTURE PLANS: In parallel with the completion of data collection (final follow-up November 2019), BASIC study data are currently analysed in multiple subprojects. Since 2012, we are conducting an ongoing follow-up study on the participants and their children up to 6 years of age (U-BIRTH). Researchers interested in collaboration may contact Professor Alkistis Skalkidou (corresponding author) with their request to be considered by the BASIC study steering committee.
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- Celsing, F, et al.
(författare)
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Effects of chronic iron deficiency anaemia on myoglobin content, enzyme activity, and capillary density in the human skeletal muscle.
- 1988
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Ingår i: Acta medica Scandinavica. - 0001-6101. ; 223:5, s. 451-7
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Tidskriftsartikel (refereegranskat)abstract
- The influence of chronic iron deficiency anaemia on myoglobin content, maximal enzyme activities and capillarization in the human skeletal muscle was investigated. Muscle samples from musculus vastus lateralis were screened in an Indonesian population. The causes of iron deficiency were chronic intestinal bleeding or repeated pregnancy combined with low iron intake. The maximal activities of iron-dependent and non-iron-dependent glycolytic and oxidative enzymes as well as myoglobin showed similar values in the iron-deficient group and the matched control group. The activities of the oxidative enzymes in both the iron-deficient group and the controls were lower, however, compared even to untrained Swedish subjects. The capillary density was essentially within a normal range in both groups. It is concluded that chronic iron deficiency anaemia of a moderate or severe degree, with Hb concentrations of about 80-100 g.1(-1), does not cause an impaired biochemical function of the human skeletal muscle.
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- Comasco, Erika, et al.
(författare)
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Postpartum depression symptoms : a case-control study on monoaminergic functional polymorphisms and environmental stressors
- 2011
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Ingår i: Psychiatric Genetics. - 0955-8829 .- 1473-5873. ; 21:1, s. 19-28
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:Postpartum depression (PPD) is an under diagnosed and under treated mood disorder, with negative impact on both the mother and the infant's health. The aim of this study is to examine whether genetic variations in the monoaminergic neurotransmitter system, together with environmental stressors, contribute to the development of PPD symptoms.METHODS:This nested case-control study included 275 women from a population-based cohort of delivering women in Sweden. A questionnaire containing the Edinburgh Postnatal Depression Scale was collected at 6 weeks and 6 months postpartum. Three functional polymorphisms were genotyped, catechol-O-methyltransferase (COMT)-ValMet, monoamine oxidase A (MAOA)-upstream variable number tandem repeat (uVNTR) and serotonin transporter linked polymorphic region (5HTT-LPR). Stressful life events, maternity stressors and previous psychiatric contact were considered as potential risk factors.RESULTS:COMT-ValMet was significantly associated with PPD symptoms at 6 weeks, but not at 6 months postpartum. A significant gene-gene interaction effect was present between COMT-ValMet and MAOA-uVNTR. In a gene-environment multivariate model, COMT-ValMet, psychiatric contact and maternity stressors were significantly associated with PPD symptoms. Among those with history of psychiatric problems, the COMT-ValMet and 5HTT-LPR risk variants were associated with PPD symptoms, whereas in the absence of previous psychiatric contact only maternity stressors were related to PPD symptoms.CONCLUSION:The interaction effect between monoaminergic genes and environmental stressors is likely to contribute to vulnerability for PPD. The different patterns of association according to history of psychiatric problems, if replicated, might be helpful in screening strategies.
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- Comasco, Erika, et al.
(författare)
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Postpartum depressive symptoms and the BDNF Val66Met functional polymorphism: effect of season of delivery :
- 2011
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Ingår i: Archives of Women's Mental Health. - : Springer Science and Business Media LLC. - 1434-1816 .- 1435-1102. ; 14:6, s. 453-463
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Tidskriftsartikel (refereegranskat)abstract
- Postpartum depression (PPD) is an often underdiagnosed and undertreated mood disorder, with negative impact on the mother's and infant's health. Seasonal variation has been discussed as a risk factor for PPD. Candidate genes, such as those encoding for the brain-derived neurotrophic factor (BDNF), serotonin transporter (5-HTT), and Period2 (PER2), have been associated with depression and seasonal disorders. The present study is aimed to examine whether functional polymorphic variants, BDNF Val66Met, 5-HTTLPR, or PER2 SNP 10870, are associated with PPD symptoms and whether these genetic polymorphisms interact with season in predicting PPD symptoms. This case-control study comprised of 275 women from a population-based cohort of delivering women in Sweden, who completed a questionnaire containing the Edinburgh postnatal depression scale (EPDS) at 6 weeks and 6 months postpartum. Stressful life events (SLEs) and maternity stressors were also assessed. The results did not reveal any statistically significant overall association between the studied genetic polymorphisms and PPD symptoms. However, a significant association between BDNF Met66 carrier status and development of PPD symptoms at 6 weeks postpartum, even when controlling for prepartum and postpartum environmental risk factors, was evident among mothers delivering during autumn/winter. No gene-gene interactions were found but a cumulative effect was detected with carriers of a greater number of 5-HTTLPR S and BDNFVal66Met Met alleles reporting higher EPDS scores, if delivered during autumn/winter. Our findings propose a role of the BDNF gene in the development of PPD symptoms, potentially mediated by season of delivery.
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