Etween the two means of high and low work stress groups divided by the standard deviation for the complete data. B. 
Results of the initial main effects model using 
METsum as dependent variable. (DOC)AcknowledgmentsWe thank the participating nurses from the Finnish Public I-BRD9 Sector study. We also thank members of the Finnish Institute for Molecular Medicine for technical assistance and sequencing services.Author ContributionsConceived and designed the experiments: JSA ML HMO AT MK JV EK MH SP TP. Performed the experiments: JSA AT. Analyzed the data: JSA AT HMO EK. Contributed reagents/materials/analysis tools: MK JV MK SP TP. Wrote the paper: JSA ML HMO AT MK JV EK MH SP TP.Stress Affects Serotonin Transporter Methylation
Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissue. This common disease, primarily initiated by periodontal pathogens, is an outcome of a 58-49-1 custom synthesis complex interaction between periodontal microorganisms and the 18334597 host inflammatory response [1]. The host response involves proinflammatory cytokines, chemokines, prostaglandins, Toll-like receptors and proteolytic enzymes, which have all been demonstrated to play an important role in the pathogenesis of periodontitis [2,3]. Studies have been performed combining in vivo and in vitro approaches to identify genes responsible for periodontitis. To date, there are a few published microarray studies investigating the gene expression profile in periodontits. One microarray study reported no significant differences in gene expression at different pathological sites in PD 168393 biological activity patients with chronic and aggressive periodontitis [4], whereas Kim et al. [5] and Demmer et al. [6] showed a number ofgenes that were upregulated in periodontitis compared to healthy controls. In addition, Beikler et al. [7] demonstrated that in periodontitis sites, the expression of immune and inflammatory genes was down-regulated following ITI-007 non-surgical therapy. With regard to in vitro studies, gene expression profiling has been performed on gingival fibroblasts from inflamed and healthy gingival tissues, for a limited number of inflammatory markers, such as interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor- a (TNF-a) and CD14 [8]. Furthermore, microarray analysis has also been performed on periodontal ligament cells and gingival keratinocytes [9,10]. With regard to disease susceptibility at a genomic level, one genome-wide association study (GWAS) has been conducted in patients with aggressive periodontitis showing an association between aggressive periodontitis and intronic single nucleotide polymorphism rs1537415, which is located in the glycosyltransferase gene GLT6D1 [11].Gene Expression in PeriodontitisMaterials and Methods Ethics StatementThe study was performed in accordance with the Declaration of Helsinki and the current legislation in Sweden and after approval from the Karolinska Institutet Ethical Research Board. The Regional Ethics Board in Stockholm approved the collection of the biopsies and informed 
consent was obtained from all patients.Collection of gingival tissue samplesA total of 10 nonsmoking individuals (20 biopsies), were included in the study. Four patients in the study group had other types of diseases: patient 2 was undergoing investigations for the disease sarcoidosis, patient 3 had diabetes type-2, patient 7 had a history of osteoarthritis and patient 10 was diagnosed with asthma. All participants were examined for periodontal disease and those wit.Etween the two means of high and low work stress groups divided by the standard deviation for the complete data. B. Results of the initial main effects model using METsum as dependent variable. (DOC)AcknowledgmentsWe thank the participating nurses from the Finnish Public Sector study. We also thank members of the Finnish Institute for Molecular Medicine for technical assistance and sequencing services.Author ContributionsConceived and designed the experiments: JSA ML HMO AT MK JV EK MH SP TP. Performed the experiments: JSA AT. Analyzed the data: JSA AT HMO EK. Contributed reagents/materials/analysis tools: MK JV MK SP TP. Wrote the paper: JSA ML HMO AT MK JV EK MH SP TP.Stress Affects Serotonin Transporter Methylation
Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissue. This common disease, primarily initiated by periodontal pathogens, is an outcome of a complex interaction between periodontal microorganisms and the 18334597 host inflammatory response [1]. The host response involves proinflammatory cytokines, chemokines, prostaglandins, Toll-like receptors and proteolytic enzymes, which have all been demonstrated to play an important role in the pathogenesis of periodontitis [2,3]. Studies have been performed combining in vivo and in vitro approaches to identify genes responsible for periodontitis. To date, there are a few published microarray studies investigating the gene expression profile in periodontits. One microarray study reported no significant differences in gene expression at different pathological sites in patients with chronic and aggressive periodontitis [4], whereas Kim et al. [5] and Demmer et al. [6] showed a number ofgenes that were upregulated in periodontitis compared to healthy controls. In addition, Beikler et al. [7] demonstrated that in periodontitis sites, the expression of immune and inflammatory genes was down-regulated following non-surgical therapy. With regard to in vitro studies, 
gene expression profiling has been performed on gingival fibroblasts from inflamed and healthy gingival tissues, for a limited number of inflammatory markers, such as interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor- a (TNF-a) and CD14 [8]. Furthermore, microarray analysis has also been performed on periodontal ligament cells and gingival keratinocytes [9,10]. With regard to disease susceptibility at a genomic level, one genome-wide association study (GWAS) has been conducted in patients with aggressive periodontitis showing an association between aggressive periodontitis and intronic single nucleotide polymorphism rs1537415, which is located in the glycosyltransferase gene GLT6D1 [11].Gene Expression in PeriodontitisMaterials and Methods Ethics StatementThe study was performed in accordance with the Declaration of Helsinki and the current legislation in Sweden and after approval from the Karolinska Institutet Ethical Research Board. The Regional Ethics Board in Stockholm approved the collection of the biopsies and informed consent was obtained from all patients.Collection of gingival tissue samplesA total of 10 nonsmoking individuals (20 biopsies), were included in the study. Four patients in the study group had other types of diseases: patient 2 was undergoing investigations for the disease sarcoidosis, patient 3 had diabetes type-2, patient 7 had a history of osteoarthritis and patient 10 was diagnosed with asthma. All participants were examined for periodontal disease and those wit.Etween the two means of high and low work stress groups divided by the standard deviation for the complete data. B. Results of the initial main effects model using METsum as dependent variable. (DOC)AcknowledgmentsWe thank the participating nurses from the Finnish Public Sector study. We also thank members of the Finnish Institute for Molecular Medicine for technical assistance and sequencing services.Author ContributionsConceived and designed the experiments: JSA ML HMO AT MK JV EK MH SP TP. Performed the experiments: JSA AT. Analyzed the data: JSA AT HMO EK. Contributed reagents/materials/analysis tools: MK JV MK SP TP. Wrote the paper: JSA ML HMO AT MK JV EK MH SP TP.Stress Affects Serotonin Transporter Methylation
Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissue. This common disease, primarily initiated by periodontal pathogens, is an outcome of a complex interaction between periodontal microorganisms and the 18334597 host inflammatory response [1]. The host response involves proinflammatory cytokines, chemokines, prostaglandins, Toll-like receptors and proteolytic enzymes, which have all been demonstrated to play an important role in the pathogenesis of periodontitis [2,3]. Studies have been performed combining in vivo and in vitro approaches to identify genes responsible for periodontitis. To date, there are a few published microarray studies investigating the gene expression profile in periodontits. One microarray study reported no significant differences in gene expression at different pathological sites in patients with chronic and aggressive periodontitis [4], whereas Kim et al. [5] and Demmer et al. [6] showed a number ofgenes that were upregulated in periodontitis compared to healthy controls. In addition, Beikler et al. [7] demonstrated that in periodontitis sites, the expression of immune and inflammatory genes was down-regulated following non-surgical therapy. With regard to in vitro studies, gene expression profiling has been performed on gingival fibroblasts from inflamed and healthy gingival tissues, for a limited number of inflammatory markers, such as interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor- a (TNF-a) and CD14 [8]. Furthermore, microarray analysis has also been performed on periodontal ligament cells and gingival keratinocytes [9,10]. With regard to disease susceptibility at a genomic level, one genome-wide association study (GWAS) has been conducted in patients with aggressive periodontitis showing an association between aggressive periodontitis and intronic single nucleotide polymorphism rs1537415, which is located in the glycosyltransferase gene GLT6D1 [11].Gene Expression in PeriodontitisMaterials and Methods Ethics StatementThe study was performed in accordance with the Declaration of Helsinki and the current legislation in Sweden and after approval from the Karolinska Institutet Ethical Research Board. The Regional Ethics Board in Stockholm approved the collection of the biopsies and informed consent was obtained from all patients.Collection of gingival tissue samplesA total of 10 nonsmoking individuals (20 biopsies), were included in the study. Four patients in the study group had other types of diseases: patient 2 was undergoing investigations for the disease sarcoidosis, patient 3 had diabetes type-2, patient 7 had a history of osteoarthritis and patient 10 was diagnosed with asthma. All participants were examined for periodontal disease and those wit.Etween the two means of high and low work stress groups divided by the standard deviation for the complete data. B. Results of the initial main effects model using METsum as dependent variable. (DOC)AcknowledgmentsWe thank the participating nurses from the Finnish Public Sector study. We also thank members of the Finnish Institute for Molecular Medicine for technical assistance and sequencing services.Author ContributionsConceived and designed the experiments: JSA ML HMO AT MK JV EK MH SP TP. Performed the experiments: JSA AT. Analyzed the data: JSA AT HMO EK. Contributed reagents/materials/analysis tools: MK JV MK SP TP. Wrote the paper: JSA ML HMO AT MK JV EK MH SP TP.Stress Affects Serotonin Transporter Methylation
Periodontitis is a chronic inflammatory disease characterized by the destruction of periodontal tissue. This common disease, primarily initiated by periodontal pathogens, is an outcome of a complex interaction between periodontal microorganisms and the 18334597 host inflammatory response [1]. The host response involves proinflammatory cytokines, chemokines, prostaglandins, Toll-like receptors and proteolytic enzymes, which have all been demonstrated to play an important role in the pathogenesis of periodontitis [2,3]. Studies have been performed combining in vivo and in vitro approaches to identify genes responsible for periodontitis. To date, there are a few published microarray studies investigating the gene expression profile in periodontits. One microarray study reported no significant differences in gene expression at different pathological sites in patients with chronic and aggressive periodontitis [4], whereas Kim et al. [5] and Demmer et al. [6] showed a number ofgenes that were upregulated in periodontitis compared to healthy controls. In addition, Beikler et al. [7] demonstrated that in periodontitis sites, the expression of immune and inflammatory genes was down-regulated following non-surgical therapy. With regard to in vitro studies, gene expression profiling has been performed on gingival fibroblasts from inflamed and healthy gingival tissues, for a limited number of inflammatory markers, such as interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor- a (TNF-a) and CD14 [8]. Furthermore, microarray analysis has also been performed on periodontal ligament cells and gingival keratinocytes [9,10]. With regard to disease susceptibility at a genomic level, one genome-wide association study (GWAS) has been conducted in patients with aggressive periodontitis showing an association between aggressive periodontitis and intronic single nucleotide polymorphism rs1537415, which is located in the glycosyltransferase gene GLT6D1 [11].Gene Expression in PeriodontitisMaterials and Methods Ethics StatementThe study was performed in accordance with the Declaration of Helsinki and the current legislation in Sweden and after approval from the Karolinska Institutet Ethical Research Board. The Regional Ethics Board in Stockholm approved the collection of the biopsies and informed consent was obtained from all patients.Collection of gingival tissue samplesA total of 10 nonsmoking individuals (20 biopsies), were included in the study. Four patients in the study group had other types of diseases: patient 2 was undergoing investigations for the disease sarcoidosis, patient 3 had diabetes type-2, patient 7 had a history of osteoarthritis and patient 10 was diagnosed with asthma. All participants were examined for periodontal disease and those wit.
