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Article ; Online: Identification of a potential molecular link between the glucocorticoid and serotonergic signaling systems.

Falkenberg, Virginia R / Rajeevan, Mangalathu S

2010 Volume 41, Issue 2, Page(s) 322–327

Abstract: Glucocorticoid receptor (GR) and serotonin (5-hydroxytryptamine (5-HT)) signaling systems play a pivotal role in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis, but the molecular nature of interactions between these two systems remain ... ...

Abstract	Glucocorticoid receptor (GR) and serotonin (5-hydroxytryptamine (5-HT)) signaling systems play a pivotal role in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis, but the molecular nature of interactions between these two systems remain largely unidentified. We used computational and experimental approaches to evaluate if DNA-protein interactions would provide a molecular link for the interaction between 5-HT and GR systems. Bioinformatic analysis identified nine binding sites in various serotonin receptors (HTR1D, HTR1F, HTR2A, HTR3A, and HTR6) for transcription factors in the GR family. Electrophoretic mobility shift assays (EMSA) using HeLa nuclear extract and purified full-length GR verified most of the predicted DNA-protein interactions. Six binding sites verified by EMSA results were evolutionarily conserved in multiple species. Multiple lines of evidence from computational and experimental analyses in this study support the potential of a molecular link between 5-HT and GR signaling systems. This finding provides new approaches to studies directed at mechanisms for glucocorticoid negative feedback regulation of the HPA axis involving 5-HT and interventional studies directed to neuropsychiatric diseases.
MeSH term(s)	Animals ; Base Sequence ; Databases, Genetic ; Evolution, Molecular ; Glucocorticoids/metabolism ; HeLa Cells ; Humans ; Hypothalamo-Hypophyseal System/metabolism ; Molecular Sequence Data ; Pituitary-Adrenal System/metabolism ; Promoter Regions, Genetic ; Receptors, Glucocorticoid/metabolism ; Receptors, Serotonin/metabolism ; Serotonin/metabolism ; Signal Transduction/physiology
Chemical Substances	Glucocorticoids ; Receptors, Glucocorticoid ; Receptors, Serotonin ; Serotonin (333DO1RDJY)
Language	English
Publishing date	2010-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1043392-2
ISSN	1559-1166 ; 0895-8696
ISSN (online)	1559-1166
ISSN	0895-8696
DOI	10.1007/s12031-009-9320-6
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Zs.A 3006: Show issues

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Article ; Online: Pathway-focused genetic evaluation of immune and inflammation related genes with chronic fatigue syndrome.

Rajeevan, Mangalathu S / Dimulescu, Irina / Murray, Janna / Falkenberg, Virginia R / Unger, Elizabeth R

Human immunology

2015 Volume 76, Issue 8, Page(s) 553–560

Abstract: Recent evidence suggests immune and inflammatory alterations are important in chronic fatigue syndrome (CFS). This study was done to explore the association of functionally important genetic variants in inflammation and immune pathways with CFS. ... ...

Abstract	Recent evidence suggests immune and inflammatory alterations are important in chronic fatigue syndrome (CFS). This study was done to explore the association of functionally important genetic variants in inflammation and immune pathways with CFS. Peripheral blood DNA was isolated from 50 CFS and 121 non-fatigued (NF) control participants in a population-based study. Genotyping was performed with the Affymetrix Immune and Inflammation Chip that covers 11K single nucleotide polymorphisms (SNPs) following the manufacturer's protocol. Genotyping accuracy for specific genes was validated by pyrosequencing. Golden Helix SVS software was used for genetic analysis. SNP functional annotation was done using SPOT and GenomePipe programs. CFS was associated with 32 functionally important SNPs: 11 missense variants, 4 synonymous variants, 11 untranslated regulatory region (UTR) variants and 6 intronic variants. Some of these SNPs were in genes within pathways related to complement cascade (SERPINA5, CFB, CFH, MASP1 and C6), chemokines (CXCL16, CCR4, CCL27), cytokine signaling (IL18, IL17B, IL2RB), and toll-like receptor signaling (TIRAP, IRAK4). Of particular interest is association of CFS with two missense variants in genes of complement activation, rs4151667 (L9H) in CFB and rs1061170 (Y402H) in CFH. A 5' UTR polymorphism (rs11214105) in IL18 also associated with physical fatigue, body pain and score for CFS case defining symptoms. This study identified new associations of CFS with genetic variants in pathways including complement activation providing additional support for altered innate immune response in CFS. Additional studies are needed to validate the findings of this exploratory study.
MeSH term(s)	Adult ; Alleles ; Complement C2/genetics ; Fatigue Syndrome, Chronic/epidemiology ; Fatigue Syndrome, Chronic/etiology ; Fatigue Syndrome, Chronic/metabolism ; Female ; Follow-Up Studies ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Georgia/epidemiology ; Humans ; Immunity ; Inflammation/complications ; Linkage Disequilibrium ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Population Surveillance ; Risk Factors ; Signal Transduction ; Young Adult
Chemical Substances	Complement C2
Language	English
Publishing date	2015-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	801524-7
ISSN	1879-1166 ; 0198-8859
ISSN (online)	1879-1166
ISSN	0198-8859
DOI	10.1016/j.humimm.2015.06.014
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Article ; Online: Acute Psychosocial Stress-Mediated Changes in the Expression and Methylation of Perforin in Chronic Fatigue Syndrome

Virginia R. Falkenberg / Toni Whistler / Janna R. Murray / Elizabeth R. Unger / Mangalathu S. Rajeevan

Genetics and Epigenetics, Vol 2013, Iss 5, Pp 1-

2013 Volume 9

Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Libertas Academica
Document type	Article ; Online
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Article: The Genomics Education Partnership: First findings on genomics research in community colleges.

Croonquist, Paula / Falkenberg, Virginia / Minkovsky, Natalie / Sawa, Alexa / Skerritt, Matthew / Sustacek, Maire Kate / Diotti, Raffaella / Aragon, Anthony D / Mans, Tamara / Sherr, Goldie L / Ward, Catherine / Hall-Woods, Monica / Goodman, Anya L / Reed, Laura K / Lopatto, David

Scholarship and practice of undergraduate research

2023 Volume 6, Issue 3, Page(s) 17–28

Abstract: The Genomics Education Partnership (GEP), a consortium of diverse colleges/universities, provides support for integrating genomics research into undergraduate curricula. To increase research opportunities for underrepresented students, GEP is expanding ... ...

Abstract	The Genomics Education Partnership (GEP), a consortium of diverse colleges/universities, provides support for integrating genomics research into undergraduate curricula. To increase research opportunities for underrepresented students, GEP is expanding to more community colleges (CC). Genomics research, requiring only a computer with internet access, may be particularly accessible for 2-year institutions with limited research capacity and significant budget constraints. To understand how GEP supports student research at CCs, we analyzed student knowledge and self-reported outcomes. We found that CC student gains are comparable to non-CC student gains, with improvements in attitudes toward science and thriving in science. Our early findings suggest that the GEP model of centralized support with flexible CURE implementation benefits CC students and may help mitigate barriers to implementing research at CCs.
Language	English
Publishing date	2023-09-20
Publishing country	United States
Document type	Journal Article
ISSN	2476-101X
ISSN	2476-101X
DOI	10.18833/spur/6/3/1
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Article: Acute psychosocial stress-mediated changes in the expression and methylation of perforin in chronic fatigue syndrome.

Falkenberg, Virginia R / Whistler, Toni / Murray, Janna R / Unger, Elizabeth R / Rajeevan, Mangalathu S

Genetics & epigenetics

2013 Volume 5, Page(s) 1–9

Abstract: ... with PRF1 expression at all TSST time points in both CFS (r = -0.56, P = <0.0001) and NF (r = -0.38, P = <0 ...

Abstract	Perforin (PRF1) is essential for immune surveillance and studies report decreased perforin in chronic fatigue syndrome (CFS), an illness potentially associated with stress and/or infection. We hypothesize that stress can influence regulation of PRF1 expression, and that this regulation will differ between CFS and non-fatigued (NF) controls. We used the Trier Social Stress Test (TSST) as a standardized acute psychosocial stress, and evaluated its effect on PRF1 expression and methylation in CFS (n = 34) compared with NF (n = 47) participants. During the TSST, natural killer (NK) cells increased significantly in both CFS (P = <0.0001) and NF subjects (P = <0.0001). Unlike previous reports, there was no significant difference in PRF1 expression at baseline or during TSST between CFS and NF. However, whole blood PRF1 expression increased 1.6 fold during the TSST in both CFS (P = 0.0003) and NF (P = <0.0001). Further, the peak response immediately following the TSST was lower in CFS compared with NF (P = 0.04). In addition, at 1.5 hours post TSST, PRF1 expression was elevated in CFS compared with NF (whole blood, P = 0.06; PBMC, P = 0.02). Methylation of seven CpG sites in the methylation sensitive region of the PRF1 promoter ranged from 38%-79% with no significant differences between CFS and NF. Although, the average baseline methylation of all seven CpG sites did not differ between CFS and NF groups, it showed a significant negative correlation with PRF1 expression at all TSST time points in both CFS (r = -0.56, P = <0.0001) and NF (r = -0.38, P = <0.0001). Among participants with high average methylation (≥65%), PRF1 expression was significantly lower in CFS than NF subjects immediately following TSST. These findings suggest methylation could be an important epigenetic determinant of inter-individual differences in PRF1 expression and that the differences in PRF1 expression and methylation between CFS and NF in the acute stress response require further investigation.
Language	English
Publishing date	2013-01-28
Publishing country	United States
Document type	Journal Article
ISSN	1179-237X
ISSN	1179-237X
DOI	10.4137/GEG.S10944
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Article ; Online: Functional genomics of serotonin receptor 2A (HTR2A): interaction of polymorphism, methylation, expression and disease association.

Falkenberg, Virginia R / Gurbaxani, Brian M / Unger, Elizabeth R / Rajeevan, Mangalathu S

Neuromolecular medicine

2010 Volume 13, Issue 1, Page(s) 66–76

Abstract: Serotonergic neurotransmission plays a key role in the pathophysiology of neuropsychiatric illnesses. The functional significance of a promoter polymorphism, -1438G/A (rs6311), in one of the major genes of this system (serotonin receptor 2A, HTR2A) ... ...

Abstract	Serotonergic neurotransmission plays a key role in the pathophysiology of neuropsychiatric illnesses. The functional significance of a promoter polymorphism, -1438G/A (rs6311), in one of the major genes of this system (serotonin receptor 2A, HTR2A) remains poorly understood in the context of epigenetic factors, transcription factors and endocrine influences. We used functional and structural equation modeling (SEM) approaches to assess the contributions of the polymorphism (rs6311), DNA methylation and clinical variables to HTR2A expression in chronic fatigue syndrome (CFS) subjects from a population-based study. HTR2A was up-regulated in CFS through allele-specific expression modulated by transcription factors at critical sites in its promoter: an E47 binding site at position -1,438, (created by the A-allele of rs6311 polymorphism), a glucocorticoid receptor (GR) binding site encompassing a CpG at position -1,420, and Sp1 binding at CpG methylation site -1,224. Methylation at -1,420 was strongly correlated with methylation at -1,439, a CpG site that is dependent upon the G-allele of rs6311 at position -1,438. SEM revealed a strong negative interaction between E47 and GR binding (in conjunction with cortisol level) on HTR2A expression. This study suggests that the promoter polymorphism (rs6311) can affect both transcription factor binding and promoter methylation, and this along with an individual's stress response can impact the rate of HTR2A transcription in a genotype and methylation-dependent manner. This study can serve as an example for deciphering the molecular determinants of transcriptional regulation of major genes of medical importance by integrating functional genomics and SEM approaches. Confirmation in an independent study population is required.
MeSH term(s)	Adult ; Alleles ; DNA Methylation ; Epigenesis, Genetic ; Fatigue Syndrome, Chronic/genetics ; Fatigue Syndrome, Chronic/physiopathology ; Female ; Gene Expression Regulation ; Genomics ; Genotype ; Humans ; Male ; Middle Aged ; Models, Genetic ; Nervous System Diseases/genetics ; Nervous System Diseases/physiopathology ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Receptor, Serotonin, 5-HT2A/genetics
Chemical Substances	Receptor, Serotonin, 5-HT2A
Language	English
Publishing date	2010-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-010-8138-2
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Zs.A 5818: Show issues

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Article ; Online: Determination of quantitative and site-specific DNA methylation of perforin by pyrosequencing.

Narasimhan, Supraja / Falkenberg, Virginia R / Khin, Maung M / Rajeevan, Mangalathu S

BMC research notes

2009 Volume 2, Page(s) 104

Abstract: Background: Differential expression of perforin (PRF1), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site-specific ... ...

Abstract	Background: Differential expression of perforin (PRF1), a gene with a pivotal role in immune surveillance, can be attributed to differential methylation of CpG sites in its promoter region. A reproducible method for quantitative and CpG site-specific determination of perforin methylation is required for molecular epidemiologic studies of chronic diseases with immune dysfunction. Findings: We developed a pyrosequencing based method to quantify site-specific methylation levels in 32 out of 34 CpG sites in the PRF1 promoter, and also compared methylation pattern in DNAs extracted from whole blood drawn into PAXgene blood DNA tubes (whole blood DNA) or DNA extracted from peripheral blood mononuclear cells (PBMC DNA) from the same normal subjects. Sodium bisulfite treatment of DNA and touchdown PCR were highly reproducible (coefficient of variation 1.63 to 2.18%) to preserve methylation information. Application of optimized pyrosequencing protocol to whole blood DNA revealed that methylation level varied along the promoter in normal subjects with extremely high methylation (mean 86%; range 82-92%) in the distal enhancer region (CpG sites 1-10), a variable methylation (range 49%-83%) in the methylation sensitive region (CpG sites 11-17), and a progressively declining methylation level (range 12%-80%) in the proximal promoter region (CpG sites 18-32) of PRF1. This pattern of methylation remained the same between whole blood and PBMC DNAs, but the absolute values of methylation in 30 out of 32 CpG sites differed significantly, with higher values for all CpG sites in the whole blood DNA. Conclusion: This reproducible, site-specific and quantitative method for methylation determination of PRF1 based on pyrosequencing without cloning is well suited for large-scale molecular epidemiologic studies of diseases with immune dysfunction. PBMC DNA may be better suited than whole blood DNA for examining methylation levels in genes associated with immune function.
Language	English
Publishing date	2009-06-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/1756-0500-2-104
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Article ; Online: Identification of Phosphoglycerate Kinase 1 (PGK1) as a reference gene for quantitative gene expression measurements in human blood RNA.

Falkenberg, Virginia R / Whistler, Toni / Murray, Janna' R / Unger, Elizabeth R / Rajeevan, Mangalathu S

BMC research notes

2011 Volume 4, Page(s) 324

Abstract: Background: Blood is a convenient sample and increasingly used for quantitative gene expression measurements with a variety of diseases including chronic fatigue syndrome (CFS). Quantitative gene expression measurements require normalization of target ... ...

Abstract	Background: Blood is a convenient sample and increasingly used for quantitative gene expression measurements with a variety of diseases including chronic fatigue syndrome (CFS). Quantitative gene expression measurements require normalization of target genes to reference genes that are stable and independent from variables being tested in the experiment. Because there are no genes that are useful for all situations, reference gene selection is an essential step to any quantitative reverse transcription-PCR protocol. Many publications have described appropriate genes for a wide variety of tissues and experimental conditions, however, reference genes that may be suitable for the analysis of CFS, or human blood RNA derived from whole blood as well as isolated peripheral blood mononuclear cells (PBMCs), have not been described. Findings: Literature review and analyses of our unpublished microarray data were used to narrow down the pool of candidate reference genes to six. We assayed whole blood RNA from Tempus tubes and cell preparation tube (CPT)-collected PBMC RNA from 46 subjects, and used the geNorm and NormFinder algorithms to select the most stable reference genes. Phosphoglycerate kinase 1 (PGK1) was one of the optimal normalization genes for both whole blood and PBMC RNA, however, additional genes differed for the two sample types; Ribosomal protein large, P0 (RPLP0) for PBMC RNA and Peptidylprolyl isomerase B (PPIB) for whole blood RNA. We also show that the use of a single reference gene is sufficient for normalization when the most stable candidates are used. Conclusions: We have identified PGK1 as a stable reference gene for use with whole blood RNA and RNA derived from PBMC. When stable genes are selected it is possible to use a single gene for normalization rather than two or three. Optimal normalization will improve the ability of results from PBMC RNA to be compared with those from whole blood RNA and potentially allows comparison of gene expression results from blood RNA collected and processed by different methods with the intention of biomarker discovery. Results of this study should facilitate large-scale molecular epidemiologic studies using blood RNA as the target of quantitative gene expression measurements.
Language	English
Publishing date	2011-09-06
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/1756-0500-4-324
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Article ; Online: Identification of Phosphoglycerate Kinase 1 ( PGK1 ) as a reference gene for quantitative gene expression measurements in human blood RNA

Unger Elizabeth R / Murray Janna' R / Whistler Toni / Falkenberg Virginia R / Rajeevan Mangalathu S

BMC Research Notes, Vol 4, Iss 1, p

2011 Volume 324

Abstract: Abstract Background Blood is a convenient sample and increasingly used for quantitative gene expression measurements with a variety of diseases including chronic fatigue syndrome (CFS). Quantitative gene expression measurements require normalization of ... ...

Abstract	Abstract Background Blood is a convenient sample and increasingly used for quantitative gene expression measurements with a variety of diseases including chronic fatigue syndrome (CFS). Quantitative gene expression measurements require normalization of target genes to reference genes that are stable and independent from variables being tested in the experiment. Because there are no genes that are useful for all situations, reference gene selection is an essential step to any quantitative reverse transcription-PCR protocol. Many publications have described appropriate genes for a wide variety of tissues and experimental conditions, however, reference genes that may be suitable for the analysis of CFS, or human blood RNA derived from whole blood as well as isolated peripheral blood mononuclear cells (PBMCs), have not been described. Findings Literature review and analyses of our unpublished microarray data were used to narrow down the pool of candidate reference genes to six. We assayed whole blood RNA from Tempus tubes and cell preparation tube (CPT)-collected PBMC RNA from 46 subjects, and used the geNorm and NormFinder algorithms to select the most stable reference genes. Phosphoglycerate kinase 1 (PGK1) was one of the optimal normalization genes for both whole blood and PBMC RNA, however, additional genes differed for the two sample types; Ribosomal protein large, P0 (RPLP0 ) for PBMC RNA and Peptidylprolyl isomerase B ( PPIB) for whole blood RNA. We also show that the use of a single reference gene is sufficient for normalization when the most stable candidates are used. Conclusions We have identified PGK1 as a stable reference gene for use with whole blood RNA and RNA derived from PBMC. When stable genes are selected it is possible to use a single gene for normalization rather than two or three. Optimal normalization will improve the ability of results from PBMC RNA to be compared with those from whole blood RNA and potentially allows comparison of gene expression results from blood RNA collected and processed by different methods with the intention of biomarker discovery. Results of this study should facilitate large-scale molecular epidemiologic studies using blood RNA as the target of quantitative gene expression measurements.
Keywords	Medicine ; R ; Biology (General) ; QH301-705.5 ; Science (General) ; Q1-390
Subject code	612
Language	English
Publishing date	2011-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article: An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol.

Smith, Alicia K / Maloney, Elizabeth M / Falkenberg, Virginia R / Dimulescu, Irina / Rajeevan, Mangalathu S

Psychoneuroendocrinology

2009 Volume 34, Issue 4, Page(s) 597–606

Abstract: Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. AL is operationalized by a composite index of multiple biomarkers. Accordingly, genes, behavior ... ...

Abstract	Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. AL is operationalized by a composite index of multiple biomarkers. Accordingly, genes, behavior and environment contribute to AL. To determine if individual differences in AL may be influenced by inherent genetic variation, we calculated an allostatic load index (ALI) for 182 Caucasian subjects derived from a population-based study of chronic fatigue syndrome. Nearly 65% of the subjects in this study sample reported fatiguing illness. ALI was calculated based on 11 measures representing metabolic, cardiovascular, inflammatory, hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) activities. Subjects were dichotomized into high (ALI > or = 3) or low (ALI < 3) AL groups, and the association between high AL and 129 polymorphisms in 32 genes related to the HPA axis, neurotransmission, inflammation, cardiovascular and metabolic functions were evaluated. Polymorphisms in angiotensin-1 converting enzyme (ACE), corticotropin-releasing hormone receptor 1 (CRHR1), and serotonin receptors (HTR3A and HTR4) were associated with AL (p=0.0007-0.0486), but only one polymorphism, rs4968591, in ACE remained significant after correction for multiple comparisons. The T allele of ACE rs4968591 was more common in subjects with high AL (67.5%) than in subjects with low AL (49.3%) (p=0.0007), and this effect appeared independent of age, sex, body mass index and fatigue status. Additionally, high interleukin-6 (IL-6; p(trend)=0.04), and C-reactive protein (CRP; p(trend)=0.01) levels, as well as low urinary cortisol levels in females (p=0.03) were associated with the T allele, which may result in allele-specific binding of the transcription factor, E2F1. Our results suggest a role for ACE in the bidirectional communication between the central nervous and immune systems in response to stress. Further studies will be needed (a) to replicate the association between AL and ACE polymorphisms in population studies designed to differentiate the effects of sex, age and racial/ethnic background, (b) to evaluate the effect of allele-specific binding of E2F1 at rs4968591, and (c) to examine the role of ACE in the co-regulation of CRP, IL-6 and cortisol.
MeSH term(s)	Adolescent ; Adult ; Aged ; Allostasis/genetics ; Analysis of Variance ; C-Reactive Protein/analysis ; Computational Biology ; E2F1 Transcription Factor/metabolism ; Fatigue Syndrome, Chronic/blood ; Fatigue Syndrome, Chronic/genetics ; Female ; Humans ; Hydrocortisone/urine ; Interleukin-6/analysis ; Male ; Middle Aged ; Odds Ratio ; Peptidyl-Dipeptidase A/genetics ; Polymorphism, Genetic ; Receptors, Corticotropin-Releasing Hormone/genetics ; Receptors, Serotonin/genetics ; Receptors, Serotonin, 5-HT3 ; Receptors, Serotonin, 5-HT4/genetics ; Sex Factors ; Statistics, Nonparametric ; Young Adult
Chemical Substances	CRF receptor type 1 ; E2F1 Transcription Factor ; E2F1 protein, human ; HTR3A protein, human ; Interleukin-6 ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Serotonin ; Receptors, Serotonin, 5-HT3 ; Receptors, Serotonin, 5-HT4 (158165-40-3) ; C-Reactive Protein (9007-41-4) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2009-05
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/j.psyneuen.2008.10.022
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