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The American journal of pathology 22건

  1. [해외논문]   Table of Contents   SCI SCIE


    The American journal of pathology v.188 no.7 ,pp. A3 - A3 , 2018 , 0002-9440 ,

    초록

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  2. [해외논문]   Editorial Board   SCI SCIE


    The American journal of pathology v.188 no.7 ,pp. A1 - A2 , 2018 , 0002-9440 ,

    초록

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  3. [해외논문]   This Month in AJP   SCI SCIE


    The American journal of pathology v.188 no.7 ,pp. 1509 - 1509 , 2018 , 0002-9440 ,

    초록

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  4. [해외논문]   High Frequency of Ovarian Cyst Development in Vhl 2B/+ ;Snf5 +/− Mice   SCI SCIE

    Kuwahara, Yasumichi (Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina ) , Kennedy, Leslie M. (Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina ) , Karnezis, Anthony N. (Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada ) , Mora-Blanco, E. Lorena (Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital Boston and Harvard University, Boston, Massachusetts ) , Rogers, Arlin B. (Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina ) , Fletcher, Christopher D. (Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts ) , Huntsman, David G. (Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada ) , Roberts, Charles W.M. (Department of Pediatric Oncology, Dana-Farber Cancer Institute, Children's Hospital Boston and Harvard University, Boston, Massachusetts ) , Rathmell, W. Kimryn (Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina ) , Weissman, Bernard E. (Lineb)
    The American journal of pathology v.188 no.7 ,pp. 1510 - 1516 , 2018 , 0002-9440 ,

    초록

    The new paradigm of mutations in chromatin-modifying genes as driver events in the development of cancers has proved challenging to resolve the complex influences over disease phenotypes. In particular, impaired activities of members of the SWI/SNF chromatin remodeling complex have appeared in an increasing variety of tumors. Mutations in SNF5 , a member of this ubiquitously expressed complex, arise in almost all cases of malignant rhabdoid tumor in the absence of additional genetic alterations. Therefore, we studied how activation of additional oncogenic pathways might shift the phenotype of disease driven by SNF5 loss. With the use of a genetically engineered mouse model, we examined the effects of a hypomorphic Vhl 2B allele on disease phenotype, with a modest up-regulation of the hypoxia response pathway. Snf5 +/− ;Vhl 2B/+ mice did not demonstrate a substantial difference in overall survival or a change in malignant rhabdoid tumor development. However, a high percentage of female mice showed complex hemorrhagic ovarian cysts, a phenotype rarely found in either parental mouse strain. These lesions also showed mosaic expression of SNF5 by immunohistochemistry. Therefore, our studies implicate that modest changes in angiogenic regulation interact with perturbations of SWI/SNF complex activity to modulate disease phenotypes.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  5. [해외논문]   Human Streptococcal Necrotizing Fasciitis Histopathology Mirrored in a Murine Model   SCI SCIE

    Keller, Nadia (Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland ) , Andreoni, Federica (Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland ) , Reiber, Claudine (Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland ) , Luethi-Schaller, Helga (Clinic of Preventive Dentistry, Periodontology and Cariology, Division of Oral Microbiology and Immunology, Center of Dental Medicine) , Schuepbach, Reto Andreas (University of Zurich, Zurich, Switzerland ) , Moch, Holger (Institute of Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland ) , Marques Maggio, Ewerton (Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland ) , Zinkernagel, Annelies S. (Department of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland )
    The American journal of pathology v.188 no.7 ,pp. 1517 - 1523 , 2018 , 0002-9440 ,

    초록

    Streptococcal necrotizing fasciitis (NF) causes high morbidity and mortality despite state-of-the-art therapy. Low incidence and rapid disease progression, necessitating immediate initiation of therapy, have proven challenging aspects for setting up prospective randomized trials. This has resulted in little therapeutic progress over the past decade. The validation of reliable murine NF models to study both pathogenesis and optimized therapeutic regimens of streptococcal NF are thus essential. In this study, we characterized a murine NF model and compared the pathology with an in-depth tissue analysis of streptococcal NF in patients. We found that the streptococcal murine NF model closely reflected all histologic characteristics encountered in human streptococcal NF. This murine NF model helps understanding of human NF pathology better in a time-dependent manner and will allow studying novel therapeutic options in the future.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Leukocyte Dynamics during the Evolution of Human Coronary Atherosclerosis : Conclusions from a Sevenfold, Chromogen-Based, Immunohistochemical Evaluation   SCI SCIE

    Zuiderwijk, Melissa (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden ) , Geerts, Marlieke (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden ) , van Rhijn, Connie J. (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden ) , van den Bogaerdt, Antoon (Euro Heart Valve Bank, Beverwijk, the Netherlands ) , Hamming, Jaap F. (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden ) , van Dijk, Rogier A. (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden ) , Lindeman, Jan H. (Einthoven Laboratory for Cardiovascular Medicine, Division of Vascular Surgery, Department of Surgery, Leiden University Medical Center, Leiden)
    The American journal of pathology v.188 no.7 ,pp. 1524 - 1529 , 2018 , 0002-9440 ,

    초록

    Atherosclerosis is a complex process with strong inflammatory component. We developed a straightforward sevenfold staining protocol for simultaneous assessment of dominant leukocyte classes, vascularization, and expression of the putative foam cell maker CD36. The method was applied on human coronaries covering the full spectrum of atherosclerotic disease. Results confirm the progressive association of macrophages and T cells with the process and a global presence of mast cells. B cells are exclusively present in adventitial follicles that accompany the process plaque destabilization (thin cap and ruptured lesions) and are otherwise absent. Neutrophils are only present as part of the hemorrhage that accompanies plaque rupture. This study does not classify CD36 as a key factor in foam cell formation. Observed macrophage accumulation in the neointima of stabilized fibrous calcified plaques is consistent with a process of neoatherosclerosis. This study on human coronaries shows a progressive association of macrophage and T-cell abundance with plaque progression. Follicle-like structures are transiently present during the process of plaque destabilization. Plaque healing is accompanied by cessation of the inflammatory response but followed by a new cycle of atherosclerosis.

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    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Immunolabeling of Cleared Human Pancreata Provides Insights into Three-Dimensional Pancreatic Anatomy and Pathology   SCI SCIE

    Noë (Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , , Michaë (Department of Surgery, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , l (Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , Rezaee, Neda (Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , Asrani, Kaushal (Department of Surgery, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , Skaro, Michael (Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, Maryland ) , Groot, Vincent P. (Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, Maryland ) , Wu, Pei-Hsun (Department of Pathology, Asan Medical Center, University of Ulsan Col) , Olson, Matthew T. , Hong, Seung-Mo , Kim, Sung Joo , Weiss, Matthew J. , Wolfgang, Christopher L. , Makary, Martin A. , He, Jin , Cameron, John L. , Wirtz, Denis , Roberts, Nicholas J. , Offerhaus, G. Johan A. , Brosens, Lodewijk A.A. , Wood, Laura D. , Hruban, Ralph H.
    The American journal of pathology v.188 no.7 ,pp. 1530 - 1535 , 2018 , 0002-9440 ,

    초록

    Visualizing pathologies in three dimensions can provide unique insights into the biology of human diseases. A rapid and easy-to-implement dibenzyl ether-based technique was used to clear thick sections of surgically resected human pancreatic parenchyma. Protocols were applicable to both fresh and formalin-fixed, paraffin-embedded tissue. The penetration of antibodies into dense pancreatic parenchyma was optimized using both gradually increasing antibody concentrations and centrifugal flow. Immunolabeling with antibodies against cytokeratin 19 was visualized using both light sheet and confocal laser scanning microscopy. The technique was applied successfully to 26 sections of pancreas, providing three-dimensional (3D) images of normal pancreatic tissue, pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasms, and infiltrating pancreatic ductal. adenocarcinomas. 3D visualization highlighted processes that are hard to conceptualize in two dimensions, such as invasive carcinoma growing into what appeared to be pre-existing pancreatic ducts and within venules, and the tracking of long cords of neoplastic cells parallel to blood vessels. Expanding this technique to formalin-fixed, paraffin-embedded tissue opens pathology archives to 3D visualization of unique biosamples and rare diseases. The application of immunolabeling and clearing to human pancreatic parenchyma provides detailed visualization of normal pancreatic anatomy, and can be used to characterize the 3D architecture of diseases including pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, and pancreatic ductal adenocarcinomas.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  8. [해외논문]   Obstructive Lymphangitis Precedes Colitis in Murine Norovirus–Infected Stat1-Deficient Mice   SCI SCIE

    Seamons, Audrey (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Treuting, Piper M. (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Meeker, Stacey (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Hsu, Charlie (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Paik, Jisun (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Brabb, Thea (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Escobar, Sabine S. (Department of Comparative Medicine, University of Washington, Seattle, Washington ) , Alexander, Jonathan S. (Department of Molecular and Cellular Physiology, Louisiana State University, Shreveport, Louisiana ) , Ericsson, Aaron C. (Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri ) , Smith, Jason G. (Department of Microbiology, University of Washington, Seattle, Washington ) , Maggio-Price, Lillian (Department of Comparative Medicine, University of Washington, Seattle, Washington)
    The American journal of pathology v.188 no.7 ,pp. 1536 - 1554 , 2018 , 0002-9440 ,

    초록

    Murine norovirus (MNV) is an RNA virus that can prove lethal in mice with impaired innate immunity. We found that MNV-4 infection of Stat1 −/− mice was not lethal, but produced a 100% penetrant, previously undescribed lymphatic phenotype characterized by chronic-active lymphangitis with hepatitis, splenitis, and chronic cecal and colonic inflammation. Lesion pathogenesis progressed from early ileal enteritis and regional dilated lymphatics to lymphangitis, granulomatous changes in the liver and spleen, and, ultimately, typhlocolitis. Lesion development was neither affected by antibiotics nor reproduced by infection with another enteric RNA virus, rotavirus. MNV-4 infection in Stat1 −/− mice decreased expression of vascular endothelial growth factor (Vegf) receptor 3, Vegf-c , and Vegf-d and increased interferon (Ifn)-γ, tumor necrosis factor-α, and inducible nitric oxide synthase. However, anti–IFN-γ and anti–tumor necrosis factor-α antibody treatment did not attenuate the histologic lesions. Studies in Ifnαβγr −/− mice suggested that canonical signaling via interferon receptors did not cause MNV-4–induced disease. Infected Stat1 −/− mice had increased STAT3 phosphorylation and expressed many STAT3-regulated genes, consistent with our findings of increased myeloid cell subsets and serum granulocyte colony-stimulating factor, which are also associated with increased STAT3 activity. In conclusion, in Stat1 −/− mice, MNV-4 induces lymphatic lesions similar to those seen in Crohn disease as well as hepatitis, splenitis, and typhlocolitis. MNV-4–infected Stat1 −/− mice may be a useful model to study mechanistic associations between viral infections, lymphatic dysfunction, and intestinal inflammation in a genetically susceptible host.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  9. [해외논문]   The G-Protein–Coupled Receptor ALX/Fpr2 Regulates Adaptive Immune Responses in Mouse Submandibular Glands   SCI SCIE

    Wang, Ching-Shuen (Address correspondence to Olga J. Baker, D.D.S., Ph.D., School of Dentistry, University of Utah, 383 Colorow Dr., Salt Lake City, UT 84108-1201.) , Baker, Olga J.
    The American journal of pathology v.188 no.7 ,pp. 1555 - 1562 , 2018 , 0002-9440 ,

    초록

    Lipoxin receptor (ALX)/N-formyl peptide receptor (FPR)-2 is a G-protein–coupled receptor that has multiple binding partners, including the endogenous lipid mediators resolvin D1, lipoxin A 4 , and the Ca 2+ -dependent phospholipid-binding protein annexin A1. Previous studies have demonstrated that resolvin D1 activates ALX/Fpr2 to resolve salivary gland inflammation in the NOD/ShiLtJ mouse model of SjOgren syndrome. Moreover, mice lacking the ALX/Fpr2 display an exacerbated salivary gland inflammation in response to lipopolysaccharide. Additionally, activation of ALX/Fpr2 has been shown to be important for regulating antibody production in B cells. These previous studies indicate that ALX/Fpr2 promotes resolution of salivary gland inflammation while modulating adaptive immunity, suggesting the need for investigation of the role of ALX/Fpr2 in regulating antibody production and secretory function in mouse salivary glands. Our results indicate that aging female knockout mice lacking ALX/Fpr2 display a significant reduction in saliva flow rates and weight loss, an increased expression of autoimmune-associated genes, an up-regulation of autoantibody production, and increased CD20-positive B-cell population. Although not all effects were noted among the male knockout mice, the results nonetheless indicate that ALX/Fpr2 is clearly involved in the adaptive immunity and secretory function in salivary glands, with further investigation warranted to determine the cause(s) of these between-sex differences.

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  10. [해외논문]   Characterization of the Small Intestinal Lesion in Celiac Disease by Label-Free Quantitative Mass Spectrometry   SCI SCIE

    Tutturen, Astrid E.V. (Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway ) , Dørum, Siri (Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway ) , Clancy, Trevor (Department of Immunology, Institute for Cancer Research, Oslo University Hospital-Radiumhospitalet, Oslo, Norway ) , Reims, Henrik M. (Department of Pathology, Oslo University Hospital, Oslo, Norway ) , Christophersen, Asbjørn (KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway ) , Lundin, Knut E.A. (KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway ) , Sollid, Ludvig M. (Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway ) , de Souza, Gustavo A. (Proteomics Core Facility, Oslo University Hospital-Rikshospitalet, Oslo, Norway ) , Stamnaes, Jorunn (Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway)
    The American journal of pathology v.188 no.7 ,pp. 1563 - 1579 , 2018 , 0002-9440 ,

    초록

    Global characterization of tissue proteomes from small amounts of biopsy material has become feasible because of advances in mass spectrometry and bioinformatics tools. In celiac disease (CD), dietary gluten induces an immune response that is accompanied by pronounced remodeling of the small intestine. Removal of gluten from the diet abrogates the immune response, and the tissue architecture normalizes. In this study, differences in global protein expression of small intestinal biopsy specimens from CD patients were quantified by analyzing formalin-fixed, paraffin-embedded material using liquid chromatography–mass spectrometry and label-free protein quantitation. Protein expression was compared in biopsy specimens collected from the same patients before and after 1-year treatment with gluten-free diet ( n = 10) or before and after 3-day gluten provocation ( n = 4). Differential expression of proteins in particular from mature enterocytes, neutrophils, and plasma cells could distinguish untreated from treated CD mucosa, and Ig variable region IGHV5-51 expression was found to serve as a CD-specific marker of ongoing immune activation. In patients who had undergone gluten challenge, coordinated up-regulation of wound response proteins, including the CD autoantigen transglutaminase 2, was observed. Our study provides a global and unbiased assessment of antigen-driven changes in protein expression in the celiac intestinal mucosa.

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