Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Collagen studies in congenital cutis laxa (1987)
    Springer
    Archives of dermatological research 279 (1987), S. 308-314 
    Details
    ISSN: 1432-069X
    Keywords: Congenital cutis laxa ; Collagen synthesis ; Electron microscopy ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case of congenital cutis laxa (CCL) of unclear mode of inheritance associated with multiple pulmonary artery branch stenosis was extensively investigated to assess possible correlations between clinical, ultrastructural, and biochemical features. Light microscopy revealed that elastic fibers were absent in the papillary dermis, while hypoplastic elsewhere. Transmission electron microscopy showed a poor elastin matrix content in some elastic fibers, variable diameters of collagen fibrils, and abundant glycogen granules in most dermal cells. Measurement of collagen fibril diameters, using an image analyzer, was carried out in the patient and two age- and site-matched controls. A biomodal distribution was found in the upper reticular dermis of the patient. In vitro analysis of collagen in skin fibroblast cultures of the patient showed increased collagen synthesis with a balanced production of type I and type III procollagens. Our study confirms that CCL represents a disorder both of collagen and elastic connective tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431223
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Giant vertebral notochordal rest: a new entity distinct from chordoma (2005)
    Oxford, UK : Blackwell Science Ltd
    Histopathology 47 (2005), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2559.2005.02168.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Thrombin Inhibits the Migration of Human Liver Myofibroblasts (2005)
    Oxford, UK; Malden, USA : Blackwell Science Inc
    Wound repair and regeneration 13 (2005), S. 0 
    Details
    ISSN: 1524-475X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Liver myofibroblasts are the key cells of liver fibrogenesis. Recent data show that the serine proteinase thrombin is involved in fibrogenesis through a mitogenic effect on myofibroblasts. The aim of this study was to evaluate the effects of thrombin on the migration of human liver myofibroblasts; another major parameter in fibrogenesis.In a Boyden chamber assay, thrombin dose-dependently (10−10–10−7 M) decreased spontaneous myofibroblast migration down to 49 ± 1% of control values (p = 5.10−10) without affecting cell adhesion or viability. Thrombin effect was blocked by its specific catalytic inhibitor hirudin and could be reproduced by using the proteinase-activated receptor-1 (PAR-1) agonist SFLLRNP. Thrombin also completely inhibited migration when induced by the chemotactic agent platelet-derived growth factor-BB. We then investigated the signaling mechanisms involved. The COX-2 inhibitor NS398 dose-dependently (2.5–10 μM) blunted the inhibitory effect of thrombin on spontaneous migration. However, NS398 did not reverse the inhibitory effect of thrombin on PDGF-BB-induced migration. Phosphatidylinositol 3-kinase (PI3-K) is a major determinant of chemotaxis induced by PDGF. Whereas thrombin did not itself induce PI3-K activity, as shown by the lack of detectable phosphorylation of Akt-1, it inhibited PDGF-BB-induced Akt-1 phosphorylation. This effect was dependent of the Rho/ROCK pathway since it was abolished in the presence of the ROCK inhibitor Y-27632.In summary, thrombin, acting via a proteinase-activated receptor, inhibits human liver myofibroblasts migration. Inhibition of basal migration is dependent on COX-2, while inhibition of PDGF-BB-induced migration involves decreased PI3-K activation via a Rho/ROCK mechanism. We suggest that thrombin could thus stabilize activated myofibroblasts on the site of active fibrogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1067-1927.2005.130117j.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    The sinusoidal barrier in rats with portacaval anastomosis: A morphometric study (1985)
    Springer
    Virchows Archiv 407 (1985), S. 347-357 
    Details
    ISSN: 1432-2307
    Keywords: Perisinusoidal cell ; Endothelial cell ; Portacaval anastomosis ; Rat ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Shunting of portal blood in the rat leads to liver atrophy and to an increase in arterial blood flow with microcirculatory disturbances. The aim of this study was to investigate the effects of these disturbances on the liver sinusoidal barrier (endothelial and perisinusoidal cells) using morphometric techniques. Rats with portacaval anastomosis (PCA) and sham operated pair-fed controls were studied 3 months after the shunt. Sinusoidal volume density in PCA increased but not significantly and the volume density (Vv) of total endothelial (EC) and perisinusoidal cells (PSC) increased by 104.54% compared to sham operated pair-fed rats. The increase of EC Vv was not associated with an increase in surface density (Sv) suggesting a fall in the number of small fenestrations and an increase in cell thickness. This interpretation supports the morphological observations. The increase of PSC Vv was mainly related to the increase in their subendothelial processes Vv and not to that of the cell body Vv. Lipids Vv and RER Sv expressed per sinusoidal cells remained unchanged suggesting that the balance between the 2 hypothetical functions of the PSC, namely fibrogenesis and storage of vitamin A, was maintained. In conclusion, changes of EC and PSC after PCA result mainly in thickening of the sinusoidal barrier. This increase may impair exchanges between the sinusoidal lumen and Disse space and contribute to functional abnormalities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00710659
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    The sinusoidal barrier in alcoholic patients without liver fibrosis (1986)
    Springer
    Virchows Archiv 409 (1986), S. 385-393 
    Details
    ISSN: 1432-2307
    Keywords: Alcohol ; Human ; Sinusoidal cells ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Alcohol induces morphological changes in the endothelial and perisinusoidal cells at the fibrotic stage of alcoholic liver diseases. Directly or indirectly, through hemodynamic disturbances linked to the enlargement of steatotic hepatocytes, alcohol may modify this barrier before the onset of fibrosis. Liver biopsies were obtained from control and from alcoholic patients and perfusion-fixed. Volume and surface densities of endothelial cells, perisinusoidal cells and their processes were measured. Liver histology was normal in the 2 groups except for steatosis in the alcoholics. Volume densities represented 8.2%, 4.7% and 3.2% of the sinusoid in controls for endothelial cells, perisinusoidal cells and their processes whereas surface densities represented respectively 0.5, 0.23, 0.21 m2/cm3 of sinusoid. Morphometric values were not significantly different in the alcoholic patients. In none of the alcoholic patients did fine morphological studies of sinusoidal cells give any indication of the possible evolution of the alcoholic disease towards fibrosis. These results indicate that in the group of patients studied, alcohol, before the fibrotic stage, did not significantly alter the sinusoidal barrier.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00708255
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Removal of cellular debris formed in the Disse space in patients with cholestasis (1987)
    Springer
    Virchows Archiv 410 (1987), S. 501-507 
    Details
    ISSN: 1432-2307
    Keywords: Cellular debris ; Kupffer ; Endothelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using electron microscopy, we investigated how cellular debris, formed in the Disse space during cholestasis, was cleared. Ten patients with cholestasis of varied origin and severity were studied and compared with 10 controls without liver disease. In cholestatic patients, sinusoidal cells contained variable amounts of amylase PAS-positive material. In clean perfusion-fixed sinusoids the endothelial cells often appeared swollen and active, with few fenestrations. Hepatocyte blebs and cellular debris were sometimes seen in the Disse space. Two mechanisms were apparently involved in the clearing process: phagocytosis by macrophages either infiltrated into the Disse space, or forming the barrier; and the passage of debris from the Disse space into the sinusoidal lumen through the endothelial wall. Debris was either forced through enlarged pores or through the wall, with a progressive invagination followed by an outpouching in the lumen. The force, possibly provided by endothelial massage, may not be sufficient to push out cellular debris from the Disse space; morphological data seemed to indicate that endothelial damage may be a necessary factor. Debris present in the lumen was phagocytized by numerous active macrophages. Cellular debris was not observed in the Disse space of control patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00781685
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Perisinusoidal fibrosis of the liver in patients with thrombocytopenic purpura (1987)
    Springer
    Virchows Archiv 411 (1987), S. 553-559 
    Details
    ISSN: 1432-2307
    Keywords: Thrombocytopenic purpura ; Idiopathic thrombocytopenic purpura ; Liver sinusoidal fibrosis ; Electron microscopy ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 10 patients with thrombocytopenic purpura (TP) underwent splenectomy. Eight of these patients had idiopathic TP (certain or probable). All had normal liver function tests. Liver histology of the surgical biopsy was normal with the exception of a non specific mild portal infiltration in 6 cases. On Sirius red staining the perisinusoidal network was normal in 3 cases, mildly or moderately increased in 5 cases and often associated with perivenular fibrosis. Collagen types I, III, IV, laminin and fibronectin were increased in the 8 biopsies tested. On semi-thin sections, numerous Kupffer cells were observed. Under the electron microscope, sinusoidal abnormalities were very similar in all 7 patients studied: numerous Kupffer cells containing abundant lysosomes, numerous collagen bundles in the Disse space, active endothelial cells, transformation of some perisinusoidal cells into cells with some of the characteristics of fibroblasts (increased RER) and myofibroblasts (peripheral condensations of the filamentous network), increased fragments of basement membrane-like material. In two cases there was an increase in the number of perisinusoidal cells loaded with lipids. The similarity of the lesions and the absence of other fibrogenic causes (except in 2 cases) suggest that TP may represent another group of diseases with perisinusoidal fibrosis. The aetiology of fibrosis remains unknown but platelet derived growth factor and activated macrophages may play a major role.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00713286
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Fine structure of hepatic sinusoids and sinusoidal cells in disease (1990)
    New York, NY : Wiley-Blackwell
    Journal of Electron Microscopy Technique 14 (1990), S. 257-282 
    Details
    ISSN: 0741-0581
    Keywords: Sinusoids ; Endothelial cells ; Kupffer cells ; Perisinusoidal cells ; Pit cells ; Space of Disse ; Extracellular matrix ; Disease ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Notes: Liver sinusoids are special capillaries that are limited by fenestrated endothelial cells, without a genuine basement membrane, surrounded by perisinusoidal cells storing vitamin A, and harbouring Kupffer cells and pit cells, resident macrophages, and large granular lymphocytes, respectively. Each nonparenchymal cell and parenchymal cell of the liver interacts with all others and with the extracellular matrix. Therefore, the functional ability of each cell is constantly being modified by the metabolic activity of the others.Human liver biopsies (132), needle or surgical, perfusion-fixed with glutaraldehyde and processed for transmission electron microscopy (TEM), and occasionally for scanning electron microscopy (SEM), were examined. The study included liver diseases (such as alcoholic liver diseases, benign and malignant liver tumors, cholestasis of various origins, fulminant hepatitis, acute rejection after orthotopic liver transplantation, Budd-Chiari syndrome), as well as general or extrahepatic diseases (such as diabetes, hemochromatosis, hypervitaminosis A, various hematological disorders), and normal controls.Ultrastructural abnormalities are described and illustrated under two different headings: (1) elementary lesions of sinusoidal cells (endothelial, Kupffer, perisinusoidal and pit cells), nonsinusoidal cells (in the space of Disse and/or in the lumen), the extracellular matrix; and (2) the major pathological entities including perisinusoidal fibrosis, capillarization of sinusoids, sinusoidal dilatation, and peliosis. In the discussion, an overview of the major abnormalities reported in the literature is presented, and some specific questions regarding (1) perisinusoidal fibrosis in liver with normal histology, (2) the overload of perisinusoidal cells with lipids in non-hypervitaminosis A intoxication and (3) the etiological relationship of sinusoidal dilatation, peliosis, perisinusoidal fibrosis, or sinusoidal tumors with drugs and toxic compounds are discussed. In the event that lesions are not specific to any diagnosis, the knowledge of the ultrastructure of sinusoids is extremely useful from the perspective of the liver as an ecosystem.
    Additional Material: 24 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jemt.1060140307
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...