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Histopathologic diagnosis of Allograft rejection in human - Lung

Histopathologic diagnosis of Allograft rejection in human LungLung 2007 Working Formulation for the Classification of Pulmonary Allograft Rejection By the International Society for Heart and Lung Transplantation (ISHLT ) 2013 Updated consensus J Heart Lung Transplant 2007;26:1229–42 J Heart Lung Transplant 2013;32:14-21. Xenotransplantation . 2012 ; 19(3): 144–158Overview Alloreactive injury to the donor can affect both the vasculature and the airways in acute and chronic rejection Acute rejection Perivascular mononuclear cell infiltrates ± subendothelial infiltration so-called endothelialitis or intimitis L ymphocytic bronchitis and bronchiolitis Chronic rejection F ibrous scarring : often dense and eosinophilic , involving the bronchioles (Sometimes) accelerated fibrointimal changes of pulmonary arteries and veins Key histologic discriminator between acute and chronic rejection : The presence of presumed irreversible dense eosinophilic hyaline fibrosis in airways and vessels Histologte Rejection) N ormal pulmonary parenchyma without evidence of mononuclear cell infiltration , hemorrhage or necrosis .A: ACUTE REJECTION Grade A1 (Minimal Acute Rejection ) Scattered , infrequent perivascular mononuclear infiltrates in alveolated lung parenchyma Blood vessels, particularly venules , cuffed by small, round plasmacytoid and transformed lymphocytes forming a ring of two or three cells in thickness within the perivascular adventitia Eosinophils and endothelialitis are not present Infrequent perivascular infiltrates at low-power magnification is not a reliable discriminator between Grade A1 and A2A: ACUTE REJECTION Grade A1 (Minimal Acute Rejection )A: ACUTE REJECTION Grade A2 (Mild Acute Rejection ) More frequent perivascular mononuclear infiltrates surrounding venules and arterioles A mixture of small, round lymphocytes, activated lymphocytes , plasmacytoid lymphocytes, macrophages and eosinophils Frequent endothelialitis subendothelial infiltration by mononuclear cells e perivascular, interstitial and air-space infiltrates of mononuclear cells Prominent alveolar pneumocyte damage and endothelialitis Intra-alveolar necrotic epithelial cells , macrophages, hyaline membranes, hemorrhage and neutrophils Parenchymal necrosis , infarction or necrotizing vasculitis must be distinguished from post-transplantation acute lung injury with a feature of reperfusion-related damage The nature of the tissue damage in Grade A4 has a potential relationship with an antibody-mediated form of acute rejectionA: ACUTE REJECTION Grade A4 (Severe Acute Rejection )B: AIRWAY INFLAMMATION : LYMPHOCYTIC BRONCHIOLITIS Only to small airways (bronchioles) Not the inflammation in cartilage-containing large airways The airway inflammation can be present in the absence of perivascular infiltrates (Grade A) Rigorous exclusion of infection is necessaryB: AIRWAY INFLAMMATION : LYMPHOCYTIC BRONCHIOLITIS Grade B0 (No Airway Inflammation) No evidence of bronchiolar inflammationB: AIRWAY INFthelial ulceration, fibrino -purulent exudate, cellular debris and neutrophils Dominant neutrophils infiltration within the epithelium and submucosa with submucosal mononuclear cells I nfection (rather than rejection)B: AIRWAY INFLAMMATION : LYMPHOCYTIC BRONCHIOLITIS Grade B2R (High-grade Small Airway Inflammation)B: AIRWAY INFLAMMATION : LYMPHOCYTIC BRONCHIOLITIS Grade BX ( Ungradeable Small Airways Inflammation) Due to sampling problems , infection, tangential cutting, artifact, etc .C: CHRONIC AIRWAYS REJECTION: OBLITERATIVE BRONCHIOLITIS Dense eosinophilic hyaline fibrosis in the submucosa of membranous and respiratory bronchioles, resulting in partial or complete luminal occlusion C an be concentric or eccentric M ay be associated with fragmentation and destruction of the smooth muscle and elastica of the airway wall May extend into the peribronchiolar interstitium Mucostasis and/or foamy histiocytes in the distal air spaces are commonly associated C0 : No evidence of obliterativey bacterial and viral), graft preservation injury and drug reactions  should be confirmed by capillary C4d staining J Heart Lung Transplant 2013;32:14-21.Acute Antibody-mediated ( Humoral ) Rejection Histopathologic findings Neutrophilic capillaritis Neutrophilic septal margination High-grade acute cellular rejection ( ≥ A3 ) Persistent/recurrent acute cellular rejection (any A Grade) Acute lung injury pattern/diffuse alveolar damage High-grade lymphocytic bronchiolitis (Grade B2R ) Persistent low-grade lymphocytic bronchiolitis (Grade B1R) Obliterative bronchiolitis (Grade C1 ) Arteritis in the absence of infection or cellular rejection Graft dysfunction without morphologic explanation Any histologic findings in setting of de novo DSA positivity J Heart Lung Transplant 2013;32:14-21.PULMONARY XENOGRAFT REJECTION ISSUES As with other pig vascularized organs, the pig lung can be injured by antibody binding and complement activation at the endothelial cell interface. The lung also appea

의/약학| 2013.11.27| 27페이지| 3,000원| 조회(93)

생명공학, 면역학, 병리학, 의학, 조직학, 외과, 면역반응, 거부반응, 이종이식, 이식..

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Histopathologic diagnosis of Allograft rejection in human & pig xenograft - Liver

Histopathologic diagnosis of Allograft rejection in human LiverLiver 1997 Banff schema for grading liver allograft rejection J Clin Pathol 2010;63:47–74 Hepatology 1997;25:658–63 PLoS One. 2012;7(1): e29720ACUTE CELLULAR REJECTION Portal vein endothelium and bile ducts are targets of injury Bile duct epithelium, Vascular endothelial cells in portal tracts and perivenular areas of zone 3 The infiltrates tend to cluster around with little to no spillover to the lobule through the interface hepatocytes No significant involvement in lobular regions between the portal tract and zone 3 venules  helpful in differentiating typical ACR from hepatitis In the more severe forms, infiltrates involve the perivenular parenchyma, with or without hepatocellular necrosisACUTE CELLULAR REJECTION Parameter scored Criteria* RAI score Portal inflammation Inflammation in minority of portal tracts , not expanding and mostly lymphocytic 1 Inflammation in and expanding majority or all portal tracts , mixed lymsed nucleocytoplasmic ratio, cytoplasmic vacuolisation , disordered polarity and/or irregular spacing in epithelium 2 Inflammation affecting duct epithelium in most portal tracts with marked evidence of epithelial injury in most ducts , such as increased nucleocytoplasmic ratio, cytoplasmic vacuolisation , disordered polarity and/or irregular spacing in epithelium; outright duct necrosis can be seen in some ducts 3 Venous phlebitis Subendothelial lymphocytes in some but not the majority of portal and/or hepatic venules 1 Subendothelial lymphocytes in most portal and/or hepatic venules 2 Banff 1997 criteria for scoring acute cellular rejection in liver allografts The table is modified from the Banff schema for grading liver allograft rejection: an international consensus document. *Key features differentiating one score in each parameter from the next higher score are underlined. RAI, Rejection Activity Index.ACUTE CELLULAR REJECTION Portal inflammation Usually but not always mixed celllifting of the endothelium to more plump shape Moderate ‘‘ embolisation ’’ into the vascular lumen ± nuclear atypia Severe accompanied by perivenular inflammation extension into the lobule  necrosis of surrounding hepatocytes usually around terminal hepatic venulesACUTE CELLULAR REJECTION Subendothelial inflammation Bile duct injury Bile duct injury Portal inflammation Perivenular inflammation Portal inflammation No lobular activity Hepatic vein phlebitisLATE CELLULAR REJECTION ACR occurs late ( after 6 months) Pattern and nature of inflammatory infiltrates sometimes differs More hepatitic features interface activity, central perivenulitis and lobular inflammation Monotypic/less mixed portal infiltrates Less prominent duct injuryCHRONIC REJECTION Vascular endothelial injury Hepatic artery and peribiliary plexus Bile duct injury Epithelial senescence Irregular bile duct epithelial size with non-uniform spacing, cytoplasmic eosinophilia and high nucleocytoplasmic ratio No association wi of necrosis Features mimicking preservation/reperfusion injuries (zone 3 hepatocellular ‘‘loosening’’ and cholestasis) in the less affected areas Bile duct Ischemic necrosis of bile ducts of all calibers Loss of small bile ducts Vessels (small, intermediate and sometimes large) Thromboses Vasculitis : Neutrophilic exudation and fibrin deposits in around vascular walls IHC : hardly necessary C4d , C1q or immunoglobulins (almost always IgG , ± IgM also) in vascular and sinusoidal wallsANTIBODY-MEDIATED REJECTION Less aggressive variant Not well defined Overlap with preservation/reperfusion injury Zone-3-accentuated cholestasis Portal expansion with edema Ductular proliferation (exclude obstruction/ stricturing ) In hilum Endothelial hypertrophy and myocyte necrosis, vacuolisation and thickening Necrosis of large bile ducts Congestion of peribiliary plexus IHC C4d : portal capillaries and veins and hepatic venuleHISTOPATHOLOGY OF XENOGRAFT Long-surviving ( 1 day) pig-to-baboon liver (GTKses distention) of unknown etiology ( Fig D) Frequent small fibrin thrombi in portal vessels Variable extent of ductal and occasional canalicular bile stasis PLoS One. 2012;7(1):e29720HISTOPATHOLOGY OF XENOGRAFT Long-surviving ( 1 day) pig-to-baboon liver (GTKO) Necropsy Grossly dark areas: generally similar to light areas More severe/extensive necrosis vastly increased hemorrhage Often total lobular hemorrhagic necrosis with only focal hepatocytes spared(Fig E) Occasional thrombosis Again central lobular involvement Hepatocellular cytoplasmic vacuolar change and distention Distinct infarction consistent with gross Large multifocal fibrin thrombi and severe hepatocyte disassociation/individualization Numerous bacterial colonies associated with pre-mortem retrograde migration of enteric bacterial (No inflammation was noted) PLoS One. 2012;7(1):e29720HISTOPATHOLOGY OF XENOGRAFT Immunohistopathology of liver xenografts Cellular infiltrates 2 hr Bx : No T or B cell infiltrate (very mild CD

의/약학| 2013.11.27| 18페이지| 3,000원| 조회(60)

생명공학, 면역학, 병리학, 의학, 조직학, 외과, 면역반응, 거부반응, 이종이식, 이식..

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Histopathologic diagnosis of Allograft rejection in human & pig xenograft - kidney

Histopathologic diagnosis of Allograft rejection in human KidneyKidney Banff 2007 Classification of Renal Allograft Pathology based on Banff 97 Working Classification of Renal Allograft Pathology Am J Transplant 2008; 8: 753–760 Kid Int 1999; 55: 713–723 J Clin Pathol 2010 63: 26-37 (Figure ) J Am Soc Nephrol 2012; 23(2): 225–235OVERVIEW Based on Banff 97 classification Range of findings in allograft biopsies Semiquantitative grading of changes Both acute/active rejection chronic/ sclerosing allograft nephropathy Banff 2007 updates: Addition of Scoring of peritubular capillaritis for acute antibody-mediated rejection Multiple diagnostic categories could be suggested for single biopsy specimen ex) Acute antibody-mediated rejection with Acute T-cell-mediated rejection, simultaneouslySCORE SYSTEM Acute lesion scoring Lymphocyte in epithelial layer Inflammatory cells in intimaSCORE SYSTEM Acute lesion scoring Neutrophil Interstitial inflammationSCORE SYSTEM Chronic lesion scoring Interstitial fibrosis Tubular atrophySCORE SYSTEM Chronic lesion scoring Thickened capillary loop Silver stainingSCORE SYSTEM Chronic lesion scoringSCORE SYSTEM Others : ptc scoring updated 2007 ptc 1 ptc 2 ptc 3SCORE SYSTEM IHC : C4d stainingDIAGNOSTIC CATEGORIESDIAGNOSTIC CATEGORIES (cg 0) (ci0/ct1 or ci1/ct1) (ci2/ct2) (ci3/ct3)PATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS Hyperacute rejection did not occur in GTKO kidney xenografts Acute humoral rejection : Xenograft loss by 34 days Immunotolerance -treated group : 2/4 had normal function Mild form but transient graft dysfunction reversible , mild microangiopathic glomerulopathy probably associated with preformed antibodies Severe form unstable graft function chronic xenograft glomerulopathy J Am Soc Nephrol 2012; 23(2): 225–235PATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS J Am Soc Nephrol 2012; 23(2): 225–235 Pathologic changes in the grafts of the immunotolerance protocol Mild thrombotic microangiopathic glomerulopathy (I) Recovered after 2wks(K) No cellular rejection and arteriolar changes Focal mesangial proliferation with double GBM (M) Interstitial fibrosis (N)PATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS Pathologic changes in the grafts of the immunotolerance protocol IF : Reversible glomerular injury deposition IgG (-) vs. IgM (+) C4d(+) C5b-9(+) Deposition decreased in process of time J Am Soc Nephrol 2012; 23(2): 225–235PATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS Acute humoral rejection : Xenograft loss by 34 days Immunosuppression Tx group : All 3/3 grafts failed Thrombotic microangiopathic glomerulopathy Multiple platelet-fibrin microthrombi Focal interstitial hemorrhage Acute cellular xenograft rejection IgM , IgG , C4d, and C5b-9 deposition Endothelial cell death Diffuse endothelial procoagulant activation with high expression of tissue factor and vWF Low expression of the ectonucleotidase CD39 J Am Soc Nephrol 2012; 23(2): 225–235PATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS TUNEL dead cells CD41 activated platelets J Am Soc Nephrol 2012; 23(2): 225–235 fibrin exudation fibrin thrombi Pathologic features of graft failure in the immunosuppression protocol Thrombotic microangiopathic glomerulopathy Interstitial edema Focal hemorrhage Fibrin thrombi in peritubular capillariesPATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS J Am Soc Nephrol 2012; 23(2): 225–235 Pathologic features of graft failure in the immunosuppression protocol Thrombotic microangiopathic glomerulopathy multiple thrombi fibrin exudation enlarged endothelial cells mesangial proliferativePATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS J Am Soc Nephrol 2012; 23(2): 225–235 Pathologic features of graft failure in the immunosuppression protocol Thrombotic microangiopathic glomerulopathy CD41 [red] + Fibrin [green] CD41 [red] + IgM [green] CD41 [red] + C4d [green] Thrombosis in small arteriesPATHOLOGIC CHARACTERISTICS OF TRANSPLANTED KIDNEY XENOGRAFTS Pathologic features of graft failure in the immunosuppression protocol IF: immunoglobulin and complement deposition in glomeruli and small arteries and focally along peritubular capillaries J Am Soc Nephrol 2012; 23(2): 225–235{nameOfApplication=Show}

의/약학| 2013.11.27| 20페이지| 3,000원| 조회(71)

생명공학, 면역학, 병리학, 의학, 조직학, 외과, 면역반응, 거부반응, 이종이식, 이식..

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Histopathologic diagnosis of Allograft rejection in human - heart

Histopathologic diagnosis of Allograft rejection in human HeartHeart 2007 Working Formulation for the Classification of Pulmonary Allograft Rejection By the International Society for Heart and Lung Transplantation (ISHLT ) 2011 Updated consensus J Heart Lung Transplant 2005;24:1710–20 J Heart Lung Transplant 2011;30(6): 601-11 Curr Opin Organ Transplant 2012;17(2):148–154Overview Inflammatory Infiltrate Predominantly comprised of lympho cytes, as well as macrophages and occasional eosinophils Unusual findings Neutrophils with mild rejection : healing ischemic injury, antibody-mediated ( humoral ) rejection or infection Plasma cells : Quilty lesion, healing ischemic injury or a lymphoproliferative disorder ( plasmacytoid lymphocytes ) Myocyte Damage Damage or injury to the myocardium, originally termed “ myocyte necrosis” Severe rejection : cell death Milder rejection : myocytolysis and no contraction band or coagulation necrosis Myocytolysis : clearing of the sarcoplasm and nuclei, witt associated myocyte damageACUTE CELLULAR REJECTION Grade 1 R (mild, low-grade, acute cellular rejection)ACUTE CELLULAR REJECTION Grade 2 R (moderate, intermediate-grade, acute cellular rejection) 2 or more foci of mononuclear cells (lymphocytes/macrophages ) with associated myocyte damage Eosinophils may be present Intervening areas of uninvolved myocardium are present between the foci of rejectionACUTE CELLULAR REJECTION Grade 2 R (moderate, intermediate-grade, acute cellular rejection)ACUTE CELLULAR REJECTION Grade 3 R (severe, high-grade, acute cellular rejection) Diffuse inflammatory process either predominantly lymphocytes and macrophages or a polymorphous infiltrate Intensity of the infiltrate may vary between foci Multiple areas of myocyte damage Edema , interstitial hemorrhage and vasculitis may be presentACUTE CELLULAR REJECTION Grade 3 R (severe, high-grade, acute cellular rejection )ACUTE ANTIBODY-MEDIATED (HUMORAL) REJECTION AMR 0 Negative for antibody-mediated rejectionACstIF : IgG (+) IF : C4d(+) IHC : CD68(+) IHC : C4d(+)ACUTE ANTIBODY-MEDIATED (HUMORAL) REJECTION Updated consensus (2011) For IHC, C4d is the minimum requirement CD68 should be considered. For IF, C3d and C4d is agreed for the primary panel. For C4d staining, only the interstitial capillaries should be assessed. C4d staining should be avoided in the first 2 weeks after transplant, to prevent perioperative confounding factors. Recommended surveillance protocol includes 2 biopsies in the first month ( eg , at 2 and 4 weeks) and then according to the center’s circulating antibody monitoring schedule ( eg , at 1, 3, 6, and 12 months ). After a positive biopsy, subsequent biopsies should be studied by immunostaining until a negative result is achieved. F or IF, the immunostaining intensity of 2+ or 3+ was required for a positive result. For both IF and IC, only multifocal or diffuse staining constitutes a positive result . J Heart Lung Transplant 2011;30(6 ):601-11ACUTE ANTIBODY-MEDIATED (Hntibody repertoire consists of germline encoded polyreactive antibody ( IgM ) produced in the absence of clear immune challenge. Natural antibody also includes reactivity to αGal and to blood groups A and B glycans which develop in response to intestinal microflora . Naïve human and nonhuman primate sera includes antibody reactivity to α 1,3 galactosyltransferase gene knock-out (GTKO) pig cells. In primates this in mainly IgM and in humans it is a mixture of IgG and IgM . Preformed non-Gal antibody is cytotoxic to GTKO peripheral blood mononuclear cells in most human sera and about 64% of baboon sera. The level of non-Gal antibody and cytotoxicity is generally reduced compared to wild type pig cells and there is a wide range of individual variation. The impact of preformed non-Gal antibody in cardiac xenotransplantation ( CXTx ) is not evident using recipients with minimal antibody reactivity to GTKO pig cells. Recent studies using recipients with demonstrable preformed non-Gal antibodt preformed non-Gal antibody is commonly present and can induce early graft injury. This suggests that methods to deplete or block preformed non-Gal antibodies may be needed to prevent early graft injury and GTKO xenograft rejection. Curr Opin Organ Transplant 2012;17(2):148–154CARDIAC XENOGRAFT REJECTION ISSUES Fibrin and platelet rich microvascular thrombosis and myocardial coagulative necrosis are the prominent histologic features of GTKO cardiac xenograft rejection. Similar pathology is seen only in severe manifestations of antibody-mediated allograft rejection. It is unclear if this difference is the consequence of higher concentrations and greater diversity of non-Gal antibody , or due to known disparities in haemostatic regulation between pigs and humans. Dysfunction of porcine thrombomodulin , and von Willebrand factor, spontaneous porcine EC dependent aggregation of human platelets, and loss of CD39 expression from activated endothelial cell (EC)s would all promote intragraft ow}

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생명공학, 면역학, 병리학, 의학, 조직학, 외과, 면역반응, 거부반응, 이종이식, 이식..

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Anatomy of lung

Apex - Blunt superior end of the lung- Above the level of the 1st ribThree borders - Anterior- Inferior- PosteriorThree surfaces - Costal- Mediastinal- Diaphragmatic*ight lung is- -arger & heavier -shorter & wider rt. diaphragm is higher heart & pericardium bulge more to the left-straighter anterior borderleft lung has a deep cardiac notch & the lingula

의/약학| 2013.03.24| 11페이지| 1,500원| 조회(199)

간호학, 폐, 의학, 해부, Lung, anatomy

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