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Article ; Online: Patient and immunological factors associated with delayed clearance of mucosal SARS-CoV-2 RNA and symptom persistence.

Stone, Mars / Spencer, Bryan R / Warden, Donald E / Fink, Rebecca V / Saa, Paula / Leddy, Jennifer / Mulach-Vannoy, Jackie / Townsend, Rebecca / Krysztof, David / Hughes, Alexandria N / Di Germanio, Clara / Kessler, Debra A / Kleinman, Steven / Busch, Michael P / Norris, Philip J

The Journal of infectious diseases

2024

Abstract: Serial blood and mucosal samples were characterized for 102 participants enrolled a median of 7.0 days post-COVID-19 diagnosis. Mucosal RNA was detectable a median 31.5 (95% CI 20.5 - 63.5) days, with persistence ≥1 month associated with obesity (BMI ≥30, ...

Abstract	Serial blood and mucosal samples were characterized for 102 participants enrolled a median of 7.0 days post-COVID-19 diagnosis. Mucosal RNA was detectable a median 31.5 (95% CI 20.5 - 63.5) days, with persistence ≥1 month associated with obesity (BMI ≥30, OR 3.9, 95% CI 1.2 - 13.8) but not age, sex, or chronic conditions. Fifteen participants had likely reinfection; lower serum anti-S IgG levels were associated with reinfection risk. Nearly half of participants (47%) reported symptoms lasting ≥2-3 months; persistence ≥3 months was associated with BMI ≥30 (OR = 4.2 95% CI 1.1 - 12.8) and peak anti-S and anti-NC antibody levels.
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiae132
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Article: A Machine Learning Approach to Identify a Circulating MicroRNA Signature for Alzheimer Disease.

Zhao, Xuemei / Kang, John / Svetnik, Vladimir / Warden, Donald / Wilcock, Gordon / David Smith, A / Savage, Mary J / Laterza, Omar F

The journal of applied laboratory medicine

2019 Volume 5, Issue 1, Page(s) 15–28

Abstract: Background: Accurate diagnosis of Alzheimer disease (AD) involving less invasive molecular procedures and at reasonable cost is an unmet medical need. We identified a serum miRNA signature for AD that is less invasive than a measure in cerebrospinal ... ...

Abstract	Background: Accurate diagnosis of Alzheimer disease (AD) involving less invasive molecular procedures and at reasonable cost is an unmet medical need. We identified a serum miRNA signature for AD that is less invasive than a measure in cerebrospinal fluid. Methods: From the Oxford Project to Investigate Memory and Aging (OPTIMA) study, 96 serum samples were profiled by a multiplex (>500 analytes) microRNA (miRNA) reverse transcription quantitative PCR analysis, including 51 controls, 32 samples from patients with AD, and 13 samples from patients with mild cognitive impairment (MCI). Clinical diagnosis of a subset of AD and the controls was confirmed by postmortem (PM) histologic examination of brain tissue. In a machine learning approach, the AD and control samples were split 70:30 as the training and test cohorts. A multivariate random forest statistical analysis was applied to construct and test a miRNA signature for AD identification. In addition, the MCI participants were included in the test cohort to assess whether the signature can identify early AD patients. Results: A 12-miRNA signature for AD identification was constructed in the training cohort, demonstrating 76.0% accuracy in the independent test cohort with 90.0% sensitivity and 66.7% specificity. The signature, however, was not able to identify MCI participants. With a subset of AD and control participants with PM-confirmed diagnosis status, a separate 12-miRNA signature was constructed. Although sample size was limited, the PM-confirmed signature demonstrated improved accuracy of 85.7%, largely owing to improved specificity of 80.0% with comparable sensitivity of 88.9%. Conclusion: Although additional and more diverse cohorts are needed for further clinical validation of the robustness, the miRNA signature appears to be a promising blood test to diagnose AD.
MeSH term(s)	Aged ; Alzheimer Disease/blood ; Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Alzheimer Disease/mortality ; Autopsy/methods ; Brain/metabolism ; Brain/pathology ; Circulating MicroRNA/blood ; Cognitive Dysfunction/cerebrospinal fluid ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/genetics ; Early Diagnosis ; Female ; Gene Expression Profiling/methods ; Humans ; Machine Learning ; Male ; Reproducibility of Results ; Sensitivity and Specificity ; Transcriptome
Chemical Substances	Circulating MicroRNA
Language	English
Publishing date	2019-11-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2576-9456
ISSN	2576-9456
DOI	10.1373/jalm.2019.029595
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Article ; Online: Interaction of nutrition and genetics via DNMT3L-mediated DNA methylation determines cognitive decline.

Flitton, Miles / Rielly, Nicholas / Warman, Rhian / Warden, Donald / Smith, A David / Macdonald, Ian A / Knight, Helen Miranda

Neurobiology of aging

2019 Volume 78, Page(s) 64–73

Abstract: Low homocysteine levels and B vitamin treatment are reported to protect against declining cognitive health. Both B vitamins and homocysteine are involved in the production of S-adenosylmethionine, a universal methyl donor essential for the process of DNA ...

Abstract	Low homocysteine levels and B vitamin treatment are reported to protect against declining cognitive health. Both B vitamins and homocysteine are involved in the production of S-adenosylmethionine, a universal methyl donor essential for the process of DNA methylation. We investigated the effect of a damaging coding variant within the DNA methyltransferase gene DNMT3L (R278G, A/G) by examining B vitamin intake, homocysteine levels, cognitive performance, and brain atrophy in individuals in the VITACOG study of mild cognitive impairment and the TwinsUK cohort. In the VITACOG study, individuals who received a 2-year treatment of B vitamins and carried the G allele showed better "visuospatial associative memory" and slower rates of brain atrophy. In the TwinsUK study, improved "visuospatial associative memory" was evident in individuals who reported regular vitamin intake and were A/A homozygotes. In silico modeling indicated that R278G disrupts protein interaction between DNMT3L and DNMT3A, affecting the DNMT3A-3L-H3 complex required for DNA methylation. These findings show that vitamin intake and genetic variation within DNMT3L interact to influence cognitive decline.
MeSH term(s)	Aged ; Aged, 80 and over ; Atrophy ; Brain/pathology ; Cognition ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/prevention & control ; Cognitive Dysfunction/psychology ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methylation/genetics ; Female ; Homocysteine/adverse effects ; Homocysteine/metabolism ; Humans ; Male ; S-Adenosylmethionine/metabolism ; Spatial Memory ; Vitamin B Complex/administration & dosage
Chemical Substances	Homocysteine (0LVT1QZ0BA) ; Vitamin B Complex (12001-76-2) ; S-Adenosylmethionine (7LP2MPO46S) ; DNMT3L protein, human (EC 2.1.1.-) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2019-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2019.02.001
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Article: Detection of single-nucleotide polymorphisms by PCR with universal energy transfer-labeled primers: application to folate- and cobalamin-related genes.

Warden, Donald R / Refsum, Helga

Clinical chemistry

2005 Volume 51, Issue 9, Page(s) 1713–1716

MeSH term(s)	Adolescent ; Adult ; Aged ; DNA Primers ; Energy Transfer ; Fluorescent Dyes ; Folic Acid/metabolism ; Genotype ; Humans ; Membrane Transport Proteins/blood ; Membrane Transport Proteins/genetics ; Methylenetetrahydrofolate Reductase (NADPH2)/blood ; Methylenetetrahydrofolate Reductase (NADPH2)/genetics ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Reduced Folate Carrier Protein ; Transcobalamins/genetics
Chemical Substances	DNA Primers ; Fluorescent Dyes ; Membrane Transport Proteins ; Reduced Folate Carrier Protein ; SLC19A1 protein, human ; Transcobalamins ; Folic Acid (935E97BOY8) ; Methylenetetrahydrofolate Reductase (NADPH2) (EC 1.5.1.20)
Language	English
Publishing date	2005-07-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80102-1
ISSN	1530-8561 ; 0009-9147
ISSN (online)	1530-8561
ISSN	0009-9147
DOI	10.1373/clinchem.2004.045195
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Article ; Online: Cerebral amyloid angiopathy, subcortical white matter disease and dementia: literature review and study in OPTIMA.

Esiri, Margaret / Chance, Steven / Joachim, Catharine / Warden, Donald / Smallwood, Aidan / Sloan, Carolyn / Christie, Sharon / Wilcock, Gordon / Smith, A David

Brain pathology (Zurich, Switzerland)

2014 Volume 25, Issue 1, Page(s) 51–62

Abstract: Cerebral amyloid angiopathy (CAA) is of increasing clinical and research interest as the ability to detect it and its consequences by neuroimaging in living subjects has advanced. There is also increasing interest in understanding its possible role in ... ...

Abstract	Cerebral amyloid angiopathy (CAA) is of increasing clinical and research interest as the ability to detect it and its consequences by neuroimaging in living subjects has advanced. There is also increasing interest in understanding its possible role in the development of intracerebral hemorrhage, Alzheimer's disease (AD) and vascular dementia. In this article, the literature on this subject is reviewed and novel findings relating CAA to subcortical white matter damage in 224 subjects in the Oxford project to Investigate Memory and Ageing (OPTIMA) are reported. The relationship between CAA and subcortical tissue damage in the OPTIMA subjects was found to be critically dependent on ApoE genotype, there being a positive relationship between measures of CAA and subcortical small vessel disease in ApoEε4 carriers and a significant negative relationship in ApoEε2 carriers. These findings draw attention, as have many other studies, to the importance of ApoE genotype as a major risk factor not only for dementia but also for damage to blood vessels in the aging brain.
MeSH term(s)	Aged ; Aged, 80 and over ; Animals ; Apolipoproteins E/genetics ; Brain/pathology ; Cerebral Amyloid Angiopathy/complications ; Cerebral Amyloid Angiopathy/epidemiology ; Cerebral Amyloid Angiopathy/genetics ; Cerebral Amyloid Angiopathy/pathology ; Dementia/complications ; Dementia/epidemiology ; Dementia/genetics ; Dementia/pathology ; Dementia/therapy ; Female ; Humans ; Leukoencephalopathies/genetics ; Leukoencephalopathies/pathology ; Longitudinal Studies ; Male
Chemical Substances	Apolipoproteins E
Language	English
Publishing date	2014-12-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.12221
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Article ; Online: The vitamin D receptor gene is associated with Alzheimer's disease.

Lehmann, Donald J / Refsum, Helga / Warden, Donald R / Medway, Christopher / Wilcock, Gordon K / Smith, A David

Neuroscience letters

2011 Volume 504, Issue 2, Page(s) 79–82

Abstract: Vitamin D may have a role in brain function. Low levels have been frequently associated with cognitive decline and may contribute to diseases of the nervous system. The vitamin D receptor (VDR) is widely expressed in human brain. Vitamin D appears to be ... ...

Abstract	Vitamin D may have a role in brain function. Low levels have been frequently associated with cognitive decline and may contribute to diseases of the nervous system. The vitamin D receptor (VDR) is widely expressed in human brain. Vitamin D appears to be neuroprotective and may regulate inflammation in the brain. We examined two VDR polymorphisms, Apa1 and Taq1. We used DNA from 255 Alzheimer's disease (AD) cases and 260 cognitively screened elderly controls from the longitudinal cohort of the Oxford Project to Investigate Memory and Ageing (OPTIMA). The presence of each of the linked alleles, Apa1 T and Taq1 G, was associated with the risk of AD, particularly in people <75 years old: odds ratios ≥3.0 and p≤0.005. We also found preliminary evidence of interactions associated with AD between these polymorphisms and two other genes involved in the regulation of inflammation, interleukin-10 (IL10) and dopamine β-hydroxylase (DBH): synergy factors ≥3.4, uncorrected p<0.05. These associations are biologically plausible and are consistent with a role for vitamin D in AD. Nevertheless, we consider this to be a hypothesis-generating study, which needs to be replicated in a larger dataset.
MeSH term(s)	Alleles ; Alzheimer Disease/genetics ; Apolipoproteins E/genetics ; Cohort Studies ; DNA/genetics ; Dopamine beta-Hydroxylase/genetics ; Humans ; Inflammation/genetics ; Interleukin-10/genetics ; Odds Ratio ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Receptors, Calcitriol/genetics ; Risk
Chemical Substances	Apolipoproteins E ; Receptors, Calcitriol ; Interleukin-10 (130068-27-8) ; DNA (9007-49-2) ; Dopamine beta-Hydroxylase (EC 1.14.17.1)
Language	English
Publishing date	2011-09-03
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2011.08.057
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Article ; Online: PSEN1 polymorphisms alter the rate of cognitive decline in sporadic Alzheimer's disease patients.

Belbin, Olivia / Beaumont, Helen / Warden, Donald / Smith, A David / Kalsheker, Noor / Morgan, Kevin

Neurobiology of aging

2009 Volume 30, Issue 12, Page(s) 1992–1999

Abstract: Mutations in amyloid precursor protein (APP) and presenilin (PSEN) genes are known to cause familial early-onset Alzheimer's disease (AD), which account for around 5% of AD cases. Genetic associations for the remaining "sporadic" cases, other than the ... ...

Abstract	Mutations in amyloid precursor protein (APP) and presenilin (PSEN) genes are known to cause familial early-onset Alzheimer's disease (AD), which account for around 5% of AD cases. Genetic associations for the remaining "sporadic" cases, other than the risks associated with the apolipoprotein (APOE) epsilon4 allele are currently not fully established. The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) in PSEN1 are associated with a modified risk for sporadic AD or a modified disease phenotype. Eight tag SNPs were identified using linkage disequilibrium (LD) data from the International HapMap project providing coverage of the entire PSEN1 gene. These SNPs were investigated for AD susceptibility in a case-control haplotype association study (N=714) and for genotype-specific effects on cognitive performance in AD patients (N=169) using non-linear mixed effects modelling. Replication of a mild associated-risk of an intronic PSEN1 polymorphism with AD was achieved (P=0.03). No other single SNPs or haplotypes were associated with AD risk. However, 3 SNPs were associated with an altered rate of cognitive decline underlining their role as genetic modifiers of disease.
MeSH term(s)	Age of Onset ; Aged ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Case-Control Studies ; Cognition Disorders/epidemiology ; Cognition Disorders/genetics ; Disease Progression ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Haplotypes ; Humans ; Linkage Disequilibrium ; Male ; Models, Genetic ; Phenotype ; Polymorphism, Single Nucleotide ; Presenilin-1/genetics ; Psychiatric Status Rating Scales ; Time Factors
Chemical Substances	PSEN1 protein, human ; Presenilin-1
Language	English
Publishing date	2009-12
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2008.02.013
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Article ; Online: Association of the aromatase gene with Alzheimer's disease in women.

Butler, Helen T / Warden, Donald R / Hogervorst, Eva / Ragoussis, Jiannis / Smith, A David / Lehmann, Donald J

Neuroscience letters

2009 Volume 468, Issue 3, Page(s) 202–206

Abstract: Associations have been reported of aromatase polymorphisms with Alzheimer's disease (AD). We studied nine polymorphisms in 207 cases of AD, 23 cases of mild cognitive impairment (MCI) and 233 controls, all from the OPTIMA cohort. We replicated two ... ...

Abstract	Associations have been reported of aromatase polymorphisms with Alzheimer's disease (AD). We studied nine polymorphisms in 207 cases of AD, 23 cases of mild cognitive impairment (MCI) and 233 controls, all from the OPTIMA cohort. We replicated two reported associations and found others. Our findings were consistent between AD and MCI. Further, our results were sex-specific, i.e. there were significant interactions between certain polymorphisms and gender, and the associations with AD were almost entirely in women. Aromatase catalyses the conversion of androgens to estrogens. It is expressed in the human brain. In the hippocampus, it is upregulated in postmenopausal women and is lowered in AD. These sex-specific results are therefore plausible. However, our results now need to be replicated in a larger dataset.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Aromatase/genetics ; Cognition Disorders/genetics ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; INDEL Mutation ; Linkage Disequilibrium ; Longitudinal Studies ; Male ; Microsatellite Repeats ; Polymorphism, Single Nucleotide ; Sex Factors
Chemical Substances	Aromatase (EC 1.14.14.1)
Language	English
Publishing date	2009-10-30
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2009.10.089
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Article ; Online: The Epistasis Project: A Multi-Cohort Study of the Effects of BDNF, DBH, and SORT1 Epistasis on Alzheimer's Disease Risk.

Journal of Alzheimer's disease : JAD

2019 Volume 68, Issue 4, Page(s) 1535–1547

Abstract: Pre-synaptic secretion of brain-derived neurotrophic factor (BDNF) from noradrenergic neurons may protect the Alzheimer's disease (AD) brain from amyloid pathology. While the BDNF polymorphism (rs6265) is associated with faster cognitive decline and ... ...

Abstract	Pre-synaptic secretion of brain-derived neurotrophic factor (BDNF) from noradrenergic neurons may protect the Alzheimer's disease (AD) brain from amyloid pathology. While the BDNF polymorphism (rs6265) is associated with faster cognitive decline and increased hippocampal atrophy, a replicable genetic association of BDNF with AD risk has yet to be demonstrated. This could be due to masking by underlying epistatic interactions between BDNF and other loci that encode proteins involved in moderating BDNF secretion (DBH and Sortilin). We performed a multi-cohort case-control association study of the BDNF, DBH, and SORT1 loci comprising 5,682 controls and 2,454 AD patients from Northern Europe (87% of samples) and Spain (13%). The BDNF locus was associated with increased AD risk (odds ratios; OR = 1.1-1.2, p = 0.005-0.3), an effect size that was consistent in the Northern European (OR = 1.1-1.2, p = 0.002-0.8) but not the smaller Spanish (OR = 0.8-1.6, p = 0.4-1.0) subset. A synergistic interaction between BDNF and sex (synergy factor; SF = 1.3-1.5 p = 0.002-0.02) translated to a greater risk of AD associated with BDNF in women (OR = 1.2-1.3, p = 0.007-0.00008) than men (OR = 0.9-1.0, p = 0.3-0.6). While the DBH polymorphism (rs1611115) was also associated with increased AD risk (OR = 1.1, p = 0.04) the synergistic interaction (SF = 2.2, p = 0.007) between BDNF (rs6265) and DBH (rs1611115) contributed greater AD risk than either gene alone, an effect that was greater in women (SF = 2.4, p = 0.04) than men (SF = 2.0, p = 0.2). These data support a complex genetic interaction at loci encoding proteins implicated in the DBH-BDNF inflammatory pathway that modifies AD risk, particularly in women.
MeSH term(s)	Adaptor Proteins, Vesicular Transport/genetics ; Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Brain-Derived Neurotrophic Factor/genetics ; Dopamine beta-Hydroxylase/genetics ; Epistasis, Genetic ; Female ; Genetic Loci ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Polymorphism, Single Nucleotide ; Sex Factors
Chemical Substances	Adaptor Proteins, Vesicular Transport ; Brain-Derived Neurotrophic Factor ; Dopamine beta-Hydroxylase (EC 1.14.17.1) ; sortilin (Z020Y8WIJ4)
Language	English
Publishing date	2019-03-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-181116
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Article ; Online: Peripheral reductive capacity is associated with cognitive performance and survival in Alzheimer's disease

Combrinck Marc / Puopolo Maria / Greco Anita / Minghetti Luisa / Warden Donald / Smith A David

Journal of Neuroinflammation, Vol 3, Iss 1, p

2006 Volume 4

Abstract: Abstract Background Oxidative stress is believed to be an early event and a key factor in Alzheimer's disease (AD) pathogenesis and progression. In spite of an intensive search for surrogate markers to monitor changes related to oxidative stress in the ... ...

Abstract	Abstract Background Oxidative stress is believed to be an early event and a key factor in Alzheimer's disease (AD) pathogenesis and progression. In spite of an intensive search for surrogate markers to monitor changes related to oxidative stress in the brain, there is as yet no consensus about which markers to use in clinical studies. The measurement of peripheral anti-oxidants is an alternative way of evaluating the involvement of oxidative stress in the course of the disease. Given the complexity of peripheral anti-oxidant defence, variations in the levels of individual anti-oxidant species may not fully reflect the overall capacity to fight oxidant conditions. We therefore chose to evaluate the total reductive capacity (herein defined as anti-oxidant capacity, AOC) in serum from control subjects and AD patients in order to study the association between peripheral anti-oxidant defence, cognitive impairment and patient survival. Methods We measured the levels of AOC in serum samples from 26 cognitively normal controls and 25 AD patients (12 post-mortem confirmed) who completed the Cambridge Cognitive Assessment. Cognitive decline was assessed in a subgroup of 19 patients who underwent a second cognitive assessment 2 years after the initial visit. Results Serum AOC levels were lower in AD patients than in controls and were correlated with their cognitive test scores, although AOC levels were unrelated to cognitive decline assessed two years later. On the other hand, AOC levels were predictive of the length of patients' survival, with higher levels giving longer survival. Conclusion This study indicates that peripheral anti-oxidant defences are depleted in AD patients. The results suggest that serum AOC is a good index of the general health status and prognosis of patients but does not necessarily reflect the extent to which vulnerable neuronal populations are protected from oxidant processes. Further studies are required to establish whether peripheral AOC measurements may be useful in identifying asymptomatic individuals or those with early symptoms at high risk of developing significant cognitive impairment or dementia.
Keywords	Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; DOAJ:Neurology
Subject code	616
Language	English
Publishing date	2006-03-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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