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  1. Book: Atlas of medical renal pathology

    Bonsib, Stephen M.

    (Atlas of anatomic pathology)

    2013  

    Title variant Medical renal pathology
    Author's details Stephen M. Bonsib
    Series title Atlas of anatomic pathology
    Keywords Kidneys--Diseases--Atlases
    Language English
    Size XVI, 266 S. : überw. Ill., 28 cm
    Publisher Springer
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT017683725
    ISBN 978-1-4614-7149-3 ; 9781461471509 ; 1-4614-7149-4 ; 1461471508
    Database Catalogue ZB MED Medicine, Health

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    2013 A 1484 available for loan (reading room) Lesesaal EG

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  2. Article ; Online: Renal Hypoplasia, From Grossly Insufficient to Not Quite Enough: Consideration for Expanded Concepts Based Upon the Author's Perspective With Historical Review.

    Bonsib, Stephen M

    Advances in anatomic pathology

    2020  Volume 27, Issue 5, Page(s) 311–330

    Abstract: Hypoplasia is defined in the Merriman-Webster dictionary as "a condition of arrested development in which an organ, or part, remains below the normal size, or in an immature state." The degree of reduced size is not definitional. Renal hypoplasia, ... ...

    Abstract Hypoplasia is defined in the Merriman-Webster dictionary as "a condition of arrested development in which an organ, or part, remains below the normal size, or in an immature state." The degree of reduced size is not definitional. Renal hypoplasia, however, has historically been defined as a more marked reduction in renal mass such that presentation in childhood is the norm. There are 3 commonly recognized types of renal hypoplasia, simple hypoplasia, oligomeganephronic hypoplasia (oligomeganephronia) and segmental hypoplasia (Ask-Upmark kidney). They have in common a reduction in the number of renal lobes. A fourth type, not widely recognized, is cortical hypoplasia where nephrogenesis is normal but there is a reduction in the number of nephron generations. Recently there has been great interest in milder degrees of reduced nephron mass, known as oligonephronia because of its association with risk of adult-onset hypertension and chronic kidney disease. Since the last pathology review of this topic was published by Jay Bernstein in 1968, an update of the renal pathology findings in renal hypoplasia is provided with a review of 18 new cases. The renal hypoplasias are then framed within the modern concept of oligonephronia, its diverse causes and prognostic implications.
    MeSH term(s) Humans ; Kidney/pathology ; Kidney Diseases/pathology
    Language English
    Publishing date 2020-06-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1212493-x
    ISSN 1533-4031 ; 1072-4109
    ISSN (online) 1533-4031
    ISSN 1072-4109
    DOI 10.1097/PAP.0000000000000269
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Urologic Diseases Germane to the Medical Renal Biopsy: Review of a Large Diagnostic Experience in the Context of the Renal Architecture and Its Environs.

    Bonsib, Stephen M

    Advances in anatomic pathology

    2018  Volume 25, Issue 5, Page(s) 333–352

    Abstract: The kidney is one of the most complicated organs in development and is susceptible to more types of diseases than other organs. The disease spectrum includes developmental and cystic diseases, involvement by systemic diseases, iatrogenic complications, ... ...

    Abstract The kidney is one of the most complicated organs in development and is susceptible to more types of diseases than other organs. The disease spectrum includes developmental and cystic diseases, involvement by systemic diseases, iatrogenic complications, ascending infections and urinary tract obstruction, and neoplastic diseases. The diagnosis of kidney disease is unique involving 2 subspecialties, urologic pathology and renal pathology. Both renal and urologic pathologists employ the renal biopsy as a diagnostic modality. However, urologic pathologists commonly have a generous specimen in the form of a nephrectomy or partial nephrectomy while a renal pathologist requires ancillary modalities of immunofluorescence and electron microscopy. The 2 subspecialties differ in the disease spectrum they diagnose. This separation is not absolute as diseases of one subspecialty not infrequently appear in the diagnostic materials of the other. The presence of medical renal diseases in a nephrectomy specimen is well described and recommendations for reporting these findings have been formalized. However, urologic diseases appearing in a medical renal biopsy have received less attention. This review attempts to fill that gap by first reviewing the perirenal anatomy to illustrate why inadvertent biopsy of adjacent organs occurs and determine its incidence in renal biopsies followed by a discussion of gross anatomic features relevant to the microscopic domain of the medical renal biopsy. Unsuspected neoplasms and renal cysts and cystic kidney diseases will then be discussed as they create a diagnostic challenge for the renal pathologist who often has limited training and experience in these diseases.
    MeSH term(s) Biopsy ; Clinical Competence ; Humans ; Kidney/pathology ; Kidney/surgery ; Kidney Diseases/pathology ; Kidney Diseases/surgery ; Nephrectomy ; Nephrology/education ; Pathologists/education ; Predictive Value of Tests ; Prognosis ; Specialization ; Urologic Diseases/pathology ; Urologic Diseases/surgery ; Urology/education
    Language English
    Publishing date 2018-07-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1212493-x
    ISSN 1533-4031 ; 1072-4109
    ISSN (online) 1533-4031
    ISSN 1072-4109
    DOI 10.1097/PAP.0000000000000199
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4118: Show issues Location:
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  4. Article ; Online: Nephronophthisis: a pathological and genetic perspective.

    Wolf, Matthias T F / Bonsib, Stephen M / Larsen, Christopher P / Hildebrandt, Friedhelm

    Pediatric nephrology (Berlin, Germany)

    2023  

    Abstract: Nephronophthisis (NPHP) is an autosomal recessive cystic kidney disease and is one of the most frequent genetic causes for kidney failure (KF) in children and adolescents. Over 20 genes cause NPHP and over 90 genes contribute to renal ciliopathies often ... ...

    Abstract Nephronophthisis (NPHP) is an autosomal recessive cystic kidney disease and is one of the most frequent genetic causes for kidney failure (KF) in children and adolescents. Over 20 genes cause NPHP and over 90 genes contribute to renal ciliopathies often involving multiple organs. About 15-20% of NPHP patients have additional extrarenal symptoms affecting other organs than the kidneys. The involvement of additional organ systems in syndromic forms of NPHP is explained by shared expression of most NPHP gene products in centrosomes and primary cilia, a sensory organelle present in most mammalian cells. This finding resulted in the classification of NPHP as a ciliopathy. If extrarenal symptoms are present in addition to NPHP, these disorders are defined as NPHP-related ciliopathies (NPHP-RC) and can involve the retina (e.g., with Senior-Løken syndrome), CNS (central nervous system) (e.g., with Joubert syndrome), liver (e.g., Boichis and Arima syndromes), or bone (e.g., Mainzer-Saldino and Sensenbrenner syndromes). This review focuses on the pathological findings and the recent genetic advances in NPHP and NPHP-RC. Different mechanisms and signaling pathways are involved in NPHP ranging from planar cell polarity, sonic hedgehog signaling (Shh), DNA damage response pathway, Hippo, mTOR, and cAMP signaling. A number of therapeutic interventions appear to be promising, ranging from vasopressin receptor 2 antagonists such as tolvaptan, cyclin-dependent kinase inhibitors such as roscovitine, Hh agonists such as purmorphamine, and mTOR inhibitors such as rapamycin.
    Language English
    Publishing date 2023-11-06
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-023-06174-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book: Atlas of medical renal pathology

    Bonsib, Stephen M

    (Atlas of anatomic pathology)

    2013  

    Author's details Stephen M. Bonsib
    Series title Atlas of anatomic pathology
    MeSH term(s) Kidney Diseases/pathology ; Kidney/pathology
    Language English
    Size xvi, 266 pages :, illustrations
    Document type Book
    ISBN 9781461471493 ; 9781461471509 ; 1461471494 ; 1461471508
    Database Catalogue of the US National Library of Medicine (NLM)

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  6. Article ; Online: The classification of renal cystic diseases and other congenital malformations of the kidney and urinary tract.

    Bonsib, Stephen M

    Archives of pathology & laboratory medicine

    2010  Volume 134, Issue 4, Page(s) 554–568

    Abstract: Context: Renal cystic diseases and congenital abnormalities of the kidney and urinary tract comprise a heterogeneous group of lesions whose pathogenesis has eluded physicians for centuries. Recent advances in molecular and genetic understanding of these ...

    Abstract Context: Renal cystic diseases and congenital abnormalities of the kidney and urinary tract comprise a heterogeneous group of lesions whose pathogenesis has eluded physicians for centuries. Recent advances in molecular and genetic understanding of these diseases may provide the solution to this riddle.
    Objective: The formulation of an effective classification system for these disorders has been elusive but is needed to introduce order while providing a conceptual framework for diagnosis.
    Data sources: This review discusses the evolution, beginning in the 19th century, of postulates regarding the pathogenesis of cystic and developmental renal diseases. Selected classification systems proffered during this period are discussed in pursuit of an ideal classification schema that would account for morphologic features and their clinical importance, with logical links to pathogenesis and treatment. Although this remains an elusive target, its general outline is becoming clearer. A classification approach favored by the author is presented, which incorporates many of the strengths contained in several previous classifications.
    Conclusions: Genetic-and molecular-based postulates regarding the pathogenesis of the renal cystic and developmental diseases have implicated mutated master genes and the modification of genes that are crucial in renal development and genes that are central to the sensory effects of the renal tubular primary cilium on cell physiology. These scientific advances provide pathogenetic links between morphologically and genetically distinct entities and certain cystic and neoplastic entities, associations that seemed implausible not long ago. These advances may eventually provide the basis for future classification systems while suggesting targets for therapeutic approaches in the prevention and treatment of these diseases.
    MeSH term(s) History, 19th Century ; History, 20th Century ; History, 21st Century ; Humans ; Kidney/abnormalities ; Kidney Diseases, Cystic/classification ; Kidney Diseases, Cystic/etiology ; Kidney Diseases, Cystic/history ; Kidney Diseases, Cystic/pathology ; Models, Anatomic ; Urinary Tract/abnormalities
    Language English
    Publishing date 2010-02-11
    Publishing country United States
    Document type Historical Article ; Journal Article ; Review
    ZDB-ID 194119-7
    ISSN 1543-2165 ; 0363-0153 ; 0096-8528 ; 0003-9985
    ISSN (online) 1543-2165
    ISSN 0363-0153 ; 0096-8528 ; 0003-9985
    DOI 10.1043/1543-2165-134.4.554
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Renal cystic diseases and renal neoplasms: a mini-review.

    Bonsib, Stephen M

    Clinical journal of the American Society of Nephrology : CJASN

    2009  Volume 4, Issue 12, Page(s) 1998–2007

    Abstract: The past two decades have witnessed recognition of several new types of renal cell carcinoma, each with distinct cytogenetic abnormalities. Included are several genetic and acquired cystic kidney diseases associated with development of renal cell ... ...

    Abstract The past two decades have witnessed recognition of several new types of renal cell carcinoma, each with distinct cytogenetic abnormalities. Included are several genetic and acquired cystic kidney diseases associated with development of renal cell carcinoma, the topic of this review. The risk in patients with autosomal dominant polycystic kidney disease is not accurately known but may be slightly increased. The risk for patients with von Hippel-Lindau disease is substantial, and death from renal cancer is common. For patients with tuberous sclerosis complex, the challenge is recognition of the occasional malignancy arising in a field of many benign tumors. Patients with end-stage kidney disease and acquired cystic kidney disease may develop a variety of renal cell carcinoma types. Progress in understanding the molecular basis of renal cyst formation and neoplastic disease has fostered development of targeted therapies that now hold promise for a group of neoplasms whose cure was traditionally dependent on surgical approaches.
    MeSH term(s) Carcinoma, Renal Cell/epidemiology ; Carcinoma, Renal Cell/physiopathology ; Carcinoma, Renal Cell/therapy ; Humans ; Kidney Diseases, Cystic/epidemiology ; Kidney Diseases, Cystic/physiopathology ; Kidney Diseases, Cystic/therapy ; Kidney Neoplasms/epidemiology ; Kidney Neoplasms/physiopathology ; Kidney Neoplasms/therapy ; Risk Factors
    Language English
    Publishing date 2009-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.02020309
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Book ; Online: Atlas of Medical Renal Pathology

    Bonsib, Stephen M

    (Atlas of Anatomic Pathology)

    2013  

    Abstract: The kidney is an organ with complex organogenesis susceptible to numerous misadventures in development and is exposed to a diverse array of insults of hematogenous and lower urinary tract origin. This Atlas of Medical Renal Pathology provides an overview ...

    Author's details by Stephen M. Bonsib
    Series title Atlas of Anatomic Pathology
    Abstract The kidney is an organ with complex organogenesis susceptible to numerous misadventures in development and is exposed to a diverse array of insults of hematogenous and lower urinary tract origin. This Atlas of Medical Renal Pathology provides an overview of the development, macroscopic and microscopic features of the normal kidney. This is followed by a comprehensive survey of developmental and cystic kidney diseases, vascular diseases and tubulointerstitial diseases. An emphasis is placed on gross diagnostic findings with detailed histological correlates. In addition, the histological, immunofluorescent, immunohistochemical and ultrastructural features of the major glomerular diseases and renal transplantation pathology are presented. This compendium of non-neoplastic kidney diseases illustrates the vast majority diseases you are likely to encounter in surgical and autopsy pathology
    Keywords Medicine ; Pathology
    Language English
    Size Online-Ressource (XVI, 266 p. 746 illus., 677 illus. in color), digital
    Publisher Springer
    Publishing place New York, NY
    Document type Book ; Online
    Note Includes bibliographical references and index
    ISBN 9781461471493 ; 9781461471509 ; 1461471494 ; 1461471508
    DOI 10.1007/978-1-4614-7150-9
    Database Former special subject collection: coastal and deep sea fishing

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  9. Article ; Online: Fluorescence in situ hybridization for the diagnosis of NPHP1 deletion-related nephronophthisis on renal biopsy.

    Larsen, Christopher P / Bonsib, Stephen M / Beggs, Marjorie L / Wilson, Jon D

    Human pathology

    2018  Volume 81, Page(s) 71–77

    Abstract: Nephronophthisis is an autosomal recessive tubulointerstitial nephropathy that is a leading genetic etiology of end-stage renal disease in children and young adults. Approximately 60% of patients with a known genetic etiology of nephronophthisis are due ... ...

    Abstract Nephronophthisis is an autosomal recessive tubulointerstitial nephropathy that is a leading genetic etiology of end-stage renal disease in children and young adults. Approximately 60% of patients with a known genetic etiology of nephronophthisis are due to homozygous deletion of the NPHP1 gene. We identified a total of 45 renal biopsies from young patients with chronic kidney disease of undetermined etiology and analyzed them for the possibility of nephronophthisis due to NPHP1 deletion using interphase fluorescence in situ hybridization and/or polymerase chain reaction. Homozygous NPHP1 deletion was identified in 9 patients (20%). In cases with adequate tissue, both assays were performed and showed 100% agreement. Blinded histopathologic analysis was then performed and identified 6 lesions that were significantly more common in biopsies from patients with NPHP1 deletion-proven nephronophthisis than chronic kidney injury of other known etiologies. Many of the classically described nephronophthisis biopsy lesions such as tubular basement membrane duplication, presence of cysts, and mononuclear interstitial inflammation were not significantly associated with this disease when compared with biopsies from patients with chronic kidney injury due to other etiologies. There were, however, morphologic lesions that were strongly associated with NPHP1 deletion including tubular abnormalities such as diverticulum, florets, and macula densa-like change as well as interstitial Tamm-Horsfall aggregates, periglomerular fibrosis, and the absence of arteriosclerosis. Awareness of the histopathologic pattern of injury in nephronophthisis combined with testing for NPHP1 deletion enables renal pathologists to provide a definitive pathologic and genetic diagnosis in a subset of patients with this disease.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adolescent ; Adult ; Biopsy ; Child ; Child, Preschool ; Female ; Gene Deletion ; Genetic Markers ; Genetic Predisposition to Disease ; Homozygote ; Humans ; In Situ Hybridization, Fluorescence ; Kidney/pathology ; Kidney Diseases, Cystic/complications ; Kidney Diseases, Cystic/congenital ; Kidney Diseases, Cystic/genetics ; Kidney Diseases, Cystic/pathology ; Male ; Membrane Proteins/genetics ; Phenotype ; Polymerase Chain Reaction ; Predictive Value of Tests ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/pathology ; Risk Factors ; Young Adult
    Chemical Substances Adaptor Proteins, Signal Transducing ; Genetic Markers ; Membrane Proteins ; NPHP1 protein, human
    Language English
    Publishing date 2018-06-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207657-3
    ISSN 1532-8392 ; 0046-8177
    ISSN (online) 1532-8392
    ISSN 0046-8177
    DOI 10.1016/j.humpath.2018.06.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 722: Show issues Location:
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  10. Article: Renal veins and venous extension in clear cell renal cell carcinoma.

    Bonsib, Stephen M

    Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

    2006  Volume 20, Issue 1, Page(s) 44–53

    Abstract: The 2002 TNM formulation defines a pT3b tumor as one that 'extends into the renal vein or its segmental (muscle containing) branches.' This definition elicits uncertainty when veins with little muscle are involved or the relationship to the main renal ... ...

    Abstract The 2002 TNM formulation defines a pT3b tumor as one that 'extends into the renal vein or its segmental (muscle containing) branches.' This definition elicits uncertainty when veins with little muscle are involved or the relationship to the main renal vein is unknown. The diameter and medial thickness of 10 normal renal venous systems were studied and compared to sinus veins involved in 54 pT3b clear cell renal cell carcinomas (CC). All tumors were grossly examined and sampled for histology by the author. An immunoperoxidase cocktail containing CD 31 and actin, Masson trichrome and elastic stains were employed to aid identification of intravenous tumor. The venous dissections showed variable numbers of primary and secondary divisions with substantial overlap in diameter and medial thickness. The medial thickness decreased with each proximal division and ranged from being nonexistent to being thick. Study of the 54 pT3b CC revealed that the initial phase of extrarenal extension involved large caliber veins draining the primary tumor. With extensive venous involvement, tumor invaded through the vein wall into sinus fat or demonstrated retrograde venous extension into adjacent cortex. Correlation between gross and histology revealed that most nodules of tumor within the sinus fat contained evidence of pre-existing veins. The following observations were made: (1) the diameter of a sinus vein or the quantity of muscle is a poor indicator of vein segment or relationship to the main renal vein; therefore, the wording used to define pT3b should be clarified; (2) extrarenal spread in CC begins with intravenous extension whereas sinus fat invasion is usually secondary; (3) retrograde venous extension occurs in cases with massive renal vein involvement; and (4) nodules within the sinus fat usually represent venous involvement.
    MeSH term(s) Actins/analysis ; Carcinoma, Renal Cell/chemistry ; Carcinoma, Renal Cell/pathology ; Humans ; Immunohistochemistry ; Kidney/blood supply ; Kidney/pathology ; Kidney Neoplasms/chemistry ; Kidney Neoplasms/pathology ; Muscle, Smooth, Vascular/pathology ; Neoplasm Invasiveness ; Neoplasm Staging ; Platelet Endothelial Cell Adhesion Molecule-1/analysis ; Practice Guidelines as Topic ; Renal Veins/chemistry ; Renal Veins/immunology ; Renal Veins/pathology ; Staining and Labeling/methods ; Terminology as Topic
    Chemical Substances Actins ; Platelet Endothelial Cell Adhesion Molecule-1
    Language English
    Publishing date 2006-11-17
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 645073-8
    ISSN 1530-0285 ; 0893-3952
    ISSN (online) 1530-0285
    ISSN 0893-3952
    DOI 10.1038/modpathol.3800726
    Database MEDical Literature Analysis and Retrieval System OnLINE

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