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  • 1.
    Abels, Esther
    et al.
    PathAI, MA USA.
    Pantanowitz, Liron
    Univ Pittsburgh, PA USA.
    Aeffner, Famke
    Amgen Inc, CA USA.
    Zarella, Mark D.
    Drexel Univ, PA 19104 USA.
    van der Laak, Jeroen
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk patologi. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Radboud Univ Nijmegen, Netherlands.
    Bui, Marilyn M.
    H Lee Moffitt Canc Ctr and Res Inst, FL USA.
    Vemuri, Venkata N. P.
    Chan Zuckerberg Biohub, CA USA.
    Parwani, Anil V.
    Ohio State Univ, OH 43210 USA.
    Gibbs, Jeff
    Hyman Phelps and McNamara PC, DC USA.
    Agosto-Arroyo, Emmanuel
    H Lee Moffitt Canc Ctr and Res Inst, FL USA.
    Beck, Andrew H.
    PathAI, MA USA.
    Kozlowski, Cleopatra
    Genentech Inc, CA 94080 USA.
    Computational pathology definitions, best practices, and recommendations for regulatory guidance: a white paper from the Digital Pathology Association2019Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    In this white paper, experts from the Digital Pathology Association (DPA) define terminology and concepts in the emerging field of computational pathology, with a focus on its application to histology images analyzed together with their associated patient data to extract information. This review offers a historical perspective and describes the potential clinical benefits from research and applications in this field, as well as significant obstacles to adoption. Best practices for implementing computational pathology workflows are presented. These include infrastructure considerations, acquisition of training data, quality assessments, as well as regulatory, ethical, and cyber-security concerns. Recommendations are provided for regulators, vendors, and computational pathology practitioners in order to facilitate progress in the field. (c) 2019 The Authors. The Journal of Pathology published by John Wiley amp; Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

  • 2.
    Hofvander, Jakob
    et al.
    Lund University, Sweden.
    Arbajian, Elsa
    Lund University, Sweden.
    Stenkula, Karin G.
    Lund University, Sweden.
    Lindkvist-Petersson, Karin
    Lund University, Sweden.
    Larsson, Malin
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Bioinformatik. Linköpings universitet, Tekniska fakulteten.
    Nilsson, Jenny
    Lund University, Sweden.
    Magnusson, Linda
    Lund University, Sweden.
    Vult von Steyern, Fredrik
    Lund University, Sweden; Skåne University Hospital, Sweden.
    Rissler, Pehr
    Department Pathol, Lund, Sweden.
    Hornick, Jason L.
    Harvard Medical Sch, MA 02115 USA.
    Mertens, Fredrik
    Lund University, Sweden; Department Clin Genet, Sweden.
    Frequent low-level mutations of protein kinase D2 in angiolipoma2017Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 241, nr 5, s. 578-582Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tumours displaying differentiation towards normal fat constitute the most common subgroup of soft tissue neoplasms. A series of such tumours was investigated by whole-exome sequencing followed by targeted ultra-deep sequencing. Eighty per cent of angiolipomas, but not any other tumour type, displayed mutations in the protein kinase D2 (PRKD2) gene, typically in the part encoding the catalytic domain. The absence of other aberrations at the chromosome or RNA level suggests that PRKD2 mutations are critical for angiolipoma development. Consistently, the mutated PRKD2 alleles were present at low (3-15%) frequencies, indicating that only a subset of the tumour cells is affected. Indeed, by sequencing mature fat cells and other cells separately, the former typically showed the highest mutation frequencies. Thus, we hypothesize that altered PRKD2 signalling in the adipocytic cells drives tumourigenesis and, in agreement with its pivotal role in angiogenesis, induces the vessel formation that is characteristic for angiolipoma. Copyright (c) 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley amp; Sons, Ltd.

  • 3.
    Keita, Åsa
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin.
    Salim, Sa´ad
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi.
    Jiang, T.
    Department of Clinical and Experimental Medicine Linköping University.
    Yang, P-C
    Intestinal Disease Research Program McMaster University, Hamilton, Canada.
    Franzén, Lennart
    Aleris Medilab Täby.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Magnusson, Karl-Eric
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi.
    Söderholm, Johan D
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Increased uptake of non-pathogenic E. coli via the follicle-associated epithelium in longstanding ileal Crohn's disease2008Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 215, nr 2, s. 135-144Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In Crohn's disease (CD), inflammation is driven by luminal commensal micro-organisms, however, mechanisms of early phases of inflammation need further clarification. The earliest observable lesions of recurrent CD are microscopic erosions at the specialized follicle-associated epithelium (FAE), which lines the Peyer's patches. Therefore, our aim was to investigate the mucosal barrier to non-pathogenic bacteria in FAE of CD. The FAE of macroscopically normal ileum from patients with longstanding CD, ulcerative colitis, and controls was studied in Ussing chambers regarding electrophysiology and permeability to 51Cr-EDTA, horseradish peroxidase, and non-pathogenic E. coli strains. Transepithelial passage routes and uptake into dendritic cells were studied by confocal and electron microscopy. FAE of CD showed increased numbers of adherent bacteria, after E. coli exposure in Ussing chambers, as well as spontaneously in non-exposed archival surgical tissues. Further, we found increased uptake of fluorescent E. coli K-12 and HB101 across FAE of CD, but not in ulcerative colitis. Microscopy demonstrated intercellular and transcellular uptake of E. coli in CD, but only transcellular in controls. FAE exposed to E. coli demonstrated changes in conductance and 51Cr-EDTA permeability, suggesting that bacteria affected the paracellular pathway in CD mucosa. Following bacterial uptake, CD mucosa also demonstrated an increased percentage of E. coli co-localizing with dendritic cells, and augmented tissue release of TNF-α. Our data present novel insights into the pathophysiology of CD by demonstrating a previously unrecognized defect of FAE barrier to bacteria in ileal CD, leading to increased load of commensal bacteria to the inductive sites of mucosal immunity. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

  • 4.
    Mucchiano, Gerd
    et al.
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär och immunologisk patologi. Linköpings universitet, Hälsouniversitetet.
    Häggqvist, Bo
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär och immunologisk patologi. Linköpings universitet, Hälsouniversitetet.
    Sletten, Knut
    Department of Biochemistry and Biotechnology Center of Oslo, University of Oslo, Norway.
    Westermark, Per
    Department of Genetics and Pathology, Uppsala University, Sweden.
    Apolipoprotein A-1-derived amyloid in atherosclerotic plaques of the human aorta2001Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 193, nr 2, s. 270-275Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Previous studies have shown that the amyloid localized to the aortic intima may be a biochemical entity different from other forms of localized amyloid. The amyloid fibril protein in one patient studied consisted of an N-terminal fragment of apolipoprotein A-1 (apo A-1). Since this patient was later shown to carry a missense mutation in the apo A-1 gene, leading to a deletion at position 107 of the mature protein, the question remained whether wild-type apo A-1 is amyloidogenic. In autopsy specimens from the thoracic aorta from 69 individuals, intimal atherosclerotic plaque-related amyloid was present in 11 cases (16%) and amyloid outside plaques in 37 cases (54%). The immunoreactivity of amyloid localized to the aortic intima was evaluated with the aid of antisera against N-terminal segments of apo A-1. The amyloid in association with atherosclerotic plaques was positively labelled by immunohistochemistry. The amyloid fibril protein from one patient, previously shown not to carry any mutation in the apo A-1 gene, was purified and shown by amino acid sequence analysis to be of apo A-1 nature. The result shows that wild-type apo A-1 is amyloidogenic and gives rise to a common localized form of amyloid associated with atherosclerosis.

  • 5.
    Peng, S.
    et al.
    Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Westermark, Gunilla
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Naslund, J.
    Näslund, J., Department of Clinical Neuroscience, Occupational Therapy, and Elderly Care Research (NEUROTEC), Section for Geriatrics, Karolinska Institute, Huddinge, Sweden.
    Häggqvist, Bo
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär och immunologisk patologi.
    Glennert, J.
    Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Westermark, P.
    Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden, Rudbeck Laboratory, Uppsala University, SE-751 85 Uppsala, Sweden.
    A computer-based training system for breast fine needle aspiration cytology2002Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 196, nr 1, s. 113-121Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Fine-needle aspiration (FNA) cytology is a rapid and inexpensive technique used extensively in the diagnosis of breast disease. To remove diagnostic subjectivity, a diagnostic decision support system (DDSS) called CytoInform© has been developed, based on a Bayesian belief network (BBN) for the diagnosis of breast FNAs. In addition to acting as a DDSS, the system implements a computer-based training (CBT) system, providing a novel approach to breast cytology training. The system guides the trainee cytopathologist through the diagnostic process, allowing the user to grade each diagnostic feature using a set of on-screen reference images as visual clues. The trainee positions a slider on a spectrum relative to these images, reflecting the similarity between the reference image and the microscope image. From this, an evidence vector is generated, allowing the current diagnostic probability to be updated by the BBN. As the trainee assesses each clue, the evidence entered is compared with that of the expert through the use of a defined teaching file. This file records the relative severity of each clue and a tolerance band within which the trainee must position the slider. When all clues in the teaching case have been completed, the system informs the user of inaccuracies and offers the ability to reassess problematic features. In trials with two pathologists of different experience and a series of ten cases, the system provided an effective tool in conveying diagnostic evidence and protocols to trainees. This is evident from the fact that each pathologist only misinterpreted one case and a total of 86%/88% (experienced/inexperienced) of all clues assessed were interpreted correctly. Significantly, in all cases that produced the correct final diagnostic probability, the route taken to that solution was consistent with the expert's solution. Copyright © 2001 John Wiley & Sons, Ltd.

  • 6. Peng, Siwei
    et al.
    Westermark, Gunilla
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi.
    Näslund, Jan
    Häggqvist, Bo
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär och immunologisk patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Glennert, Johanna
    Westermark, Per
    Medin and medin-amyloid in ageing inflamed and non-inflamed temporal arteries2002Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 196, s. 91-96Artikel i tidskrift (Refereegranskat)
  • 7.
    Terman, Alexei
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Geriatrik.
    Gustafsson, Bertil
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Brunk, Ulf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi.
    Autophagy, organelles and ageing2007Ingår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 211, nr 2, s. 134-143Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy and other degradative systems, long-lived postmitotic cells, such as cardiac myocytes, neurons and retinal pigment epithelial cells, progressively accumulate biological 'garbage' ('waste' materials). The latter include lipofuscin (a non-degradable intralysosomal polymeric substance), defective mitochondria and other organelles, and aberrant proteins, often forming aggregates (aggresomes). An interaction between senescent lipofuscin-loaded lysosomes and mitochondria seems to play a pivotal role in the progress of cellular ageing. Lipofuscin deposition hampers autophagic mitochondrial turnover, promoting the accumulation of senescent mitochondria, which are deficient in ATP production but produce increased amounts of reactive oxygen species. Increased oxidative stress, in turn, further enhances damage to both mitochondria and lysosomes, thus diminishing adaptability, triggering mitochondrial and lysosomal pro-apoptotic pathways, and culminating in cell death. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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