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Wanders, A.
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Publications (10 of 69) Show all publications
Nordling, S., Brännström, J., Carlsson, F., Lu, B., Salvaris, E., Wanders, A., . . . Magnusson, P. U. (2018). Enhanced protection of the renal vascular endothelium improves early outcome in kidney transplantation: peclinical investigations in pig and mouse. Scientific Reports, 8, Article ID 5220.
Open this publication in new window or tab >>Enhanced protection of the renal vascular endothelium improves early outcome in kidney transplantation: peclinical investigations in pig and mouse
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2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 5220Article in journal (Refereed) Published
Abstract [en]

Ischemia reperfusion injury is one of the major complications responsible for delayed graft function in kidney transplantation. Applications to reduce reperfusion injury are essential due to the widespread use of kidneys from deceased organ donors where the risk for delayed graft function is especially prominent. We have recently shown that coating of inflamed or damaged endothelial cells with a unique heparin conjugate reduces thrombosis and leukocyte recruitment. In this study we evaluated the binding capacity of the heparin conjugate to cultured human endothelial cells, to kidneys from brain-dead porcine donors, and to murine kidneys during static cold storage. The heparin conjugate was able to stably bind cultured endothelial cells with high avidity, and to the renal vasculature of explanted kidneys from pigs and mice. Treatment of murine kidneys prior to transplantation reduced platelet deposition and leukocyte infiltration 24 hours post-transplantation, and significantly improved graft function. The present study thus shows the benefits of enhanced protection of the renal vasculature during cold storage, whereby increasing the antithrombotic and anti-adhesive properties of the vascular endothelium yields improved renal function early after transplantation.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Surgery Urology and Nephrology
Identifiers
urn:nbn:se:umu:diva-146562 (URN)10.1038/s41598-018-21463-1 (DOI)000428235200024 ()29581529 (PubMedID)
Available from: 2018-05-16 Created: 2018-05-16 Last updated: 2018-06-09Bibliographically approved
Lampinen, M., Fredricsson, A., Vessby, J., Wanders, A., Rorsman, F. & Carlson, M. (2016). Expression of the liver homing receptor CXCR3+on colonic CD8+T lymphocytes in patients with primary sclerosing cholangitis provides a possible link between colonic and biliary duct inflammation. Journal of Crohn's & Colitis, 10, S109-S109
Open this publication in new window or tab >>Expression of the liver homing receptor CXCR3+on colonic CD8+T lymphocytes in patients with primary sclerosing cholangitis provides a possible link between colonic and biliary duct inflammation
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2016 (English)In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 10, p. S109-S109Article in journal, Meeting abstract (Other academic) Published
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-122583 (URN)10.1093/ecco-jcc/jjw019.158 (DOI)000374496600160 ()
Note

Supplement: 1. Meeting abstract: P039

Available from: 2016-12-15 Created: 2016-06-20 Last updated: 2018-06-09Bibliographically approved
Rönnblom, A., Holmström, T., Tanghöj, H., Wanders, A. & Sjöberg, D. (2015). Celiac disease, collagenous sprue and microscopic colitis in IBD: observations from a population-based cohort of IBD (ICURE). Scandinavian Journal of Gastroenterology, 50(10), 1234-1240
Open this publication in new window or tab >>Celiac disease, collagenous sprue and microscopic colitis in IBD: observations from a population-based cohort of IBD (ICURE)
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2015 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 50, no 10, p. 1234-1240Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Inflammatory bowel disease (IBD), microscopic colitis and celiac disease are all diseases with worldwide distribution and increased incidence has been reported from many areas. There is a shortage of studies investigating the occurrence of these diseases in the same individual and whether those affected demonstrate any particular phenotype. The aim of the study was to describe the concomitant incidence of microscopic colitis and celiac disease in a population-based IBD cohort. METHODS: All 790 individuals in a prospective population-based cohort included 2005-09 from Uppsala region, Sweden, were reviewed regarding the appearance of microscopic or celiac disease before or after IBD diagnosis. RESULTS: Fifty percent (396/790) of the patients had been examined for the possibility of celiac disease. Seventeen patients with celiac disease were found, representing 2.2% of the cohort. Patients with celiac disease were younger compared to the non-celiac patients and those with colitis had more often an extensive inflammation of the colon. Seventy-one percent (12/17) were women. The majority of the patients were diagnosed with celiac disease before IBD. Five patients with IBD had an earlier diagnosis of microscopic colitis or developed it after the IBD diagnosis. One teenager developed collagenous sprue, misinterpreted as a severe relapse of ulcerative colitis (UC) resulting in colectomy. CONCLUSIONS: The risk for celiac disease seems not to be increased in IBD, but those affected by both diseases seem to be predominantly women with extensive UC. There is a potential association between microscopic colitis and IBD.

Place, publisher, year, edition, pages
Taylor & Francis, 2015
Keywords
celiac disease, collagenous sprue, epidemiology, inflammatory bowel diseases, microscopic colitis
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-110927 (URN)10.3109/00365521.2015.1041152 (DOI)000361324600007 ()25921772 (PubMedID)1502-7708 (Electronic) 0036-5521 (Linking) (ISBN)
Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07Bibliographically approved
Klar, J., Raykova, D., Gustafson, E., Tothova, I., Ameur, A., Wanders, A. & Dahl, N. (2015). Phenotypic expansion of visceral myopathy associated with ACTG2 tandem base substitution. European Journal of Human Genetics, 23(12), 1679-1683
Open this publication in new window or tab >>Phenotypic expansion of visceral myopathy associated with ACTG2 tandem base substitution
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2015 (English)In: European Journal of Human Genetics, ISSN 1018-4813, E-ISSN 1476-5438, Vol. 23, no 12, p. 1679-1683Article in journal (Refereed) Published
Abstract [en]

Familial visceral myopathy (FVM) is a rare heritable and heterogeneous condition due to impaired smooth muscle function. We identified a family segregating 11 individuals with a spectrum of visceral symptoms involving the small intestine, colon, biliary tract, urinary tract and uterus. Whole-exome sequencing revealed a novel heterozygous tandem base substitution c.806_807delinsAA (p.(Gly269Glu)) in ACTG2, encoding smooth muscle actin gamma-2, in affected family members. Variants in ACTG2 were recently identified in FVM with intestinal pseudo-obstruction as well as with the congenital megacystics-microcolon-intestinal hypoperistalsis syndrome. In our family, eight affected members presented with severe complications from the biliary and/or the urinary tracts in addition to gastrointestinal pseudo-obstructions. Furthermore, all affected mothers had a history of assisted deliveries owing to poor progress during labor and weak uterine contractions. The variable involvement of multiple smooth muscle-dependent organs in our family, including the biliary tract and the uterus, add to the phenotypic spectrum associated with ACTG2 missense variants.

Place, publisher, year, edition, pages
Nature Publishing Group, 2015
National Category
Basic Medicine Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-110917 (URN)10.1038/ejhg.2015.49 (DOI)000365129700015 ()25782675 (PubMedID)
Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07Bibliographically approved
Gremel, G., Wanders, A., Cedernaes, J., Fagerberg, L., Hallström, B., Edlund, K., . . . Pontén, F. (2015). The human gastrointestinal tract-specific transcriptome and proteome as defined by RNA sequencing and antibody-based profiling. Journal of gastroenterology, 50(1), 46-57
Open this publication in new window or tab >>The human gastrointestinal tract-specific transcriptome and proteome as defined by RNA sequencing and antibody-based profiling
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2015 (English)In: Journal of gastroenterology, ISSN 0944-1174, E-ISSN 1435-5922, Vol. 50, no 1, p. 46-57Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The gastrointestinal tract (GIT) is subdivided into different anatomical organs with many shared functions and characteristics, but also distinct differences. We have combined a genome-wide transcriptomics analysis with immunohistochemistry-based protein profiling to describe the gene and protein expression patterns that define the human GIT. METHODS: RNA sequencing data derived from stomach, duodenum, jejunum/ileum and colon specimens were compared to gene expression levels in 23 other normal human tissues analysed with the same method. Protein profiling based on immunohistochemistry and tissue microarrays was used to sub-localize the corresponding proteins with GIT-specific expression into sub-cellular compartments and cell types. RESULTS: Approximately 75% of all human protein-coding genes were expressed in at least one of the GIT tissues. Only 51 genes showed enriched expression in either one of the GIT tissues and an additional 83 genes were enriched in two or more GIT tissues. The list of GIT-enriched genes with validated protein expression patterns included various well-known but also previously uncharacterised or poorly studied genes. For instance, the colon-enriched expression of NXPE family member 1 (NXPE1) was established, while NLR family, pyrin domain-containing 6 (NLRP6) expression was primarily found in the human small intestine. CONCLUSIONS: We have applied a genome-wide analysis based on transcriptomics and antibody-based protein profiling to identify genes that are expressed in a specific manner within the human GIT. These genes and proteins constitute important starting points for an improved understanding of the normal function and the different states of disease associated with the GIT.

Place, publisher, year, edition, pages
Springer, 2015
Keywords
RNA expression, Immunohistochemistry, Gastrointestinal tract
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:umu:diva-110913 (URN)10.1007/s00535-014-0958-7 (DOI)000348982100006 ()24789573 (PubMedID)
Note

First online: 01 May 2014

Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07Bibliographically approved
Sangfelt, P., Sundin, A., Wanders, A., Rasmussen, I., Karlson, B. M., Bergquist, A. & Rorsman, F. (2014). Monitoring dominant strictures in primary sclerosing cholangitis with brush cytology and FDG-PET. J Hepatol, 61(6), 1352-7
Open this publication in new window or tab >>Monitoring dominant strictures in primary sclerosing cholangitis with brush cytology and FDG-PET
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2014 (English)In: J Hepatol, Vol. 61, no 6, p. 1352-7Article in journal (Refereed) Published
Abstract [en]

BACKGROUND & AIMS: Despite a high risk of cholangiocellular adenocarcinoma (CCA) it is unclear how surveillance of patients with primary sclerosing cholangitis (PSC) should be performed. METHODS: We evaluated a follow-up algorithm of brush cytology and positron emission tomography/computed tomography with [(18)F] fluorodeoxyglucose ([(18)F]FDG-PET/CT), measured as maximum standardized uptake values, normalized to the liver background (SUVmax/liver) at 180 min, in PSC patients with dominant bile duct strictures. RESULTS: Brush cytology with high grade dysplasia (HGD) was detected in 12/70 patients (17%), yielding a diagnostic sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of 56%, 89%, 75%, and 88%, respectively. Preemptive liver transplantations due to repeated HGD before manifest CCA were performed in six patients. Receiver operating characteristic (ROC) analysis of [(18)F]FDG uptake showed that a SUVmax/liver quotient of 3.3 was able to discriminate between CCA and non-malignant disease with a sensitivity, specificity, PPV and NPV for CCA of 89%, 92%, 62%, 98%, respectively. A SUVmax/liver >3.3 detected CCA in 8/9 patients whereas a quotient <2.4 excluded CCA. Combining brush cytology and quantitative [(18)F]FDG-PET/CT yielded a sensitivity for HGD and/or CCA of 100% and a specificity of 88%. CONCLUSION: Early detection of HGD before manifest CCA is feasible with repeated brush cytology and may allow for preemptive liver transplantation. [(18)F]FDG-PET/CT has a high sensitivity for manifest CCA and a negative scan indicates a non-malignant state of the disease. Brush cytology and [(18)F]FDG-PET/CT are complementary in monitoring and managing PSC patients with dominant strictures.

Keywords
Adenocarcinoma/diagnosis/pathology/radionuclide imaging, Adult, Aged, Aged, 80 and over, Bile Duct Neoplasms/diagnosis/pathology/radionuclide imaging, Bile Ducts, Intrahepatic, Cholangiocarcinoma/diagnosis/pathology/radionuclide imaging, Cholangitis, Sclerosing/*pathology/*radionuclide imaging, Constriction, Pathologic/pathology/radionuclide imaging, Cytological Techniques/*methods, *Disease Progression, Feasibility Studies, Female, *Fluorodeoxyglucose F18, Follow-Up Studies, Humans, Liver Transplantation, Male, Middle Aged, Positron-Emission Tomography/*methods, Prospective Studies, Sensitivity and Specificity, Biliary dysplasia, Brush cytology, Cholangiocellular adenocarcinoma, Endoscopic retrograde cholangiography, Positron emission tomography, [(18)f]fdg
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-110928 (URN)1600-0641 (Electronic) 0168-8278 (Linking) (ISBN)
Note

Sangfelt, Per Sundin, Anders Wanders, Alkwin Rasmussen, Ib Karlson, Britt-Marie Bergquist, Annika Rorsman, Fredrik eng Evaluation Studies Research Support, Non-U.S. Gov't Netherlands 2014/08/12 06:00 J Hepatol. 2014 Dec;61(6):1352-7. doi: 10.1016/j.jhep.2014.07.032. Epub 2014 Aug 9.

Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07
Hallén, K., Sangfelt, P., Nilsson, T., Nordgren, H., Wanders, A. & Molin, D. (2014). Vanishing bile duct-like syndrome in a patient with Hodgkin lymphoma: pathological development and restitution [Letter to the editor]. Acta Oncologica, 53(9), 1271-5
Open this publication in new window or tab >>Vanishing bile duct-like syndrome in a patient with Hodgkin lymphoma: pathological development and restitution
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2014 (English)In: Acta Oncologica, ISSN 0284-186X, E-ISSN 1651-226X, Vol. 53, no 9, p. 1271-5Article in journal, Letter (Refereed) Published
Place, publisher, year, edition, pages
Informa Healthcare, 2014
National Category
Basic Medicine Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-110915 (URN)10.3109/0284186X.2014.897001 (DOI)000342282100020 ()24697745 (PubMedID)1651-226X (Electronic) 0284-186X (Linking) (ISBN)
Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07Bibliographically approved
Dieterich, L. C., Schiller, P., Huang, H., Wawrousek, E. F., Loskog, A., Wanders, A., . . . Dimberg, A. (2013). alphaB-Crystallin regulates expansion of CD11b(+)Gr-1(+) immature myeloid cells during tumor progression. FASEB J, 27(1), 151-62
Open this publication in new window or tab >>alphaB-Crystallin regulates expansion of CD11b(+)Gr-1(+) immature myeloid cells during tumor progression
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2013 (English)In: FASEB J, Vol. 27, no 1, p. 151-62Article in journal (Refereed) Published
Abstract [en]

The molecular chaperone alphaB-crystallin has emerged as a target for cancer therapy due to its expression in human tumors and its role in regulating tumor angiogenesis. alphaB-crystallin also reduces neuroinflammation, but its role in other inflammatory conditions has not been investigated. Here, we examined whether alphaB-crystallin regulates inflammation associated with tumors and ischemia. We found that CD45(+) leukocyte infiltration is 3-fold increased in tumors and ischemic myocardium in alphaB-crystallin-deficient mice. Notably, alphaB-crystallin is prominently expressed in CD11b(+) Gr-1(+) immature myeloid cells (IMCs), known as regulators of angiogenesis and immune responses, while lymphocytes and mature granulocytes show low alphaB-crystallin expression. alphaB-Crystallin deficiency results in a 3-fold higher accumulation of CD11b(+) Gr-1(+) IMCs in tumors and a significant rise in CD11b(+) Gr-1(+) IMCs in spleen and bone marrow. Similarly, we noted a 2-fold increase in CD11b(+) Gr-1(+) IMCs in chronically inflamed livers in alphaB-crystallin-deficient mice. The effect of alphaB-crystallin on IMC accumulation is limited to pathological conditions, as CD11b(+) Gr-1(+) IMCs are not elevated in naive mice. Through ex vivo differentiation of CD11b(+) Gr-1(+) cells, we provide evidence that alphaB-crystallin regulates systemic expansion of IMCs through a cell-intrinsic mechanism. Our study suggests a key role of alphaB-crystallin in limiting expansion of CD11b(+) Gr-1(+) IMCs in diverse pathological conditions.

Keywords
Animals, Antigens, CD11b/*immunology, Base Sequence, Bone Marrow Cells/*immunology, Cell Differentiation, Crystallins/*physiology, DNA Primers, Disease Progression, Humans, Mice, Mice, Inbred C57BL, Teratocarcinoma/immunology/*pathology
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-110902 (URN)1530-6860 (Electronic) 0892-6638 (Linking) (ISBN)
Note

Dieterich, Lothar C Schiller, Petter Huang, Hua Wawrousek, Eric F Loskog, Angelica Wanders, Alkwin Moons, Lieve Dimberg, Anna eng 2012/10/04 06:00 FASEB J. 2013 Jan;27(1):151-62. doi: 10.1096/fj.12-213017. Epub 2012 Oct 2.

Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07
Ramachandran, M., Yu, D., Wanders, A., Essand, M. & Eriksson, F. (2013). An infection-enhanced oncolytic adenovirus secreting H. pylori neutrophil-activating protein with therapeutic effects on neuroendocrine tumors. Mol Ther, 21(11), 2008-18
Open this publication in new window or tab >>An infection-enhanced oncolytic adenovirus secreting H. pylori neutrophil-activating protein with therapeutic effects on neuroendocrine tumors
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2013 (English)In: Mol Ther, Vol. 21, no 11, p. 2008-18Article in journal (Refereed) Published
Abstract [en]

Helicobacter pylori neutrophil-activating protein (HP-NAP) is a major virulence factor involved in H. pylori infection. HP-NAP can mediate antitumor effects by recruiting neutrophils and inducing Th1-type differentiation in the tumor microenvironment. It therefore holds strong potential as a therapeutic gene. Here, we armed a replication-selective, infection-enhanced adenovirus with secretory HP-NAP, Ad5PTDf35-[Delta24-sNAP], and evaluated its therapeutic efficacy against neuroendocrine tumors. We observed that it could specifically infect and eradicate a wide range of tumor cells lines from different origin in vitro. Insertion of secretory HP-NAP did not affect the stability or replicative capacity of the virus and infected tumor cells could efficiently secrete HP-NAP. Intratumoral administration of the virus in nude mice xenografted with neuroendocrine tumors improved median survival. Evidence of biological HP-NAP activity was observed 24 hours after treatment with neutrophil infiltration in tumors and an increase of proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha and MIP2-alpha in the systemic circulation. Furthermore, evidence of Th1-type immune polarization was observed as a result of increase in IL-12/23 p40 cytokine concentrations 72 hours postvirus administration. Our observations suggest that HP-NAP can serve as a potent immunomodulator in promoting antitumor immune response in the tumor microenvironment and enhance the therapeutic effect of oncolytic adenovirus.

Keywords
Adenoviridae/*genetics/metabolism, Animals, Bacterial Proteins/genetics/immunology/*therapeutic use, Cell Differentiation/drug effects, Cell Line, Tumor, Cytokines/metabolism, Female, Genetic Therapy, Genetic Vectors, Humans, Mice, Mice, Nude, Neuroendocrine Tumors/immunology/*therapy, Neutrophils/drug effects/metabolism, Oncolytic Virotherapy, Oncolytic Viruses/*genetics/metabolism, Recombination, Genetic, Tumor Microenvironment/drug effects/immunology, Virulence Factors/metabolism, Xenograft Model Antitumor Assays
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-110926 (URN)1525-0024 (Electronic) 1525-0016 (Linking) (ISBN)
Note

Ramachandran, Mohanraj Yu, Di Wanders, Alkwin Essand, Magnus Eriksson, Fredrik eng Research Support, Non-U.S. Gov't 2013/07/03 06:00 Mol Ther. 2013 Nov;21(11):2008-18. doi: 10.1038/mt.2013.153. Epub 2013 Jul 2.

Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07
Hogberg, N., Stenback, A., Carlsson, P. O., Wanders, A. & Lilja, H. E. (2013). Genes regulating tight junctions and cell adhesion are altered in early experimental necrotizing enterocolitis. J Pediatr Surg, 48(11), 2308-12
Open this publication in new window or tab >>Genes regulating tight junctions and cell adhesion are altered in early experimental necrotizing enterocolitis
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2013 (English)In: J Pediatr Surg, Vol. 48, no 11, p. 2308-12Article in journal (Refereed) Published
Abstract [en]

BACKGROUND/PURPOSE: Necrotizing enterocolitis (NEC) represents one of the gravest complications in preterm infants and carries significant morbidity and mortality. Increased intestinal permeability may play an important role in the pathogenesis of NEC. In this study we investigated the genes regulating structural proteins such as tight junctions (TJ) and cell adhesion in a neonatal rat model of early NEC. METHODS: The studies were performed on Sprague-Dawley rat pups. Experimental NEC was induced using hypoxia/re-oxygenation treatment on day 1 after birth. Intestinal specimens from the ileum were obtained, mRNA was purified, and the transcriptome was analyzed using microarray. RESULTS: We found several TJ genes such as claudins 1, 8, 14, 15, and gap junction protein to be affected. Alterations in genes involved in the inflammatory response was confirmed, along with several genes regulating proteins used as biomarkers for NEC. CONCLUSION: This study indicates that tight junctions and cell adhesion may play a critical role in the pathogenesis of early experimental NEC. Better understanding of the pathogenesis of NEC may lead to novel strategies for the prevention and treatment of NEC.

Keywords
Animals, Animals, Newborn, Anoxia/genetics, Cell Adhesion/*genetics, Cell Adhesion Molecules/biosynthesis/genetics, Disease Models, Animal, Enterocolitis, Necrotizing/etiology/*genetics, Gene Expression Profiling, *Gene Expression Regulation, Hypercapnia/genetics, Ileum/*metabolism, Inflammation, Oligonucleotide Array Sequence Analysis, Oxygen/toxicity, Rats, Rats, Sprague-Dawley, Tight Junctions/*metabolism, Transcriptome, Cell adhesion, Genes, Microarray, Necrotizing enterocolitis, Tight junction
National Category
Basic Medicine
Identifiers
urn:nbn:se:umu:diva-110916 (URN)1531-5037 (Electronic) 0022-3468 (Linking) (ISBN)
Note

Hogberg, Niclas Stenback, Anders Carlsson, Per-Ola Wanders, Alkwin Lilja, Helene Engstrand eng Research Support, Non-U.S. Gov't 2013/11/12 06:00 J Pediatr Surg. 2013 Nov;48(11):2308-12. doi: 10.1016/j.jpedsurg.2013.06.027.

Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2018-06-07

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