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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cardiac and Cardiovascular Systems) ;lar1:(hkr)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cardiac and Cardiovascular Systems) > Högskolan Kristianstad

  • Resultat 1-10 av 18
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1.
  • Persson, Christina, 1985, et al. (författare)
  • Cardiovascular risk factors in relation to dietary patterns in 50-year-old men and women: a feasibility study of a short FFQ
  • 2019
  • Ingår i: Public Health Nutrition. - : Cambridge University Press. - 1475-2727 .- 1368-9800. ; 22:4, s. 645-653
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: We aimed to assess the feasibility of a simple new fifteen-item FFQ as a tool for screening risk of poor dietary patterns in a healthy middle-aged population and to investigate how the results of the FFQ correlated with cardiovascular risk factors and socio-economic factors. DESIGN: A randomized population-based cross-sectional study. Metabolic measurements for cardiovascular risk factors and information about lifestyle were collected. A fifteen-item FFQ was created to obtain information about dietary patterns. From the FFQ, a healthy eating index was created with three dietary groups: good, average and poor. Multivariate logistic regression was used to assess relationships between dietary patterns and cardiovascular risk factors. SETTING: Sweden. SUBJECTS: Men and women aged 50 years and living in Gothenburg, Sweden. RESULTS: In total, 521 middle-aged adults (257 men, 264 women) were examined. With good dietary pattern as the reference, there was a gradient association of having obesity, hypertension and high serum TAG in those with average and poor dietary patterns. After adjustment for education and lifestyle factors, individuals with a poor dietary pattern still had significantly higher risk (OR; 95 % CI) of obesity (2.33; 1.10, 4.94), hypertension (2.73; 1.44, 5.20) and high serum TAG (2.62; 1.33, 5.14) compared with those with a good dietary pattern. CONCLUSIONS: Baseline data collected by a short FFQ can predict cardiovascular risk factors in middle-aged Swedish men and women. The FFQ could be a useful tool in health-care settings, when screening for risk of poor dietary patterns.
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2.
  • Lanke, E., et al. (författare)
  • Co-segregation of the PROS1 locus and protein S deficiency in families having no detectable mutations in PROS1
  • 2004
  • Ingår i: Journal of Thrombosis and Haemostasis. - : Wiley-Blackwell. - 1538-7933 .- 1538-7836. ; 2:11, s. 1918-1923
  • Tidskriftsartikel (refereegranskat)abstract
    • Inherited deficiency of protein S constitutes an important risk factor of venous thrombosis. Many reports have demonstrated that causative mutations in the protein S gene are found only in approximately 50% of the cases with protein S deficiency. It is uncertain whether the protein S gene is causative in all cases of protein S deficiency or if other genes are involved in cases where no mutation is identified. The aim of the current study was to determine whether haplotypes of the protein S gene cosegregate with the disease phenotype in cases where no mutations have been found. Eight protein S-deficient families comprising 115 individuals where previous DNA sequencing had failed to detect any causative mutations were analyzed using four microsatellite markers in the protein S gene region. Co-segregation between microsatellite haplotypes and protein S deficiency was found in seven of the investigated families, one family being uninformative. This suggests that the causative genetic defects are located in or close to the protein S gene in a majority of such cases where no mutations have been found.
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3.
  • Lanke, E., et al. (författare)
  • Genetic analysis of 31 Swedish type 1 von Willebrand disease families reveals incomplete linkage to the von Willebrand factor gene and a high frequency of a certain disease haplotype
  • 2005
  • Ingår i: Journal of Thrombosis and Haemostasis. - : Wiley-Blackwell. - 1538-7933 .- 1538-7836. ; 3:12, s. 2656-2663
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The most common type of von Willebrand disease (VWD), type 1, has in only a few cases been explained by an identified causative mutation in the von Willebrand factor (VWF) gene. The ABO blood group and other modifier loci outside the VWF gene may contribute to the development of type 1 VWD. OBJECTIVES AND METHODS: Our aim was to determine whether there was genetic linkage to the VWF gene in 31 Swedish type 1 VWD families. Stringent diagnostic criteria in accordance with ISTH guidelines were used. Genetic linkage was investigated by using two highly informative dinucleotide microsatellite markers, which we have recently identified, located in introns six and 15 of the VWF gene. We also investigated the existence of common disease haplotypes and the relation between type 1 VWD and ABO blood group. RESULTS: We found genetic linkage to the VWF gene in 27 (87%) of the families. However, in four (13%) of the families, there was clearly no genetic linkage. We found the 4751A>G (Tyr1584Cys) sequence variation in exon 28, which is a common mutation in the Canadian VWD population (14.3%), in only one of the 31 families (3.2%). A possible common mutation was identified in six of the 27 (22%) families with genetic linkage. Blood group O was over-represented among type 1 VWD patients. CONCLUSION: We conclude that there is linkage between the VWF gene and hereditary type 1 VWD in a majority of families.
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4.
  • Manderstedt, Eric, et al. (författare)
  • Genetic variation of the blood coagulation regulator tissue factor pathway inhibitor and venous thromboembolism among middle-aged and older adults: A population-based cohort study
  • 2022
  • Ingår i: Research and practice in thrombosis and haemostasis. - : Elsevier BV. - 2475-0379. ; 6:7
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Tissue factor is the main initiator of blood coagulation, and tissue factor pathway inhibitor (TFPI) is the primary inhibitor of the initiation of blood coagulation. The genetic variation of TFPI and the relation to venous thromboembolism (VTE), that is, venous thrombosis and pulmonary embolism, remains to be clarified. This exome sequencing study aimed to determine the molecular epidemiology of the TFPI gene and the relation to VTE in a large population-based cohort of middle-aged and older adults. Methods: The exomes of TFPI were analyzed for variants in 28,794 subjects without previous VTE (born 1923–1950, 60% women), who participated in the Malmö Diet and Cancer Study (1991–1996). Patients were followed until the first event of VTE, death, or 2018. Qualifying variants were defined as loss-of-function or nonbenign (PolyPhen-2) missense variants with minor allele frequency less than 0.1%. Results: No common variant was associated with VTE. Nine rare variants (two loss-of-function and seven nonbenign missense) were classified as qualifying and included in collapsing analysis. Prevalence of qualifying variants was 0.09%. Five individuals with VTE compared to 17 individuals without VTE carried one qualifying variant. Cox multivariate regression analysis adjusted for age, sex, body mass index, systolic blood pressure, smoking and alcohol consumption, rs6025, rs1799963, and ancestry showed a hazard ratio of 2.9 (95% CI, 1.2–7.1) for rare qualifying variants. Conclusion: Rare qualifying TFPI variants were associated with VTE, suggesting that rare variants in TFPI contribute to the development of VTE. The qualifying TFPI gene variants were very rare, suggesting a constrained gene. © 2022 The Authors. Research and Practice in Thrombosis and Haemostasis published by Wiley Periodicals LLC on behalf of International Society on Thrombosis and Haemostasis (ISTH).
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5.
  • Widen, Cecilia, et al. (författare)
  • Systemic inflammatory impact of periodontitis on acute coronary syndrome
  • 2016
  • Ingår i: Journal of Clinical Periodontology. - : Wiley. - 0303-6979 .- 1600-051X. ; 43:9, s. 713-719
  • Tidskriftsartikel (refereegranskat)abstract
    • AimA causative relationship between acute coronary syndrome (ACS) and periodontitis has yet to be defined. The aim of this study was to assess differences in levels of serum cytokines between individuals with or without ACS or periodontal comorbidity. Material and MethodsIn a case-control study, individuals with ACS (78 individuals, 10.3% females) and matching healthy controls (78 individuals, 28.2% females) were included. Medical and dental examinations were performed to diagnose ACS and periodontitis. Serum levels of cytokines were assessed, using Luminex technology. ResultsA diagnosis of periodontitis in the ACS and control group was diagnosed in 52.6% and 12.8% of the individuals, respectively. The unadjusted odds-ratio that individuals with ACS also had periodontitis was 7.5 (95% CI: 3.4, 16.8, p<0.001). Independent of periodontal conditions, individuals with ACS had significantly higher serum levels of IL8 (mean: 44.3 and 40.0pg/ml) and vascular endothelial growth factor (VEGF) (mean: 82.3 and 55.3pg/ml) than control individuals. A diagnosis of periodontitis made no difference in serum cytokine expressions. ConclusionElevated serum levels of VEGF were associated with ACS. Serum cytokine expression in individuals with ACS is unrelated to periodontal conditions.
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6.
  • Zöller, Bengt, et al. (författare)
  • Rare-variant collapsing and bioinformatic analyses for different types of cardiac arrhythmias in the UK Biobank reveal novel susceptibility loci and candidate amyloid-forming proteins
  • 2024
  • Ingår i: Cardiovascular Digital Health Journal. - : Elsevier Inc.. - 2666-6936. ; 5:1, s. 15-18
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Cardiac arrhythmias are a common health problem. Both common and rare genetic risk factors exist for cardiac arrhythmias. Cardiac amyloidosis is a rare disease that may manifest various arrhythmias. Few large-scale whole exome sequencing studies elucidating the contribution of rare variations to arrhythmias have been published. Objective: To access gene collapsing analysis of rare variations for different types of cardiac arrhythmias in UK Biobank. Identified genes were analyzed in silico for probability to form amyloid fibrils. Methods: We used 2 published UK Biobank portals (https://azphewas.com/ and https://app.genebass.org/) to access gene collapsing analysis of rare variations for different types of cardiac arrhythmias. Diagnosis of arrhythmia was based on the International Classification of Diseases, 10th Revision (ICD-10) codes: conduction disorders (I44, I45), paroxysmal tachycardia (I47), atrial fibrillation (I48), and other arrhythmias (I49). Results: Rare variations in 5 genes were linked to conduction disorders (SCN5A, LMNA, SMAD6, HSPB9, TMEM95). The TTN gene was associated with both paroxysmal tachycardia and other arrhythmias. Atrial fibrillation was associated with rare variations in 8 genes (TTN, RPL3L, KLF1, TET2, NME3, KDM5B, PKP2, PMVK). Two of the genes linked to heart conduction disorders were potential amyloid-forming proteins (HSPB9, TMEM95), while none of the 8 genes linked to other types of arrhythmias were potential amyloid-forming proteins. Conclusion: Rare variations in 13 genes were associated with arrhythmias in the UK Biobank. Two of the heart conduction disorder–linked genes are potential amyloid-forming candidates. Amyloid formation may be an underestimated cause of heart conduction disorders.
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7.
  • Halldén, Christer, et al. (författare)
  • Origin of Swedish hemophilia B mutations
  • 2013
  • Ingår i: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 11:11, s. 2001-2008
  • Tidskriftsartikel (refereegranskat)abstract
    • Background More than 1100 mutations that cause hemophilia B (HB) have been identified. At the same time, specific F9 mutations are present at high frequencies in certain populations, which raise questions about the origin of HB mutations. ObjectivesTo describe the mutation spectrum of all HB families in Sweden and investigate if mutations appearing in several families are due to independent recurrent mutations (RMs) or to a common mutation event (i.e. are identical by descent (IBD)). Patients/MethodsThe registered Swedish HB population consists of patients from 86 families. Mutations were identified by resequencing and identical haplotypes were defined using 74 markers and a control population of 285 individuals. The ages of IBD mutations were estimated using ESTIAGE. ResultsOut of 77 presumably unrelated patients with substitution mutations, 47 patients (61%) had mutations in common with other patients. Haplotyping of the 47 patients showed that 24 patients had IBD mutations (51%) with estimated ages of between two and 23 generations. A majority of these patients had mild disease. Eight of the 15 mutations observed in more than one family were C>T transitions in CpG sites and all eight were RMs. ConclusionsThe association of IBD mutations with a mild phenotype is similar to what has been previously observed in hemophilia A. Noteworthy features of the mutations that are common to more than one family are the equal proportions of patients with RM and IBD mutations and the correlation between the occurrence of RMs and C>T transitions at CpG sites.
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8.
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9.
  • Mäntylä, Päivi, et al. (författare)
  • Subgingival Aggregatibacter actinomycetemcomitans associates with the risk of coronary artery disease
  • 2013
  • Ingår i: Journal of Clinical Periodontology. - : Blackwell Munksgaard. - 0303-6979 .- 1600-051X. ; 40:6, s. 583-590
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim We investigated the association between angiographically verified coronary artery disease (CAD) and subgingival Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. Materials and Methods The cross-sectional study population (n = 445) comprised 171 (38.4%) patients with Stable CAD, 158 (35.5%) with acute coronary syndrome (ACS) and 116 (26.1%) with no significant CAD (No CAD). All patients participated in clinical and radiological oral health examinations. Pooled subgingival bacterial samples were analysed by checkerboard DNA–DNA hybridization assays. Results In all study groups, the presence of P. gingivalis, T. forsythia and T. denticola indicated a significant (p ≤ 0.001) linear association with the extent of alveolar bone loss (ABL), but A. actinomycetemcomitans did not (p = 0.074). With a threshold level of bacterial cells 1 × 105 A. actinomycetemcomitans was significantly more prevalent in the Stable CAD group (42.1%) compared to the No CAD group (30.2%) (p = 0.040). In a multi-adjusted logistic regression analysis using this threshold, A. actinomycetemcomitans positivity associated with Stable CAD (OR 1.83, 95% CI 1.00–3.35, p = 0.049), but its level or levels of other bacteria did not. Conclusions The presence of subgingival A. actinomycetemcomitans associates with an almost twofold risk of Stable CAD independently of alveolar bone loss.
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10.
  • Manderstedt, Eric, et al. (författare)
  • Thrombotic Risk Determined by Protein C Receptor (PROCR) Variants among Middle-Aged and Older Adults : A Population-Based Cohort Study
  • 2022
  • Ingår i: Thrombosis and Haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 122:8, s. 1326-1332
  • Tidskriftsartikel (refereegranskat)abstract
    • Background The protein C (PC) anticoagulant system has a key role in maintaining hemostatic balance. One missense (Ser219Gly) variant in the PC receptor (PROCR) was associated with venous thromboembolism (VTE) in genome-wide association studies. Objectives This study aimed to determine the thrombotic risk of rare and common PROCR variants in a large population-based cohort of middle-aged and older adults. Methods The exonic sequence of PROCR was analyzed for the Ser219Gly variant and other qualifying variants in 28,794 subjects (born 1923-1950, 60% women) without previous VTE, who participated in the Malmö Diet and Cancer study (1991-1996). Incidence of VTE was followed up until 2018. Qualifying variants were defined as loss-of-function or nonbenign (PolyPhen-2) missense variants with minor allele frequencies (MAFs) <0.1%. Results Re-sequencing identified 36 PROCR variants in the study population (26,210 non-VTE exomes and 2,584 VTE exomes), 11 synonymous, 22 missense, and three loss-of-function variants. Kaplan-Meier analysis of the known Ser219Gly variant (rs867186) showed that homozygosity for this variant increased the risk of disease, whereas heterozygosity showed no effect. Cox multivariate regression analysis revealed an adjusted hazard ratio (HR) of 1.5 (95% confidence interval [CI]: 1.1-2.0). Fifteen rare variants were classified as qualifying and were included in collapsing analysis (burden test and SKAT-O). They did not contribute to risk. However, a Arg113Cys missense variant (rs146420040; MAF = 0.004) showed an increased VTE risk (HR = 1.3; 95% CI: 1.0-1.9). Conclusion Homozygosity for the Ser219Gly variant and a previously identified functional PROCR variant (Arg113Cys) was associated with VTE. Other variants did not contribute to VTE.
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