Skip header and navigation

Refine By

9 records – page 1 of 1.

Cerebrospinal fluid CXCL13 in multiple sclerosis: a suggestive prognostic marker for the disease course.

https://arctichealth.org/en/permalink/ahliterature138820
Source
Mult Scler. 2011 Mar;17(3):335-43
Publication Type
Article
Date
Mar-2011
Author
Mohsen Khademi
Ingrid Kockum
Magnus L Andersson
Ellen Iacobaeus
Lou Brundin
Finn Sellebjerg
Jan Hillert
Fredrik Piehl
Tomas Olsson
Author Affiliation
Department of Clinical Neuroscience, Neuroimmunology Unit, Karolinska University Hospital, Stockholm, Sweden. mohsen.khademi@ki.se
Source
Mult Scler. 2011 Mar;17(3):335-43
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Biological Markers - cerebrospinal fluid
Chemokine CXCL13 - cerebrospinal fluid
Demyelinating Diseases - cerebrospinal fluid - diagnosis - immunology
Disability Evaluation
Disease Progression
Enzyme-Linked Immunosorbent Assay
Female
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Multiple Sclerosis, Chronic Progressive - cerebrospinal fluid - diagnosis - immunology
Multiple Sclerosis, Relapsing-Remitting - cerebrospinal fluid - diagnosis - immunology
Oligoclonal Bands - cerebrospinal fluid
Predictive value of tests
Prognosis
Reproducibility of Results
Sweden
Time Factors
Up-Regulation
Young Adult
Abstract
Levels of CXCL13, a potent B-cell chemoattractant, are elevated in the cerebrospinal fluid (CSF) during multiple sclerosis (MS) and are associated with markers of MS activity. Levels decrease upon effective treatments.
Here we validate the potential role of CSF CXCL13 as a biomarker for aspects of MS in a large amount of clinical material, the majority collected at early diagnostic work-up.
CXCL13 was measured by ELISA in 837 subjects: relapsing-remitting MS (RRMS; n=323), secondary progressive MS (SPMS; n=40), primary progressive MS (PPMS; n=24), clinically isolated syndrome (CIS; n=79), other neurological diseases (ONDs; n=181), ONDs with signs of inflammation or viral/bacterial infections (iONDs; n=176) and healthy controls (n=14).
Subjects with viral/bacterial infections had extremely high CXCL13 levels compared to all included groups (p
PubMed ID
21135023 View in PubMed
Less detail

Cytokine mapping in cerebrospinal fluid and blood in multiple sclerosis patients without oligoclonal bands.

https://arctichealth.org/en/permalink/ahliterature130806
Source
Mult Scler. 2012 May;18(5):669-73
Publication Type
Article
Date
May-2012
Author
M. Vrethem
M. Kvarnström
J. Stenstam
P. Cassel
M. Gustafsson
A M Landtblom
J. Ernerudh
Author Affiliation
Department of Neurology, Division of Neuroscience, Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden. magnus.vrethem@lio.se
Source
Mult Scler. 2012 May;18(5):669-73
Date
May-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Biological Markers - blood - cerebrospinal fluid
Case-Control Studies
Cells, Cultured
Chi-Square Distribution
Cytokines - blood - cerebrospinal fluid
Female
Humans
Inflammation Mediators - blood - cerebrospinal fluid
Leukocytes, Mononuclear - immunology
Male
Middle Aged
Multiple Sclerosis - blood - cerebrospinal fluid - classification - diagnosis - immunology
Oligoclonal Bands - cerebrospinal fluid
Regression Analysis
Sweden
Young Adult
Abstract
Since there are clinical and genetic differences between MS patients with intrathecal oligoclonal bands (OCB+) in the cerebrospinal fluid (CSF) compared with those without (OCB-), the aim was to find out if OCB- patients showed a different pattern of cytokine immune activation compared with OCB+ patients.
The study included 25 MS patients (10 OCB- and 15 OCB+) and 13 controls. A panel of cytokines was measured; IL-1ß, IL-6, IL-8/CXCL8, IL-10, TNF and GM-CSF in serum, CSF and in supernatants from polyclonally stimulated blood mononuclear cells, where also levels of IL-12p40, IL-13, IL-15, IL-17 and IFN-? were measured. The concentrations of soluble (s) VCAM-1 and sCD14 were measured in serum and CSF.
In general, there were no extensive differences in cytokine concentrations between the OCB- and OCB+ groups.
OCB- MS patients do not seem to constitute a separate entity concerning inflammatory parameters measured as cytokine concentrations in CSF and blood.
PubMed ID
21965416 View in PubMed
Less detail

HHV-6-positivity in diseases with demyelination.

https://arctichealth.org/en/permalink/ahliterature263005
Source
J Clin Virol. 2014 Oct;61(2):216-9
Publication Type
Article
Date
Oct-2014
Author
Jenna Pietiläinen-Nicklén
Jussi O Virtanen
Lasse Uotila
Oili Salonen
Markus Färkkilä
Marjaleena Koskiniemi
Source
J Clin Virol. 2014 Oct;61(2):216-9
Date
Oct-2014
Language
English
Publication Type
Article
Keywords
Adult
Blood - immunology
Cerebrospinal Fluid - immunology
Demyelinating Diseases - etiology - immunology - pathology
Female
Finland
Head - radiography
Herpesvirus 6, Human - immunology
Humans
Magnetic Resonance Imaging
Male
Oligoclonal Bands - cerebrospinal fluid
Roseolovirus Infections - diagnosis - immunology - pathology
Abstract
The triggering agent of multiple sclerosis is still unknown and many viruses, including human herpesvirus-6 (HHV-6), are under suspicion. In earlier study we found patients who had HHV-6 reactive OCBs in their CSF. We wanted to investigate whether HHV-6 has an active role in diseases with demyelination.
To analyze the HHV-6-reactive cases in detail and investigate the possible independent role of HHV-6 in the development of central nervous system involvements with demyelination.
We studied serum and CSF samples that were collected over a period of one year, from all patients who had oligoclonal bands (OCB) in cerebrospinal fluid (CSF) and were examined in the Department of Neurology, University Central Hospital of Helsinki, Finland. Clinical evaluation was accomplished blinded of HHV-6 analysis and follow-up time was two years. All patients underwent MRI of the head and clinically indicated CSF analysis.
The 17 patients with HHV-6-reactive OCBs were significantly younger and had significantly more IgG-OCBs in comparison to patients without HHV-6-reactive OCBs. Initial diagnoses in patients with HHV-6-reactive OCBs remained the same during the follow-up time.
Patients with HHV-6-positive OCBs appear to form a separable group. In progressive neurological diseases HHV-6 may have a role in long-term infection with demyelination.
PubMed ID
25088617 View in PubMed
Less detail

Impact of cerebrospinal-fluid oligoclonal immunoglobulin bands and HLA-DRB1 risk alleles on brain magnetic-resonance-imaging lesion load in Swedish multiple sclerosis patients.

https://arctichealth.org/en/permalink/ahliterature120805
Source
J Neuroimmunol. 2013 Jan 15;254(1-2):170-3
Publication Type
Article
Date
Jan-15-2013
Author
Virginija Danylaite Karrenbauer
Robert Prejs
Thomas Masterman
Jan Hillert
Anna Glaser
Kerstin Imrell
Author Affiliation
MS Research Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. virginija.karrenbauer@ki.se
Source
J Neuroimmunol. 2013 Jan 15;254(1-2):170-3
Date
Jan-15-2013
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Brain - pathology
Female
Follow-Up Studies
HLA-DRB1 Chains - genetics
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Multiple Sclerosis - cerebrospinal fluid - genetics - pathology
Oligoclonal Bands - cerebrospinal fluid
Retrospective Studies
Risk factors
Sweden - epidemiology
Young Adult
Abstract
Approximately 95% of Nordic multiple sclerosis (MS) patients display oligoclonal immunoglobulin G bands (OCB) in the cerebrospinal fluid. From a cohort of 2094 MS patients we retrieved well-characterized data from 40 OCB-negative and 60 OCB-positive patients, in an effort to determine whether lesion load on brain magnetic resonance imaging is affected by OCB status and carriage of HLA-DRB1*15 or HLA-DRB1*04. Positivity for OCB did not increase the risk of belonging to higher-lesion-load groups; nor did carrying HLA-DRB1*15 or HLA-DRB1*04. A trend was seen, however, whereby OCB positivity conferred a two-fold risk of displaying higher lesion loads infratentorially.
PubMed ID
22967351 View in PubMed
Less detail

Increased disease severity in non-Western immigrants with multiple sclerosis in Oslo, Norway.

https://arctichealth.org/en/permalink/ahliterature112433
Source
Eur J Neurol. 2013 Dec;20(12):1546-52
Publication Type
Article
Date
Dec-2013
Author
P. Berg-Hansen
C. Smestad
L. Sandvik
H F Harbo
E G Celius
Author Affiliation
Department of Neurology, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Source
Eur J Neurol. 2013 Dec;20(12):1546-52
Date
Dec-2013
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Child
Emigrants and Immigrants - statistics & numerical data
Female
Humans
Male
Middle Aged
Multiple Sclerosis - cerebrospinal fluid - epidemiology
Norway - epidemiology
Oligoclonal Bands - cerebrospinal fluid
Young Adult
Abstract
Non-Western immigrants to Norway acquire an increased risk of multiple sclerosis (MS) after migration. Ethnicity and the presence of oligoclonal bands (OCBs) in the cerebrospinal fluid (CSF) might influence the disease course. The aim of this study was to investigate differences in disease severity and in the presence of OCBs in ethnic Norwegian and immigrant MS patients.
Clinical data and CSF findings from 47 non-Western immigrants with MS were compared with those from 447 Norwegian and 48 immigrant patients from Western countries.
The non-Western immigrants had a higher mean Multiple Sclerosis Severity Score (MSSS) than the Norwegian patients (5.68 vs. 4.13, P = 0.001). Age at onset was 4 years lower amongst the non-Western immigrants (P = 0.001). After adjusting for year of birth, age at onset, gender and disease course, the mean difference in MSSS between the groups was 2.17 (P
PubMed ID
23834430 View in PubMed
Less detail

Increasing incidence of multiple sclerosis in women in Northern Finland.

https://arctichealth.org/en/permalink/ahliterature140169
Source
Mult Scler. 2011 Feb;17(2):133-8
Publication Type
Article
Date
Feb-2011
Author
O. Krökki
R. Bloigu
M. Reunanen
A M Remes
Author Affiliation
Institute of Clinical Medicine, Neurology, University of Oulu, Oulu, Finland.
Source
Mult Scler. 2011 Feb;17(2):133-8
Date
Feb-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age of Onset
Biological Markers - cerebrospinal fluid
Child
Female
Finland - epidemiology
Humans
Incidence
Magnetic Resonance Imaging
Male
Middle Aged
Multiple Sclerosis, Chronic Progressive - diagnosis - epidemiology
Multiple Sclerosis, Relapsing-Remitting - diagnosis - epidemiology
Neurologic Examination
Oligoclonal Bands - cerebrospinal fluid
Prevalence
Retrospective Studies
Risk factors
Sex Distribution
Sex Factors
Time Factors
Young Adult
Abstract
The geographical distribution of multiple sclerosis (MS) means that prevalence rates increase with latitude north or south of the equator. Temporally, a tendency for increased incidences of MS has been observed over the past two decades.
Since epidemiological studies of MS in areas close to the Arctic Circle are rare, we evaluated the incidence and prevalence of MS in Northern Ostrobothnia by means of a retrospective cohort study covering the period 1992-2007.
Patients with a definite clinical diagnosis of MS based on the Poser criteria and the early McDonald criteria of 2001 were identified in the region of Northern Ostrobothnia (population 386,972) and the incidence was calculated at 1-year time intervals, both overall and by gender.
The overall prevalence was 103/100,000 (95% CI, 93-113), with a female/male ratio of 2.17. The mean overall incidence was 6.3/100,000 (95% CI, 5.2-7.2). The incidence shows a tendency to increase over the 16-year period due to a pronounced rise in the female incidence.
Our results show a high prevalence of MS in Northern Ostrobothnia and a disproportional increase in the female MS incidence. These recent epidemiological features may be associated with environmental risk factors such as a vitamin D deficit, low life-long UV radiation and the high-latitude geographical location.
PubMed ID
20935028 View in PubMed
Less detail

A linkage study in two families with multiple sclerosis and healthy members with oligoclonal CSF immunopathy.

https://arctichealth.org/en/permalink/ahliterature78970
Source
Mult Scler. 2006 Dec;12(6):723-30
Publication Type
Article
Date
Dec-2006
Author
Haghighi S.
Andersen O.
Nilsson S.
Rydberg L.
Wahlström J.
Author Affiliation
Institute of Clinical Neuroscience, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. sara.haghighi@neuro.gu.se
Source
Mult Scler. 2006 Dec;12(6):723-30
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Adult
Chromosomes, Human, Pair 12
Chromosomes, Human, Pair 19
Chromosomes, Human, Pair 6
Family Health
Female
Genetic Predisposition to Disease
Genome, Human
Histocompatibility testing
Humans
Lod Score
Male
Multiple Sclerosis - genetics - immunology
Oligoclonal Bands - cerebrospinal fluid - genetics
Pedigree
Phenotype
Quantitative Trait Loci
Sweden
Abstract
We studied two extended families in which not only multiple sclerosis (MS) segregates, but also approximately 18% of the cerebrospinal fluid (CSF) investigated blood relatives have 'MS immunopathic trait', an oligoclonal CSF immunopathy similar to that seen in MS, but with no neurological symptoms. Both families fit a genetic model for autosomal dominant inheritance for MS immunopathic trait, although with reduced penetrance in family A. In order to identify genetic factors of importance for the development of MS immunopathic trait, we performed a genome scan using the CHLC/Weber Screening Set (ver 6A), with 285 successful markers, to test the hypothesis that a single gene is causing the MS immunopathic trait in these families. Using a parametric method, we identified regions with suggestive linkage at chromosome 6q12 with a LOD-score of 2.4, putative linkage with LOD-score 1.5 at chromosome 6p21 (HLA region), putative linkage at chromosome 12q24 with a LOD-score of 1.7 and suggestive linkage at chromosome 19q13.2 with a LOD-score of 1.8. The LOD-score at chromosome 19q13.2 increased to 2.2 when only family A was analysed. In family A, all MS patients and two of five individuals with MS immunopathic trait had HLA DRB1*(15) and in family B, all blood relatives had the rare HLA type DRB1*0103, which is associated with other autoimmune diseases. We suggest that DRB1*0103 is a necessary but not sufficient condition for the susceptibility for MS immunopathic trait in this family.
PubMed ID
17262999 View in PubMed
Less detail

Multiple sclerosis patients lacking oligoclonal bands in the cerebrospinal fluid are less likely to develop neutralizing antibodies against interferon beta.

https://arctichealth.org/en/permalink/ahliterature142986
Source
Mult Scler. 2010 Jul;16(7):796-800
Publication Type
Article
Date
Jul-2010
Author
M. Lundkvist
E. Greiner
J. Hillert
A. Fogdell-Hahn
Author Affiliation
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Source
Mult Scler. 2010 Jul;16(7):796-800
Date
Jul-2010
Language
English
Publication Type
Article
Keywords
Antibodies, Neutralizing - blood
Chi-Square Distribution
Genotype
HLA-DR Antigens - genetics - immunology
HLA-DRB1 Chains
Humans
Immunity, Humoral - genetics
Immunologic Factors - immunology - therapeutic use
Interferon-beta - immunology - therapeutic use
Logistic Models
Multiple Sclerosis - cerebrospinal fluid - drug therapy - genetics - immunology
Oligoclonal Bands - cerebrospinal fluid
Registries
Sweden
Treatment Outcome
Abstract
Multiple sclerosis patients without cerebrospinal fluid oligoclonal IgG bands have been proposed to constitute an immunogenetically distinct subgroup of multiple sclerosis that may also differ in terms of prognosis. A proportion of patients with multiple sclerosis receiving IFNbeta develop neutralizing antibodies, which interfere with treatment efficacy. Evidence suggests that the likelihood of developing neutralizing antibodies is partly genetically determined. Here, we hypothesized that absence of oligoclonal IgG bands reflects a property of B-cell responses in oligoclonal IgG band-negative patients characterized by a lessened propensity to develop neutralizing antibodies. We aimed to compare the development of neutralizing antibodies against IFNbeta between oligoclonal IgG band-negative and oligoclonal IgG band-positive multiple sclerosis patients. Treatment, oligoclonal IgG band and neutralizing antibody information was obtained for 2219 patients from the Swedish multiple sclerosis registry and the Swedish neutralizing antibody registry. Additional data on genotype was available for 532 patients. A correlation was found between oligoclonal IgG band negativity and neutralizing antibody negativity (p = 0.02). This difference was confined to neutralizing antibodies against IFNbeta-1a, since oligoclonal IgG band-negative patients were, to a lesser extent, neutralizing antibody positive compared with oligoclonal IgG band-positive patients if treated with IFNbeta-1a (12% vs. 23%; p = 0.005). No difference was observed for IFNbeta-1b-treated patients (44% vs. 46%). We propose that oligoclonal IgG band-negative patients differ immunologically from oligoclonal IgG band-positive patients, potentially influenced by distinct HLA-DRB1 alleles.
PubMed ID
20534645 View in PubMed
Less detail

Oligoclonal band status in Scandinavian multiple sclerosis patients is associated with specific genetic risk alleles.

https://arctichealth.org/en/permalink/ahliterature115733
Source
PLoS One. 2013;8(3):e58352
Publication Type
Article
Date
2013
Author
Inger-Lise Mero
Marte W Gustavsen
Hanne S Sæther
Siri T Flåm
Pål Berg-Hansen
Helle B Søndergaard
Poul Erik H Jensen
Tone Berge
Anja Bjølgerud
Aslaug Muggerud
Jan H Aarseth
Kjell-Morten Myhr
Elisabeth G Celius
Finn Sellebjerg
Jan Hillert
Lars Alfredsson
Tomas Olsson
Annette Bang Oturai
Ingrid Kockum
Benedicte A Lie
Bettina Kulle Andreassen
Hanne F Harbo
Author Affiliation
Department of Neurology, Oslo University Hospital, Ullevål, and Department of Medical Genetics, University of Oslo, Oslo, Norway.
Source
PLoS One. 2013;8(3):e58352
Date
2013
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Case-Control Studies
Denmark
Female
Gene Frequency
Genome-Wide Association Study
Genotype
HLA-DRB1 Chains - genetics
Humans
Male
Multiple Sclerosis - cerebrospinal fluid - epidemiology - genetics
Norway
Oligoclonal Bands - cerebrospinal fluid - genetics
Polymorphism, Single Nucleotide
Sweden
Abstract
The presence of oligoclonal bands (OCB) in cerebrospinal fluid (CSF) is a typical finding in multiple sclerosis (MS). We applied data from Norwegian, Swedish and Danish (i.e. Scandinavian) MS patients from a genome-wide association study (GWAS) to search for genetic differences in MS relating to OCB status. GWAS data was compared in 1367 OCB positive and 161 OCB negative Scandinavian MS patients, and nine of the most associated SNPs were genotyped for replication in 3403 Scandinavian MS patients. HLA-DRB1 genotypes were analyzed in a subset of the OCB positive (n?=?2781) and OCB negative (n?=?292) MS patients and compared to 890 healthy controls. Results from the genome-wide analyses showed that single nucleotide polymorphisms (SNPs) from the HLA complex and six other loci were associated to OCB status. In SNPs selected for replication, combined analyses showed genome-wide significant association for two SNPs in the HLA complex; rs3129871 (p?=?5.7×10(-15)) and rs3817963 (p?=?5.7×10(-10)) correlating with the HLA-DRB1*15 and the HLA-DRB1*04 alleles, respectively. We also found suggestive association to one SNP in the Calsyntenin-2 gene (p?=?8.83×10(-7)). In HLA-DRB1 analyses HLA-DRB1*15:01 was a stronger risk factor for OCB positive than OCB negative MS, whereas HLA-DRB1*04:04 was associated with increased risk of OCB negative MS and reduced risk of OCB positive MS. Protective effects of HLA-DRB1*01:01 and HLA-DRB1*07:01 were detected in both groups. The groups were different with regard to age at onset (AAO), MS outcome measures and gender. This study confirms both shared and distinct genetic risk for MS subtypes in the Scandinavian population defined by OCB status and indicates different clinical characteristics between the groups. This suggests differences in disease mechanisms between OCB negative and OCB positive MS with implications for patient management, which need to be further studied.
Notes
Cites: Ann Neurol. 2001 Jul;50(1):121-711456302
Cites: Eur J Neurol. 2011 Oct;18(10):1258-6221418440
Cites: Mol Cell Neurosci. 2002 Nov;21(3):393-40912498782
Cites: Neurology. 2003 Feb 25;60(4):647-5112601107
Cites: Tissue Antigens. 2004 Mar;63(3):237-4714989713
Cites: J Neuroimmunol. 2004 May;150(1-2):178-8515081263
Cites: Tissue Antigens. 2004 May;63(5):412-2315104673
Cites: Lancet. 1972 Jun 3;1(7762):1240-14113225
Cites: Ann Neurol. 1983 Mar;13(3):227-316847134
Cites: J Neurol Neurosurg Psychiatry. 1994 Aug;57(8):897-9028057110
Cites: Hum Immunol. 1997 Jun;55(1):59-659328791
Cites: Hum Mol Genet. 2005 Jul 15;14(14):2019-2615930013
Cites: J Neurol Sci. 2006 May 15;244(1-2):97-10216473370
Cites: Hum Mol Genet. 2006 Sep 15;15(18):2813-2416905561
Cites: Neurology. 2006 Sep 26;67(6):1062-417000979
Cites: Science. 2006 Oct 20;314(5798):475-817053149
Cites: J Neuroimmunol. 2006 Nov;180(1-2):17-2816945427
Cites: Am J Hum Genet. 2007 Jul;81(1):17-3117564960
Cites: Medicina (Kaunas). 2011;47(7):368-7322112985
Cites: J Neural Transm. 2012 Jan;119(1):77-8021643791
Cites: Mult Scler. 2012 Jul;18(7):974-8222185806
Cites: Ann Neurol. 2013 Jan;73(1):86-9423225573
Cites: Mult Scler. 2013 Apr;19(5):577-8422961214
Cites: Neurology. 2009 Sep 1;73(9):696-70119720976
Cites: Hum Mol Genet. 2001 Dec 1;10(25):2907-1611741834
Cites: Am J Hum Genet. 2007 Sep;81(3):559-7517701901
Cites: N Engl J Med. 2007 Aug 30;357(9):851-6217660530
Cites: Hum Hered. 2008;66(2):87-9818382088
Cites: Lancet. 2008 Oct 25;372(9648):1502-1718970977
Cites: J Neurol Neurosurg Psychiatry. 2009 Mar;80(3):292-618829628
Cites: J Neurol Sci. 2009 Apr 15;279(1-2):21-519181345
Cites: Mult Scler. 2009 Apr;15(4):407-819324977
Cites: J Neuroimmunol. 2009 May 29;210(1-2):128-3019327846
Cites: J Neuroimmunol. 2009 Jul 25;212(1-2):121-419457560
Cites: Ann Neurol. 2009 Jun;65(6):658-6619630074
Cites: Mult Scler. 2010 Jul;16(7):796-80020534645
Cites: J Neuroimmunol. 2010 Sep 14;226(1-2):172-620678810
Cites: Nucleic Acids Res. 2011 Jan;39(Database issue):D876-8220959295
Cites: Ann Neurol. 2011 Feb;69(2):292-30221387374
Cites: Autoimmun Rev. 2011 Jun;10(8):474-8121440682
Cites: Nature. 2011 Aug 11;476(7359):214-921833088
Cites: J Neurol Sci. 2010 Jan 15;288(1-2):63-719879597
PubMed ID
23472185 View in PubMed
Less detail

9 records – page 1 of 1.