Search

Your search keyword '"Bastholm Olesen, Thomas"' showing total 7 results
Start Over Author "Bastholm Olesen, Thomas"
7 results on '"Bastholm Olesen, Thomas"'

3. The effects of baroreflex activation therapy on blood pressure and sympathetic function in patients with refractory hypertension:the rationale and design of the Nordic BAT study*

Author

Gordin, Daniel, Fadl Elmula, Fadl Elmula M, Andersson, Bert, Gottsäter, Anders, Elf, Johan, Kahan, Thomas, Christensen, Kent Lodberg, Vikatmaa, Pirkka, Vikatmaa, Leena, Bastholm Olesen, Thomas, Groop, Per Henrik, Olsen, Michael Hecht, Tikkanen, Ilkka, and on behalf of the Nordic BAT Study Group, behalf of the Nordic BAT Study Group

Subjects
Gerontology, Adult, medicine.medical_specialty, Adolescent, Resistant hypertension, Electric Stimulation Therapy, Blood Pressure, 030204 cardiovascular system & hematology, Baroreflex, Electric Stimulation Therapy/methods, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Double-Blind Method, Internal medicine, Ambulatory blood pressure measurement, Journal Article, Internal Medicine, medicine, Humans, In patient, 030212 general & internal medicine, cardiac autonomic function, Aged, refractory hypertension, diabetes, Hypertension/physiopathology, business.industry, heart rate variability, Foundation (evidence), resistant hypertension, Heart, General Medicine, Prostheses and Implants, Middle Aged, baroreflex sensitivity, 3. Good health, baroreflex activation therapy, Blood pressure, myocardial infarction, peripheral vascular disease, Heart/physiopathology, Hypertension, Cardiology, Cardiology and Cardiovascular Medicine, business
Abstract

OBJECTIVE: To explore the effects of baroreflex activation therapy (BAT) on hypertension in patients with treatment resistant or refractory hypertension.METHODS: This investigator-initiated randomized, double-blind, 1:1 parallel-design clinical trial will include 100 patients with refractory hypertension from 6 tertiary referral hypertension centers in the Nordic countries. A Barostim Neo System will be implanted and after 1 month patients will be randomized to either BAT for 16 months or continuous pharmacotherapy (BAT off) for 8 months followed by BAT for 8 months. A second randomization will take place after 16 months to BAT or BAT off for 3 months. Eligible patients have a daytime systolic ambulatory blood pressure (ABPM) of ≥145 mm Hg, and/or a daytime diastolic ABPM of ≥95 mm Hg after witnessed drug intake (including ≥3 antihypertensive drugs, preferably including a diuretic).RESULTS: The primary end point is the reduction in 24-hour systolic ABPM by BAT at 8 months, as compared to pharmacotherapy. Secondary and tertiary endpoints are effects of BAT on home and office blood pressures, measures of indices of cardiac and vascular structure and function during follow-up, and safety.CONCLUSIONS: This academic initiative will increase the understanding of mechanisms and role of BAT in the refractory hypertension.

Published
2017
Full Text
View/download PDF

4. The effects of baroreflex activation therapy on blood pressure and sympathetic function in patients with refractory hypertension: the rationale and design of the Nordic BAT study*

Author

Gordin, Daniel, primary, Fadl Elmula, Fadl Elmula M., additional, Andersson, Bert, additional, Gottsäter, Anders, additional, Elf, Johan, additional, Kahan, Thomas, additional, Christensen, Kent Lodberg, additional, Vikatmaa, Pirkka, additional, Vikatmaa, Leena, additional, Bastholm Olesen, Thomas, additional, Groop, Per-Henrik, additional, Olsen, Michael Hecht, additional, and Tikkanen, Ilkka, additional

Published
2017
Full Text
View/download PDF

5. Polymorphisms in the Toll-Like Receptor and the IL-23/IL-17 Pathways Were Associated with Susceptibility to Inflammatory Bowel Disease in a Danish Cohort

Author

Bank, Steffen, primary, Andersen, Paal Skytt, additional, Burisch, Johan, additional, Pedersen, Natalia, additional, Roug, Stine, additional, Galsgaard, Julied, additional, Ydegaard Turino, Stine, additional, Broder Brodersen, Jacob, additional, Rashid, Shaista, additional, Kaiser Rasmussen, Britt, additional, Avlund, Sara, additional, Bastholm Olesen, Thomas, additional, Hoffmann, Hans Jürgen, additional, Andersen Nexø, Bjørn, additional, Sode, Jacob, additional, Vogel, Ulla, additional, and Andersen, Vibeke, additional

Published
2015
Full Text
View/download PDF

6. Polymorphisms in the Inflammatory Pathway Genes TLR2, TLR4, TLR9, LY96, NFKBIA, NFKB1, TNFA, TNFRSF1A, IL6R, IL10, IL23R, PTPN22, and PPARG Are Associated with Susceptibility of Inflammatory Bowel Disease in a Danish Cohort

Author

Bank, Steffen, primary, Skytt Andersen, Paal, additional, Burisch, Johan, additional, Pedersen, Natalia, additional, Roug, Stine, additional, Galsgaard, Julie, additional, Ydegaard Turino, Stine, additional, Broder Brodersen, Jacob, additional, Rashid, Shaista, additional, Kaiser Rasmussen, Britt, additional, Avlund, Sara, additional, Bastholm Olesen, Thomas, additional, Jürgen Hoffmann, Hans, additional, Kragh Thomsen, Marianne, additional, Østergaard Thomsen, Vibeke, additional, Frydenberg, Morten, additional, Andersen Nexø, Bjørn, additional, Sode, Jacob, additional, Vogel, Ulla, additional, and Andersen, Vibeke, additional

Published
2014
Full Text
View/download PDF

7. Polymorphisms in the Inflammatory Pathway Genes TLR2, TLR4, TLR9, LY96, NFKBIA, NFKB1, TNFA, TNFRSF1A, IL6R, IL10, IL23R, PTPN22, and PPARG Are Associated with Susceptibility of Inflammatory Bowel Disease in a Danish Cohort

Author

Bank, Steffen, Skytt Andersen, Paal, Burisch, Johan, Pedersen, Natalia, Roug, Stine, Galsgaard, Julie, Ydegaard Turino, Stine, Broder Brodersen, Jacob, Rashid, Shaista, Kaiser Rasmussen, Britt, Avlund, Sara, Bastholm Olesen, Thomas, Jürgen Hoffmann, Hans, Kragh Thomsen, Marianne, Østergaard Thomsen, Vibeke, Frydenberg, Morten, Andersen Nexø, Bjørn, Sode, Jacob, Vogel, Ulla, and Andersen, Vibeke

Subjects
CROHN'S disease, INFLAMMATORY bowel diseases, INTERLEUKIN-10, GENETIC regulation, SINGLE nucleotide polymorphisms, MOLECULAR biology
Abstract

Background: The inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis (UC), result from the combined effects of susceptibility genes and environmental factors. Polymorphisms in genes regulating inflammation may explain part of the genetic heritage. Methods: Using a candidate gene approach, 39 mainly functional single nucleotide polymorphisms (SNPs) in 26 genes regulating inflammation were assessed in a clinical homogeneous group of severely diseased patients consisting of 624 patients with CD, 411 patients with UC and 795 controls. The results were analysed using logistic regression. Results: Sixteen polymorphisms in 13 genes involved in regulation of inflammation were associated with risk of CD and/or UC (p≤0.05). The polymorphisms TLR2 (rs1816702), NFKB1 (rs28362491), TNFRSF1A (rs4149570), IL6R (rs4537545), IL23R (rs11209026) and PTPN22 (rs2476601) were associated with risk of CD and the polymorphisms TLR2 (rs1816702), TLR4 (rs1554973 and rs12377632), TLR9 (rs352139), LY96 (rs11465996), NFKBIA (rs696), TNFA (rs1800629), TNFRSF1A (rs4149570), IL10 (rs3024505), IL23R (rs11209026), PTPN22 (rs2476601) and PPARG (rs1801282) were associated with risk of UC. When including all patients (IBD) the polymorphisms TLR2 (rs4696480 and rs1816702), TLR4 (rs1554973 and rs12377632), TLR9 (rs187084), TNFRSF1A (rs4149570), IL6R (rs4537545), IL10 (rs3024505), IL23R (rs11209026) and PTPN22 (rs2476601) were associated with risk. After Bonferroni correction for multiple testing, both the homozygous and the heterozygous variant genotypes of IL23R G>A(rs11209026) (ORCD,adj: 0.38, 95% CI: 0.21–0.67, p = 0.03; ORIBD,adj 0.43, 95% CI: 0.28–0.67, p = 0.007) and PTPN22 1858 G>A(rs2476601) (ORCD,unadj 0.54, 95% CI: 0.41–0.72, p = 7*10−4; ORIBD,unadj: 0.61, 95% CI: 0.48–0.77, p = 0.001) were associated with reduced risk of CD. Conclusion: The biological effects of the studied polymorphisms suggest that genetically determined high inflammatory response was associated with increased risk of CD. The many SNPs found in TLRs suggest that the host microbial composition or environmental factors in the gut are involved in risk of IBD in genetically susceptible individuals. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results