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  • 1. Anderson, C.
    et al.
    Andersson, T.
    Wårdell, Karin
    Linköping University, Department of Biomedical Engineering, Biomedical Instrumentation. Linköping University, The Institute of Technology.
    Changes in skin circulation after microdialysis probe insertion visualized by laser Doppler perfusion imaging1994In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 102, no 5, p. 807-811Article in journal (Refereed)
    Abstract [en]

    Microdialysis makes possible in vivo estimation of endogenous and exogenous substances in the dermal extracellular space. Insertion of the microdialysis probe and its subsequent presence in the skin may affect both the reactivity of the skin test site and the measurement of target substances. Laser Doppler flowmetry is a non-invasive method for estimating cutaneous blood flow. A further development of this technique, laser Doppler perfusion imaging, has been used to study the time course of the circulatory changes caused in the area of microdialysis probe insertion. Laser Doppler perfusion imaging was performed prior to, during, and after microdialysis probe insertion in the skin of the ventral forearm in three subjects. Probe insertion caused an increase in skin blood perfusion in the whole test area. About 15 min after probe insertion, the flare, which is presumed to be of chiefly axon reflex origin, began to subside and the circulatory response could be seen to center around the site of insertion and the tip of the probe. Skin perfusion levels had returned to near normal levels within 60 min. Local anesthesia of the point of guide insertion inhibited the flare, but did not affect circulatory reactivity in the skin nearby. Both microdialysis and laser Doppler perfusion imaging seem to be promising new methods in dermatologic research.

  • 2.
    Anderson, Chris
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Cutaneous microdialysis: Is it worth the sweat?2006In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 126, no 6, p. 1207-1209Article in journal (Other academic)
    Abstract [en]

    Microdialysis is a minimally invasive technique for chronological study of metabolic, biochemical, and pharmacological events in living tissue. In the skin, probes are placed in the dermis or subcutis for research in two main areas, percutaneous penetration and various aspects of inflammation. Advances in technique, and the concept of data generation and analysis are leading to new areas of application.

  • 3.
    Beyer, K.
    et al.
    Division of Pediatric Allergy and Immunology, Mount Sinai Medical Center, New York, NY, United States, Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States, Department of Pediatrics, Humboldt University, Berlin, Germany.
    Nickel, R.
    Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States, Department of Pediatrics, Humboldt University, Berlin, Germany.
    Freidhoff, L.
    Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States.
    Björkstén, Bengt
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Pediatrics . Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Huang, S.-K.
    Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States.
    Barnes, K.C.
    Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States.
    MacDonald, S.
    Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States.
    Forster, J.
    Department of Pediatrics, University Hospitals, Freiburg, Germany.
    Zepp, F.
    Department of Pediatrics, University Hospitals, Mainz, Germany.
    Wahn, V.
    Department of Pediatrics, University Hospitals, Düsseldorf, Germany.
    Beaty, T.H.
    Department of Epidemiology, Johns Hopkins University, School of Hygiene and Public Health, Baltimore, United States.
    Marsh, D.G.
    Division of Pediatric Allergy and Immunology, Mount Sinai Medical Center, New York, NY, United States, Division of Clinical Immunology, Department of Medicine, Johns Hopkins University, Baltimore, United States.
    Wahn, U.
    Department of Pediatrics, Humboldt University, Berlin, Germany.
    Association and linkage of atopic dermatitis with chromosome 13q12-14 and 5q31-33 markers2000In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 115, no 5, p. 906-908Article in journal (Refereed)
    Abstract [en]

    Atopic dermatitis is a chronic inflammatory skin disease that affects 10-20% of the population. Linkage of atopy, asthma, allergic rhinitis, and total serum IgE levels to several different chromosomal regions have been described extensively, but little is known about the genetic control of atopic dermatitis. We tested for the association and linkage between atopic dermatitis and five chromosomal regions: 5q31-33, 6p21.3, 12q15-24.1, 13q12-31, and 14q11.2/14q32.1-32.3. Marker analysis was performed in two Caucasian populations: (i) 192 unrelated German children with atopic dermatitis and 59 non-atopic children from a German birth cohort study (MAS '90), parental DNA was tested in 77 of 192 children with atopic dermatitis, (ii) 40 Swedish families with at least one family member with atopic dermatitis selected from the International Study of Asthma and Allergy in Children. Evidence for linkage and allelic association for atopic dermatitis was observed for markers on chromosome 13q12-14 and 5q31-33.

  • 4.
    Bivik, Cecilia
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences.
    Verma, Deepti
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences.
    Winge, Marten C.
    Karolinska Institute, Sweden .
    Lieden, Agne
    Karolinska Institute, Sweden .
    Bradley, Maria
    Karolinska Institute, Sweden .
    Rosdahl, Inger
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Dermatology and Venerology.
    Söderkvist, Peter
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Letter: Genetic Variation in the Inflammasome and Atopic Dermatitis Susceptibility2013In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 133, no 10, p. 2486-2489Article in journal (Other academic)
    Abstract [en]

    n/a

  • 5.
    Carlström, Maria
    et al.
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Ekman, Anna-Karin
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Petersson, Stina
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Enerbäck, Charlotta
    Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Dermatology and Venerology in Östergötland. Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Lack of Evidence for Association of VEGF Polymorphisms in Swedish Patients with Psoriasis2012In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 132, no 5, p. 1510-1513Article in journal (Other academic)
    Abstract [en]

    n/a

  • 6.
    Ekman, Anna-Karin
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Bivik Eding, Cecilia
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Rundquist, Ingemar
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Enerbäck, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology.
    IL-17 and IL-22 Promote Keratinocyte Stemness in the Germinative Compartment in Psoriasis2019In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 139, no 7, p. 1564-+Article in journal (Refereed)
    Abstract [en]

    Psoriasis is an inflammatory skin disorder characterized by the hyperproliferation of basal epidermal cells. It is regarded as T-cell mediated, but the role of keratinocytes (KCs) in the disease pathogenesis has reemerged, with genetic studies identifying KC-associated genes. We applied flow cytometry on KCs from lesional and nonlesional epidermis to characterize the phenotype in the germinative compartment in psoriasis, and we observed an overall increase in the stemness markers CD29 (2.4-fold), CD44 (2.9-fold), CD49f (2.8-fold), and p63 (1.4-fold). We found a reduced percentage of cells positive for the early differentiation marker cytokeratin 10 and a greater fraction of CD29(+) and involucrin thorn cells in the psoriasis KCs than in nonlesional KCs. The up-regulation of stemness markers was more pronounced in the K10(+) cells. Furthermore, the psoriasis cells were smaller, indicating increased proliferation. Treatment with IL-17 and IL-22 induced a similar expression pattern of an up-regulation of p63, CD44, and CD29 in normal KCs and increased the colony-forming efficiency and long-term proliferative capacity, reflecting increased stem cell-like characteristics in the KC population. These data suggest that IL-17 and IL-22 link the inflammatory response to the immature differentiation and epithelial regeneration by acting directly on KCs to promote cell stemness.

  • 7.
    Erlandson, Anna
    et al.
    Sahlgrens University Hospital, Sweden.
    Appelqvist, Frida
    Sahlgrens University Hospital, Sweden.
    Wennberg, Ann-Marie
    Sahlgrens University Hospital, Sweden.
    Holm, Joanna
    Sahlgrens University Hospital, Sweden.
    Enerbäck, Charlotta
    Sahlgrens University Hospital, Sweden.
    Novel CDKN2A mutations detected in western Swedish families with hereditary malignant melanoma2007In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 127, no 6, p. 1465-1467Article in journal (Refereed)
    Abstract [en]

    We have examined alterations in the cyclin-dependent kinase inhibitor 2A (CDKN2A), a major melanoma predisposing gene, in a western-Swedish hereditary melanoma population comprising 107 patients from 68 families. Using sequence analysis and multiplex ligation-dependent probe amplification, we found a novel mutation (Asp108 Tyr), segregating with the disease in three families. This mutation has previously been detected as a somatic mutation in other cancers. We found a previously described Swedish founder mutation (ins113Arg) in one family and a large duplication encompassing the CDKN2A gene locus in another family. Moreover, a debated polymorphism (Ala148Thr) was found in nine families, in which the polymorphism did not segregate with the disease.

  • 8.
    Forslind, B
    et al.
    Karolinska Inst, Dept Med Biophys, EDRG, S-10401 Stockholm, Sweden Cox Analyt Syst AB, Gothenburg, Sweden Natl Lab Forens Lab, Linkoping, Sweden Karolinska Hosp, Dept Dermatol, S-10401 Stockholm, Sweden.
    Stocklassa, M
    Karolinska Inst, Dept Med Biophys, EDRG, S-10401 Stockholm, Sweden Cox Analyt Syst AB, Gothenburg, Sweden Natl Lab Forens Lab, Linkoping, Sweden Karolinska Hosp, Dept Dermatol, S-10401 Stockholm, Sweden.
    Aransay-Vitores, G
    Karolinska Inst, Dept Med Biophys, EDRG, S-10401 Stockholm, Sweden Cox Analyt Syst AB, Gothenburg, Sweden Natl Lab Forens Lab, Linkoping, Sweden Karolinska Hosp, Dept Dermatol, S-10401 Stockholm, Sweden.
    Nilsson, C
    Karlsson, D
    Wiegleb, B
    Karolinska Inst, Dept Med Biophys, EDRG, S-10401 Stockholm, Sweden Cox Analyt Syst AB, Gothenburg, Sweden Natl Lab Forens Lab, Linkoping, Sweden Karolinska Hosp, Dept Dermatol, S-10401 Stockholm, Sweden.
    Evaluation of a new X-ray fluorescent analysis technique for the creation of a Nordic hair database. Elemental distributions within the root and the virgin segment of hair fibres2001In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 117, no 3, p. 312-Conference paper (Other academic)
  • 9. Heilborn, Johan D
    et al.
    Frohm Nilsson, Margareta
    Kratz, Gunnar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Plastic Surgery, Hand Surgery and Burns. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Weber, Günther
    Sörensen, Ole
    Borregaard, Niels
    Ståhle-Bäckdahl, Mona
    The cathelicidin anti-microbial peptide LL-37 is involved in re-epithelialization of human skin wounds and is lacking in chronic ulcer epithelium2003In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 120, p. 379-389Article in journal (Refereed)
  • 10.
    Moore-Millar, Karena
    et al.
    Univ Strathclyde, DMEM, Glasgow, Lanark, Scotland.
    Thomson, Avril
    Univ Strathclyde, DMEM, Glasgow, Lanark, Scotland.
    Liggat, John
    Univ Strathclyde, Glasgow, Lanark, Scotland.
    Shilton, Simon
    Univ Strathclyde, Glasgow, Lanark, Scotland.
    Wiggins, Sally
    University of Strathclyde, Glasgow, Lanark, Scotland.
    Off the top of your head: What makes a wig work for alopecians2013In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 133, no 5, p. 1394-1394, article id P019Article in journal (Refereed)
    Abstract [en]

    Alopecia UK quote that 1.7% of the British population may experience alopecia areata during their lifetime. A large percentage of this population chose to wear wigs to conceal their hair loss. Since 2008 NHS Scotland has spent over £1 million per annum on the provision of wigs to medical hair loss patients, including alopecia. However, little is known about the wig users’ experience or how it affects their body image and quality of life. This study has conducted pilot focus groups, semi-structured interviews, online questionnaires, and physical testing of wig materials to gain a holistic understanding of wig users’ experiences. The findings look at identifying any relationship with fiber technology and personal experiences, and how wig design could improve their quality of life.

  • 11.
    Mörk, Cato
    et al.
    Rikshospitalet, Oslo, Norge.
    Kvernebo, Knut
    Ulleval University Hospital, Oslo, Norge.
    Asker, Claes
    IMT Linköpings universitet.
    Salerud, Göran
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Biomedical Instrumentation.
    Reduced skin capillary density during attacks of erythromelalgia implies arteriovenous shunting as pathogenetic mechanism2002In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 119, p. 949-953Article in journal (Refereed)
  • 12. Mörk, Cato
    et al.
    Salerud, Göran
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Biomedical Instrumentation.
    Asker, Claes
    Kvernebo, Knut
    The prostaglandin E1 analog misoprostol reduces symptoms and microvascular arteriovenous shunting in erythromelalgia - A double-blind, crossover, placebo-compared study2004In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 122, no 3, p. 587-593Article in journal (Refereed)
    Abstract [en]

    Based on previous experience with parenteral prostanoids, we studied the effect of misoprostol treatment, an orally administered prostaglandin E1 analog, in patients with erythromelalgia. Treatment with placebo was followed by treatment with misoprostol (0.4-0.8 mg per d), both for 6 wk. The patients (n = 21) and a study nurse who administered the trial were blinded. The endpoints were change in pain and need for cooling and global assessment of the treatment. Following central body heat provocation, global skin perfusion, capillary morphology, and change in pain were also recorded before and after each treatment period. Results were compared with data from healthy control subjects (n = 11) that did not undergo treatment. Clinical safety and tolerability evaluation included physical examinations, clinical laboratory tests, and monitoring of adverse events. All clinical outcome measures were significantly better after treatment with misoprostol (p < 0.01) as compared with placebo treatment and after a 3- mo follow-up without treatment. The heat-induced increase in global perfusion after misoprostol treatment was similar to the control group and significantly lower when compared with baseline (p < 0.01) and placebo treatment (p < 0.05), respectively. This study demonstrates that misoprostol is clinically superior to placebo in patients with erythromelalgia. The results of the perfusion studies may imply that the mechanism of action of the beneficial effect of misoprostol is reduced microvascular arteriovenous shunting in affected skin.

  • 13.
    Mørk, Cato
    et al.
    National Hospital, Department of Dermatology, Oslo, Norway.
    Asker, Claes
    Linköping University, Department of Biomedical Engineering. Linköping University, The Institute of Technology.
    Salerud, Göran
    Linköping University, Department of Biomedical Engineering. Linköping University, The Institute of Technology.
    Kvernebo, Knut
    Ullevaal Hospital, Department of Cardiothoracic Surgery, University of Oslo, Norway.
    Microvascular arteriovenous shunting is a probable pathogenetic mechanism in erythromelalgia2000In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 114, no 4, p. 643-646Article in journal (Refereed)
    Abstract [en]

    Erythromelalgia is a condition consisting of red, warm, and burning painful extremities. Symptoms are relieved by cold and aggravated by heat. A wide variety of etiologic conditions can cause erythromelalgia, but one common pathogenetic mechanism, microvascular arteriovenous shunting, has been hypothesized. The aim of this study was to test this hypothesis. Quantification of skin microvascular perfusion using laser Doppler perfusion imaging and skin temperature at rest and after central body heating was performed in 14 patients with erythromelalgia and 11 controls. Attacks of erythromelalgia were induced in eight patients after heat provocation. In the plantar region of the foot, the location of numerous anatomical arteriovenous shunts, these patients significantly increased the skin perfusion as compared with asymptomatic patients with erythromelalgia and controls. In the dorsal region with few arteriovenous shunts no significant differences between the groups were demonstrated. The results show a relation between clinical symptoms and increased perfusion in the region of numerous anatomical arteriovenous shunts, and support the hypothesis of increased thermoregulatory arteriovenous shunt flow during attacks in primary erythromelalgia.

  • 14.
    Nikamo, Pernilla
    et al.
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Cheuk, Stanley
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Lysell, Josefin
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Enerbäck, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Dermatology and Venerology.
    Bergh, Kerstin
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Xu Landén, Ning
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Eidsmo, Liv
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Ståhle, Mona
    Karolinska Institutet, Karolinska University Hospital, Stockholm.
    Genetic variants of the IL22 promoter associate to onset of psoriasis before puberty and increased IL-22 production in T cells.2014In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 134, no 6, p. 1535-1541Article in journal (Refereed)
    Abstract [en]

    Most psoriasis susceptibility genes were identified in cohorts of mixed clinical phenotypes and the exploration of genes in clinical subtypes is scarce. IL-22 has an established role in host defense and in psoriasis skin pathology, reflecting the delicate balance between control of infection and immunopathology. In a case-control study, we compared the genetic association to IL22 in psoriasis onset in patients between 0-9 (n=207), 10-20 (n=394), and 21-40 (n=468) years with healthy controls (n=1,529). Logistic regression analysis revealed association to regulatory elements in the IL22 promoter confined to onset of psoriasis before puberty (odds ratio=1.45, P<0.0007). The associated variants contain putative binding sites for AhR, a potent inducer of IL-22 expression. In a luciferase assay, transcriptional activity of a high-risk gene variant resulted in 80% higher promoter activity (P=0.012) compared with a low-risk variant. Ex vivo stimulated T cells from peripheral blood were analyzed with flow cytometry. Children with psoriasis carrying a high-risk variant produced 1.7 times more IL-22 compared with low-risk variants (P=0.042). Our combined genetic and functional data support the notion that a genetic IL22 variant that promotes epithelial barrier defense is preferentially enriched in and may precipitate the onset of psoriasis at an early age.

  • 15.
    Verma, Deepti
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Ekman, Anna-Karin
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Bivik Eding, Cecilia
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Enerbäck, Charlotta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology.
    Genome-Wide DNA Methylation Profiling Identifies Differential Methylation in Uninvolved Psoriatic Epidermis2018In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 138, no 5, p. 1088-1093Article in journal (Refereed)
    Abstract [en]

    Psoriasis is a chronic inflammatory skin disease with both local and systemic components. Genome-wide approaches have identified more than 60 psoriasis-susceptibility loci, but genes are estimated to explain only one-third of the heritability in psoriasis, suggesting additional, yet unidentified, sources of heritability. Epigenetic modifications have been linked to psoriasis and altered DNA methylation patterns in psoriatic versus healthy skin have been reported in whole-skin biopsies. In this study, focusing on epigenetic modifications in the psoriatic uninvolved skin, we compared the lesional and non-lesional epidermis from psoriasis patients with epidermis from healthy controls. We performed an exhaustive genome-wide DNA methylation profiling using reduced representation bisulfite sequencing, which interrogates the methylation status of approximately 3-4 million CpG sites. More than 2,000 strongly differentially methylated sites were identified and a striking overrepresentation of the Wnt and cadherin pathways among the differentially methylated sites was found. In particular, we observe a strong differential methylation in several psoriasis candidate genes. A substantial number of differentially methylated sites present in the uninvolved versus healthy epidermis suggests the presence of a pre-psoriatic state in the clinically healthy skin type. Our exploratory study represents a starting point for identifying biomarkers for psoriasis-prone skin before disease onset.

  • 16. Ågren, MS
    et al.
    Steenfos, HH
    Dabelsteen, S
    Hansen, JB
    Dabelsteen, E.
    Proliferation and mitogenic response to PDGF-BB of fibroblasts isolated from chronic venous leg ulcers is ulcer-age-dependent1999In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 112, p. 463-469Article in journal (Refereed)
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