Skip header and navigation

Refine By

159 records – page 1 of 16.

Additive effects of soluble TWEAK and inflammation on mortality in hemodialysis patients.

https://arctichealth.org/en/permalink/ahliterature91537
Source
Clin J Am Soc Nephrol. 2009 Jan;4(1):110-8
Publication Type
Article
Date
Jan-2009
Author
Carrero Juan J
Ortiz Alberto
Qureshi Abdul R
Martín-Ventura Jose L
Bárány Peter
Heimbürger Olof
Marrón Belén
Metry George
Snaedal Sunna
Lindholm Bengt
Egido Jesús
Stenvinkel Peter
Blanco-Colio Luis M
Author Affiliation
Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
Source
Clin J Am Soc Nephrol. 2009 Jan;4(1):110-8
Date
Jan-2009
Language
English
Publication Type
Article
Keywords
Aged
Biological Markers - blood
Cardiovascular Diseases - blood - etiology - mortality
Case-Control Studies
Chronic Disease
Cross-Sectional Studies
Female
Humans
Inflammation - blood - etiology - mortality
Inflammation Mediators - blood
Interleukin-6 - blood
Kaplan-Meiers Estimate
Kidney Diseases - blood - complications - mortality - therapy
Male
Middle Aged
Proportional Hazards Models
Renal Dialysis - mortality
Reproducibility of Results
Risk assessment
Sweden - epidemiology
Time Factors
Tumor Necrosis Factors - blood
Up-Regulation
Abstract
BACKGROUND AND OBJECTIVES: Chronic kidney disease (CKD) is characterized by an exceptionally high mortality rate, primarily due to cardiovascular disease. Reduced soluble TNF-like weak inducer of apoptosis (sTWEAK) plasma levels have been reported both in patients with subclinical atherosclerosis and CKD. DESIGN, PARTICIPANTS, & MEASUREMENTS: A cross-sectional study was conducted in 218 prevalent patients (121 men; 63 +/- 14 yr) undergoing hemodialysis (HD). sTWEAK levels in relation with the patients' outcome were studied. RESULTS: sTWEAK plasma levels were 208 [(165 to 272) pg/ml, median interquartile range], significantly lower than healthy controls (P 7.0 pg/ml), in whom high sTWEAK strongly predicted cardiovascular and all-cause mortality. These results were confirmed in a second cohort of HD patients. CONCLUSIONS: The concurrent presence of elevated sTWEAK plasma concentrations and an inflammatory environment have additive effects on mortality in HD patients. Further studies on the potential different role of sTWEAK in health and disease are warranted.
PubMed ID
18945991 View in PubMed
Less detail

a-Defensins and outcome in patients with chronic heart failure.

https://arctichealth.org/en/permalink/ahliterature126769
Source
Eur J Heart Fail. 2012 Apr;14(4):387-94
Publication Type
Article
Date
Apr-2012
Author
Heidi M Christensen
Jan Frystyk
Jens Faber
Morten Schou
Allan Flyvbjerg
Per Hildebrandt
Ilan Raymond
Tobias W Klausen
Caroline Kistorp
Author Affiliation
Department of Cardiology, Herlev University Hospital, Herlev Ringvej 75, Herlev, Denmark. heidichristensen@dadlnet.dk
Source
Eur J Heart Fail. 2012 Apr;14(4):387-94
Date
Apr-2012
Language
English
Publication Type
Article
Keywords
Aged
Analysis of Variance
Biological Markers
C-Reactive Protein
Case-Control Studies
Confidence Intervals
Denmark
Female
Heart Failure - blood - mortality - pathology
Humans
Inflammation - blood - pathology
Linear Models
Male
Natriuretic Peptide, Brain - blood
Peptide Fragments - blood
Predictive value of tests
Prognosis
Prospective Studies
Statistics as Topic
Statistics, nonparametric
Survival Analysis
Treatment Outcome
alpha-Defensins - blood
Abstract
a-Defensins are part of the innate immune system. Low-grade inflammation seems to play a crucial role in development and progression of chronic heart failure (CHF). The aims of the present study were to compare plasma levels of a-defensins in CHF patients and healthy controls and to examine the predictive ability of a-defensins, alone and combined with N-terminal pro brain natriuretic peptide (NT-proBNP), with respect to all-cause mortality.
In a prospective observational study lasting 2.6 years we examined the prognostic value of plasma a-defensins with respect to mortality in 194 CHF patients, and compared plasma levels with those of 98 age-matched healthy controls. a-Defensin levels were twice as high among CHF patients in New York Heart Association (NYHA) functional class III-IV than in patients in NYHA class I-II and healthy controls (P = 0.001). The absolute increase in risk of mortality for patients with a-defensin levels in the upper tertile vs. the lowest tertile was 30% (P = 0.002). After adjusting for potential confounders including NT-proBNP, plasma a-defensins remained independently associated with an increased risk of all-cause mortality (hazard ratio 1.65, 95% confidence interval 1.19-2.28, P = 0.002) per 1 standard deviation increment in Ln (natural logarithm)-transformed a-defensin values. The combination of high a-defensins and NT-proBNP levels provided incremental prognostic information independent of well-known prognostic biomarkers in heart failure.
Plasma a-defensins appear to have prognostic information regarding mortality among patients with CHF and seem to provide incremental information to established clinical risk markers.
PubMed ID
22357441 View in PubMed
Less detail

Adipose co-expression networks across Finns and Mexicans identify novel triglyceride-associated genes.

https://arctichealth.org/en/permalink/ahliterature118360
Source
BMC Med Genomics. 2012;5:61
Publication Type
Article
Date
2012
Author
Blake E Haas
Steve Horvath
Kirsi H Pietiläinen
Rita M Cantor
Elina Nikkola
Daphna Weissglas-Volkov
Aila Rissanen
Mete Civelek
Ivette Cruz-Bautista
Laura Riba
Johanna Kuusisto
Jaakko Kaprio
Teresa Tusie-Luna
Markku Laakso
Carlos A Aguilar-Salinas
Päivi Pajukanta
Author Affiliation
Department of Human Genetics, Gonda Center, Los Angeles, California, 90095-7088, USA.
Source
BMC Med Genomics. 2012;5:61
Date
2012
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Case-Control Studies
Finland
Gene Expression Profiling
Gene Expression Regulation
Gene Regulatory Networks - genetics
Genetic Loci - genetics
Genome-Wide Association Study
Humans
Immunity - genetics
Inflammation - blood - genetics
Mexico
Polymorphism, Single Nucleotide - genetics
Triglycerides - blood - genetics
Twins - genetics
Abstract
High serum triglyceride (TG) levels is an established risk factor for coronary heart disease (CHD). Fat is stored in the form of TGs in human adipose tissue. We hypothesized that gene co-expression networks in human adipose tissue may be correlated with serum TG levels and help reveal novel genes involved in TG regulation.
Gene co-expression networks were constructed from two Finnish and one Mexican study sample using the blockwiseModules R function in Weighted Gene Co-expression Network Analysis (WGCNA). Overlap between TG-associated networks from each of the three study samples were calculated using a Fisher's Exact test. Gene ontology was used to determine known pathways enriched in each TG-associated network.
We measured gene expression in adipose samples from two Finnish and one Mexican study sample. In each study sample, we observed a gene co-expression network that was significantly associated with serum TG levels. The TG modules observed in Finns and Mexicans significantly overlapped and shared 34 genes. Seven of the 34 genes (ARHGAP30, CCR1, CXCL16, FERMT3, HCST, RNASET2, SELPG) were identified as the key hub genes of all three TG modules. Furthermore, two of the 34 genes (ARHGAP9, LST1) reside in previous TG GWAS regions, suggesting them as the regional candidates underlying the GWAS signals.
This study presents a novel adipose gene co-expression network with 34 genes significantly correlated with serum TG across populations.
Notes
Cites: Ann Clin Res. 1973 Jun;5(3):109-414584134
Cites: Genome Biol. 2011;12(3):R2221410973
Cites: Nat Genet. 2006 Feb;38(2):218-2216429159
Cites: PLoS Genet. 2006 Aug 18;2(8):e13016934000
Cites: Am J Hum Genet. 2007 Jun;80(6):1024-3617503322
Cites: Am J Physiol Gastrointest Liver Physiol. 2007 Jul;293(1):G1-417218471
Cites: Diabetologia. 2008 Jan;51(1):62-917972059
Cites: Bioinformatics. 2008 Mar 1;24(5):719-2018024473
Cites: Genome Res. 2008 May;18(5):706-1618347327
Cites: Am J Hum Genet. 2008 Aug;83(2):180-9218674750
Cites: PLoS Comput Biol. 2008;4(8):e100011718704157
Cites: Nat Protoc. 2009;4(1):44-5719131956
Cites: Nucleic Acids Res. 2009 Jan;37(1):1-1319033363
Cites: BMC Bioinformatics. 2008;9:55919114008
Cites: Bioinformatics. 2009 May 1;25(9):1105-1119289445
Cites: Genome Biol. 2009;10(3):R2519261174
Cites: PLoS Genet. 2009 Sep;5(9):e100064219750004
Cites: Discov Med. 2009 Aug;8(41):55-6019788868
Cites: Lancet. 2010 May 8;375(9726):1634-920452521
Cites: Nat Biotechnol. 2010 May;28(5):511-520436464
Cites: Salud Publica Mex. 2010;52 Suppl 1:S44-5320585729
Cites: Nature. 2010 Aug 5;466(7307):707-1320686565
Cites: Mol Syst Biol. 2010 Dec 21;6:44121179014
Cites: PLoS Comput Biol. 2011;7(1):e100105721283776
Cites: Arterioscler Thromb Vasc Biol. 2011 May;31(5):1201-721393584
Cites: Diabetes. 2011 May;60(5):1608-1621421807
Cites: Circulation. 2011 May 24;123(20):2292-33321502576
Cites: J Lipid Res. 2011 Aug;52(8):1575-8221596930
Cites: Bioinformatics. 2011 Sep 1;27(17):2325-921697122
Cites: BMC Bioinformatics. 2011;12:32221816037
Cites: Arterioscler Thromb Vasc Biol. 2005 Sep;25(9):1985-9115976322
PubMed ID
23217153 View in PubMed
Less detail

Adiposity, aerobic fitness, muscle fitness, and markers of inflammation in children.

https://arctichealth.org/en/permalink/ahliterature119134
Source
Med Sci Sports Exerc. 2013 Apr;45(4):714-21
Publication Type
Article
Date
Apr-2013
Author
Jostein Steene-Johannessen
Elin Kolle
Lars Bo Andersen
Sigmund A Anderssen
Author Affiliation
Department of Sports, Faculty of Teacher Education and Sports, Sogn og Fjordane University College, Sogndal, Norway. jostsj@hisf.no
Source
Med Sci Sports Exerc. 2013 Apr;45(4):714-21
Date
Apr-2013
Language
English
Publication Type
Article
Keywords
Adiposity - physiology
Biological Markers - blood
Child
Exercise Test
Female
Humans
Inflammation - blood - diagnosis
Inflammation Mediators - blood
Male
Muscle Strength - physiology
Norway
Physical Fitness - physiology
Regression Analysis
Sex Distribution
Abstract
The purpose of this study was to describe levels of inflammation markers in Norwegian children and to examine the associations of adiposity, aerobic fitness, and muscle fitness with markers of inflammation.
In 2005-2006, 1467 nine-year-olds were randomly selected from all regions in Norway. The participation rate was 89%. The inflammatory markers evaluated included C-reactive protein (CRP), leptin, adiponectin, plasminogen activator inhibitor-1, tumor necrosis factor-a, hepatocyte growth factor, resistin, and interleukin-6. We assessed muscular strength by measuring explosive, isometric, and endurance strength. Aerobic fitness was measured directly during a maximal cycle ergometer test. Adiposity was expressed as waist circumference (WC).
The girls had significantly higher levels of CRP, leptin, adiponectin, and resistin and lower levels of tumor necrosis factor-a compared with the boys. We observed a graded association of CRP and leptin levels across quintiles of WC, aerobic fitness, and muscle fitness (P = 0.001 for all participants). The regression analyses revealed that WC, aerobic fitness, and muscle fitness were independently associated with the CRP (WC ß = 0.158, P
PubMed ID
23135365 View in PubMed
Less detail

Adiposity-related inflammation: effects of pregnancy.

https://arctichealth.org/en/permalink/ahliterature115475
Source
Obesity (Silver Spring). 2013 Jan;21(1):E124-30
Publication Type
Article
Date
Jan-2013
Author
Camilla M Friis
Marie C Paasche Roland
Kristin Godang
Thor Ueland
Tom Tanbo
Jens Bollerslev
Tore Henriksen
Author Affiliation
Division of Obstetrics and Gynaecology, Oslo University Hospital Rikshospitalet, Oslo, Norway. camilla.friis@ous-hf.no
Source
Obesity (Silver Spring). 2013 Jan;21(1):E124-30
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adipose Tissue
Adiposity
Adult
Body Composition
Body mass index
European Continental Ancestry Group
Female
Humans
Inflammation - blood - etiology
Inflammation Mediators - blood
Longitudinal Studies
Norway
Obesity - blood - complications
Overweight - blood
Pregnancy
Pregnancy Complications - blood
Reference Values
Statistics, nonparametric
Up-Regulation
Abstract
In the nonpregnant population, there is extensive evidence of a systemic low-grade inflammatory status in relation to excess adipose tissue. Less is known about the relation during pregnancy.
Our main objective was therefore to explore the effect of pregnancy on adiposity-related systemic inflammation.
This study is a longitudinal cohort study of 240 pregnant women of Scandinavian heritage at Oslo University hospital-Rikshospitalet, Norway from 2002 to 2005. The inflammatory markers (C-reactive protein [CRP], Interleukin-6 [IL-6], monocyte chemoattractant protein 1 [MCP-1], IL1-Ra, tumor necrosis factor receptor II, and IL-10) were measured at four timepoints during pregnancy and analyzed by enzyme immuno-assay. The women were categorized based on BMI at inclusion (BMI 30 kg/m(2)). Data were analyzed by Friedman-test, Wilcoxon signed rank test, or Kruskal-Wallis test as appropriate.
Maternal adiposity was associated with significantly higher circulatory levels of several inflammatory markers (CRP, MCP-1, IL-6, and IL-1Ra). However, this proinflammatory upregulation was not evident toward the end of pregnancy, as levels of CRP, MCP-1, and IL-6 were not any longer significantly different between the BMI categories.
Although normal pregnancy exhibits proinflammatory features, this does not seem to have additive or synergistic effects on the inflammation associated with adiposity. On the contrary, we found that the BMI-dependent increase in proinflammatory markers was not evident at the end of pregnancy.
PubMed ID
23505192 View in PubMed
Less detail

Adolescent body mass index and erythrocyte sedimentation rate in relation to colorectal cancer risk.

https://arctichealth.org/en/permalink/ahliterature283749
Source
Gut. 2016 Aug;65(8):1289-95
Publication Type
Article
Date
Aug-2016
Author
Elizabeth D Kantor
Ruzan Udumyan
Lisa B Signorello
Edward L Giovannucci
Scott Montgomery
Katja Fall
Source
Gut. 2016 Aug;65(8):1289-95
Date
Aug-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Blood Sedimentation
Body mass index
Cohort Studies
Colorectal Neoplasms - blood - diagnosis - epidemiology
Humans
Inflammation - blood - diagnosis - epidemiology
Male
Obesity - diagnosis - epidemiology
Outcome Assessment (Health Care)
Proportional Hazards Models
Risk factors
Sweden - epidemiology
Abstract
Adult obesity and inflammation have been associated with risk of colorectal cancer (CRC); however, less is known about how adolescent body mass index (BMI) and inflammation, as measured by erythrocyte sedimentation rate (ESR), relate to CRC risk. We sought to evaluate these associations in a cohort of 239 658 Swedish men who underwent compulsory military enlistment examinations in late adolescence (ages 16-20 years).
At the time of the conscription assessment (1969-1976), height and weight were measured and ESR was assayed. By linkage to the national cancer registry, these conscripts were followed for CRC through 1 January 2010. Over an average of 35 years of follow-up, 885 cases of CRC occurred, including 501 colon cancers and 384 rectal cancers. Cox regression was used to estimate adjusted HRs and corresponding 95% CIs.
Compared with normal weight (BMI 18.5 to
Notes
Cites: PLoS One. 2009 Nov 23;4(11):e795119956740
Cites: Gastroenterology. 2004 Feb;126(2):451-914762782
Cites: J Natl Cancer Inst. 1992 Sep 2;84(17):1326-311495102
Cites: BMJ Open. 2013 Jul 11;3(7):null23847269
Cites: Eur J Cancer Prev. 2013 Nov;22(6):492-50523591454
Cites: Cancer. 2003 Jan 1;97(1):46-5512491504
Cites: Gastroenterology. 2011 Mar;140(3):799-808, quiz e1121115010
Cites: Am Heart J. 2013 Feb;165(2):164-923351818
Cites: Cancer Causes Control. 2010 Dec;21(12):2069-7720680433
Cites: Int J Obes (Lond). 2012 Sep;36(9):1180-622732910
Cites: Cancer Causes Control. 2014 Apr;25(4):409-1824435936
Cites: Cancer Epidemiol Biomarkers Prev. 2011 Dec;20(12):2524-3122056504
Cites: N Engl J Med. 1992 Nov 5;327(19):1350-51406836
Cites: Gut. 2013 Jun;62(6):933-4723481261
Cites: Br J Cancer. 2013 May 14;108(9):1891-823591192
Cites: Obesity (Silver Spring). 2014 Jun;22(6):1495-50424415710
Cites: Cancer Causes Control. 1992 Jul;3(4):349-541617122
Cites: Am J Epidemiol. 2008 Jul 1;168(1):30-718477652
Cites: Arch Dis Child Educ Pract Ed. 2015 Feb;100(1):30-625205237
Cites: Clin Gastroenterol Hepatol. 2014 Aug;12(8):1342-8.e124407106
Cites: Front Biosci (Elite Ed). 2013 Jan 01;5:61-7723276970
Cites: Gastroenterology. 2010 Jun;138(6):2101-2114.e520420949
Cites: World J Gastroenterol. 2014 Aug 7;20(29):9716-3125110410
Cites: Nature. 2002 Dec 19-26;420(6917):860-712490959
Cites: Int J Cancer. 2014 Dec 15;135(12):2900-924771654
Cites: Int J Cancer. 2015 Mar 1;136(5):1181-9225043606
Cites: Cancer Prev Res (Phila). 2012 Feb;5(2):336-4222166248
Cites: Am J Clin Nutr. 2007 Sep;86(3):556-6517823417
Cites: J Natl Cancer Inst. 2010 Mar 17;102(6):391-40020208017
Cites: Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):537-4421212059
Cites: Int J Epidemiol. 1997 Oct;26(5):1003-89363521
Cites: Int J Lab Hematol. 2011 Apr;33(2):125-3221352508
Cites: Acta Radiol Oncol. 1984;23(5):305-136095600
Cites: Acta Oncol. 2009;48(1):27-3318767000
Cites: Cancer Causes Control. 2013 Dec;24(12):2059-7524022467
Cites: Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1735-4417855691
Cites: JAMA. 2008 Dec 17;300(23):2765-7819088354
Cites: Am J Epidemiol. 2007 Jul 1;166(1):36-4517449892
Cites: Cancer Causes Control. 2007 Dec;18(10):1095-10517694420
Cites: Lancet. 2014 Aug 30;384(9945):766-8124880830
Cites: Lancet. 2010 Nov 20;376(9754):1741-5020970847
Cites: Am J Epidemiol. 2012 Dec 15;176(12):1130-4023186750
Cites: JAMA Surg. 2015 Jan;150(1):17-2225372703
Cites: Gastroenterology. 2011 May;140(6):1807-1621530747
Cites: Am J Kidney Dis. 2014 Nov;64(5):723-925124945
Cites: Cancer Epidemiol Biomarkers Prev. 2014 Aug;23(8):1609-1824867266
Cites: J Clin Gastroenterol. 1986 Dec;8(6):647-503805662
Cites: Cancer Causes Control. 2014 Oct;25(10):1397-40525053407
Cites: J Neurol Neurosurg Psychiatry. 2014 Dec;85(12):1331-624681701
Cites: J Clin Oncol. 2006 Nov 1;24(31):5010-617075120
Cites: Obes Rev. 2010 Jan;11(1):19-3019538439
Cites: J Epidemiol Community Health. 2002 Oct;56(10):780-412239205
Cites: Int J Cancer. 2004 Nov 1;112(2):348-5115352051
Cites: Br J Cancer. 2011 Jun 28;105(1):162-921559014
Cites: Int J Cancer. 2011 Jun 1;128(11):2726-3420949557
Cites: Cancer Prev Res (Phila). 2014 Jul;7(7):758-6524824037
PubMed ID
25986947 View in PubMed
Less detail

An air filter intervention study of endothelial function among healthy adults in a woodsmoke-impacted community.

https://arctichealth.org/en/permalink/ahliterature137685
Source
Am J Respir Crit Care Med. 2011 May 1;183(9):1222-30
Publication Type
Article
Date
May-1-2011
Author
Ryan W Allen
Chris Carlsten
Barbara Karlen
Sara Leckie
Stephan van Eeden
Sverre Vedal
Imelda Wong
Michael Brauer
Author Affiliation
Simon Fraser University, Faculty of Health Sciences, 8888 University Drive, Burnaby, British Columbia V5A 1S6, Canada. allenr@sfu.ca
Source
Am J Respir Crit Care Med. 2011 May 1;183(9):1222-30
Date
May-1-2011
Language
English
Publication Type
Article
Keywords
Adult
Air Pollutants - blood - urine
Biological Markers - blood - urine
British Columbia
C-Reactive Protein
Cross-Over Studies
Dinoprost - urine
Endothelial Cells
Enzyme-Linked Immunosorbent Assay
Female
Filtration - methods
Humans
Hyperemia
Inflammation - blood
Inhalation Exposure
Lipid Peroxidation
Male
Malondialdehyde - urine
Middle Aged
Oxidative Stress
Reference Values
Smoke
Young Adult
Abstract
Particulate air pollution is associated with cardiovascular morbidity. One hypothesized mechanism involves oxidative stress, systemic inflammation, and endothelial dysfunction.
To assess an intervention's impact on particle exposures and endothelial function among healthy adults in a woodsmoke-impacted community. We also investigated the underlying role of oxidative stress and inflammation in relation to exposure reductions.
Portable air filters were used in a randomized crossover intervention study of 45 healthy adults exposed to consecutive 7-day periods of filtered and nonfiltered air.
Reactive hyperemia index was measured as an indicator of endothelial function via peripheral artery tonometry, and markers of inflammation (C-reactive protein, interleukin-6, and band cells) and lipid peroxidation (malondialdehyde and 8-iso-prostaglandin F(2a)) were quantified. Air filters reduced indoor fine particle concentrations by 60%. Filtration was associated with a 9.4% (95% confidence interval, 0.9-18%) increase in reactive hyperemia index and a 32.6% (4.4-60.9%) decrease in C-reactive protein. Decreases in particulate matter and the woodsmoke tracer levoglucosan were associated with reduced band cell counts. There was limited evidence of more pronounced effects on endothelial function and level of systemic inflammation among males, overweight participants, younger participants, and residents of wood-burning homes. No associations were noted for oxidative stress markers.
Air filtration was associated with improved endothelial function and decreased concentrations of inflammatory biomarkers but not markers of oxidative stress. Our results support the hypothesis that systemic inflammation and impaired endothelial function, both predictors of cardiovascular morbidity, can be favorably influenced by reducing indoor particle concentrations.
PubMed ID
21257787 View in PubMed
Less detail

Anemia, nutritional status, and inflammation in hospitalized elderly.

https://arctichealth.org/en/permalink/ahliterature92557
Source
Nutrition. 2008 Nov-Dec;24(11-12):1116-22
Publication Type
Article

An indoor air filtration study in homes of elderly: cardiovascular and respiratory effects of exposure to particulate matter.

https://arctichealth.org/en/permalink/ahliterature261646
Source
Environ Health. 2013;12:116
Publication Type
Article
Date
2013
Author
Dorina Gabriela Karottki
Michal Spilak
Marie Frederiksen
Lars Gunnarsen
Elvira Vaclavik Brauner
Barbara Kolarik
Zorana Jovanovic Andersen
Torben Sigsgaard
Lars Barregard
Bo Strandberg
Gerd Sallsten
Peter Møller
Steffen Loft
Source
Environ Health. 2013;12:116
Date
2013
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Air Pollutants - analysis - toxicity
Biological Markers - blood
Cardiovascular Physiological Phenomena - drug effects
Chromatography, High Pressure Liquid
Cities
Cross-Over Studies
Denmark
Double-Blind Method
Female
Filtration
Hematologic Tests
Humans
Inflammation - blood - etiology
Intervention Studies
Lung - drug effects - physiology
Male
Middle Aged
Particulate Matter - analysis - toxicity
Respiratory Function Tests
Abstract
Exposure to particulate air pollution increases respiratory and cardiovascular morbidity and mortality, especially in elderly, possibly through inflammation and vascular dysfunction.
We examined potential beneficial effects of indoor air filtration in the homes of elderly, including people taking vasoactive drugs.Forty-eight nonsmoking subjects (51 to 81 years) in 27 homes were included in this randomized, double-blind, crossover intervention study with consecutive two-week periods with or without the inclusion of a high-efficiency particle air filter in re-circulating custom built units in their living room and bedroom. We measured blood pressure, microvascular and lung function and collected blood samples for hematological, inflammation, monocyte surface and lung cell damage markers before and at day 2, 7 and 14 during each exposure scenario.
The particle filters reduced the median concentration of PM2.5 from approximately 8 to 4 µg/m3 and the particle number concentration from 7669 to 5352 particles/cm3. No statistically significant effects of filtration as category were observed on microvascular and lung function or the biomarkers of systemic inflammation among all subjects, or in the subgroups taking (n = 11) or not taking vasoactive drugs (n = 37). However, the filtration efficacy was variable and microvascular function was within 2 days significantly increased with the actual PM2.5 decrease in the bedroom, especially among 25 subjects not taking any drugs.
Substantial exposure contrasts in the bedroom and no confounding by drugs appear required for improved microvascular function by air filtration, whereas no other beneficial effect was found in this elderly population.
Notes
Cites: Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H944-5318083905
Cites: Occup Environ Med. 2008 May;65(5):319-2417704195
Cites: Inhal Toxicol. 2008 Apr;20(6):533-4518444007
Cites: Eur Heart J. 2008 Dec;29(24):3043-5118952612
Cites: Inhal Toxicol. 2009 Jan;21(1):38-4718752169
Cites: Environ Sci Technol. 2008 Dec 1;42(23):8641-719192775
Cites: Cardiol Rev. 2010 Jan-Feb;18(1):20-820010335
Cites: Inhal Toxicol. 2010 Feb;22(3):245-5220064088
Cites: Circulation. 2010 Jun 1;121(21):2331-7820458016
Cites: Curr Atheroscler Rep. 2010 Sep;12(5):291-30020617466
Cites: J Expo Sci Environ Epidemiol. 2011 Jan-Feb;21(1):20-3020087407
Cites: J Environ Monit. 2011 Jan;13(1):182-9121082095
Cites: Indoor Air. 2011 Apr;21(2):132-4421029183
Cites: Rev Environ Health. 2012;27(2-3):133-4923023922
Cites: Tex Heart Inst J. 2013;40(1):17-2923467296
Cites: J Am Heart Assoc. 2013 Feb;2(1):e00430923525434
Cites: Indoor Air. 2013 Jun;23(3):175-8423210563
Cites: Indoor Air. 2013 Oct;23(5):357-6823397961
Cites: Environ Health Perspect. 2011 Apr;119(4):446-5420961824
Cites: Am J Respir Crit Care Med. 2011 May 1;183(9):1222-3021257787
Cites: Inhal Toxicol. 2011 Aug;23(10):555-9221864219
Cites: Sci Total Environ. 2011 Sep 15;409(20):4217-2121835436
Cites: J Air Waste Manag Assoc. 2011 Aug;61(8):858-6321874957
Cites: Curr Allergy Asthma Rep. 2011 Oct;11(5):395-40221773748
Cites: Pediatr Pulmonol. 2012 Apr;47(4):358-6621901861
Cites: Part Fibre Toxicol. 2012;9:722452928
Cites: Future Cardiol. 2012 Jul;8(4):577-60222871197
Cites: Ann N Y Acad Sci. 2000;923:68-7711193780
Cites: Environ Health Perspect. 2001 Jun;109 Suppl 3:405-911427390
Cites: Circulation. 2002 Mar 5;105(9):1135-4311877368
Cites: Thromb Res. 2012 Jan;129(1):68-7321641633
Cites: Inhal Toxicol. 2012 Jan;24(1):47-5922220980
Cites: Environ Health Perspect. 2012 Mar;120(3):367-7222389220
Cites: Inhal Toxicol. 2003 Apr 11;15(4):305-2512635001
Cites: Eur Respir J Suppl. 2003 May;40:15s-20s12762569
Cites: J Toxicol Clin Toxicol. 1991;29(3):315-741920571
Cites: Am J Respir Crit Care Med. 1999 Feb;159(2):646-789927386
Cites: Eur Respir J. 2005 Aug;26(2):319-3816055882
Cites: Environ Health Perspect. 2005 Nov;113(11):1485-9016263500
Cites: Circulation. 2005 Dec 20;112(25):3930-616365212
Cites: Environ Health Perspect. 2006 Jan;114(1):51-816393658
Cites: Inhal Toxicol. 2006 Oct;18(11):845-5316864402
Cites: Hum Exp Toxicol. 2006 Nov;25(11):627-3517211980
Cites: Int Arch Occup Environ Health. 2007 Feb;80(4):265-7216791613
Cites: J Expo Sci Environ Epidemiol. 2007 Mar;17(2):124-3316519413
Cites: Environ Health Perspect. 2007 Aug;115(8):1177-8217687444
Cites: N Engl J Med. 2007 Sep 13;357(11):1075-8217855668
Cites: Thromb Res. 2007;120(6):849-5517321570
Cites: J Expo Sci Environ Epidemiol. 2007 Nov;17(7):613-2417440486
Cites: Am J Respir Crit Care Med. 2008 Feb 15;177(4):419-2517932377
PubMed ID
24373585 View in PubMed
Less detail

Antioxidant intake, oxidative stress and inflammation among immigrant women from the Middle East living in Sweden: associations with cardiovascular risk factors.

https://arctichealth.org/en/permalink/ahliterature84865
Source
Nutr Metab Cardiovasc Dis. 2007 Dec;17(10):748-56
Publication Type
Article
Date
Dec-2007
Author
Daryani Achraf
Basu Samar
Becker Wulf
Larsson Anders
Risérus Ulf
Author Affiliation
Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala Science Park, 751 85 Uppsala, Sweden. achraf.daryani@pubcare.uu.se
Source
Nutr Metab Cardiovasc Dis. 2007 Dec;17(10):748-56
Date
Dec-2007
Language
English
Publication Type
Article
Keywords
Adult
Antioxidants - administration & dosage
Blood Pressure - physiology
C-Reactive Protein - analysis
Cardiovascular Diseases - blood - epidemiology - etiology
Cross-Sectional Studies
Diet
Emigration and Immigration
F2-Isoprostanes - blood
Female
Food Habits - ethnology
Humans
Inflammation - blood - epidemiology
Iran - ethnology
Middle Aged
Oxidative Stress
Risk factors
Sweden - epidemiology
Turkey - ethnology
Abstract
BACKGROUND AND AIMS: Immigrant women from the Middle East have higher cardiovascular risk compared to native women. Whether low antioxidant intake, oxidative stress or inflammation contributes to risk is unknown. In a cross-sectional study of 157 randomly selected foreign-born women (Iranian and Turkish) and native women living in Sweden, we investigated antioxidant status, oxidative stress (F(2)-isoprostanes) and systemic inflammation (plasma high sensitive C-reactive protein; CRP) markers. We also investigated relationships between F(2)-isoprostanes, CRP and cardiovascular risk factors. METHODS AND RESULT: Dietary intake was assessed using 24-h dietary recalls repeated four times. Micronutrient intake was not consistently different between groups. Serum alpha-tocopherol, but not gamma-tocopherol levels, was lower in Turkish vs. Swedish women (P0.21, P values
PubMed ID
17145175 View in PubMed
Less detail

159 records – page 1 of 16.