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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 6 (1950), S. 14-16 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The effect of desoxyribonuclease and ribonuclease on suspended mitochondria is examined phase-microscopically, making use of secondary mitochondrial swelling in distilled water. The ribonucleoprotein is localized only in the mitochondrial body. The latter disappears completely under the effect of ribonuclease. The membrane possibly contains very small amounts of desoxyribonucleoprotein next to lipoid substances. The mitochondrial body on the other hand appears to be free of these substances.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 6 (1950), S. 16-17 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary It is shown that mitochondria suspended in distilled water are particularly well adapted to electron-microscopic examination, since the membrane can be loosened from the mitochondrial body by this method. The membrane is composed of short protein fibrils and globular protein molecules, and has a thickness of approximately 200 Å. The body cannot be further illuminated, but parts of the periphery show that the protein is here much more compact. It is assumed that this is dependent upon its lipoid contents.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 30 year old male patient with recurrent hemoptoe. The hemorrhages of the lung were accompanied by fever and roentgenologically slight infiltrations of the middle and lower compartments of the lung with simultaneous decrease of hemoglobine. The disease having lasted 16 months the patient has been free of complaints for the last 5 months. The biopsy of the kidney resulted in the diagnosis of a momentarily inactive proliferative focal glomerulitis. This could be confirmed by electron microscopical investigation, although there were found traces of activity. of the cell elements. Deposits of iron faintly indicated under the light microscope, were confirmed by electron microscopy. The total picture corresponds to a typical Goodpasture' syndrome.
    Notes: Zusammenfassung 30jähriger Mann mit rezidivierender Hämoptoe. Die Lungenblutungen waren von Fieber und röntgenologisch flüchtigen Lungeninfiltraten in Mittel- und Untergeschossen, gleichzeitigem Abfall des Hämoglobins begleitet. Bisherige Krankheitsdauer 16 Monate, die letzten 5 Monate war der Patient völlig beschwerdefrei. Die Nierenbiopsie ergab eine momentan inaktive proliferative Herdglomerulitis, die auch elektronenmikroskopisch nachgewiesen werden konnte. Allerdings fanden sich ultrastrukturell noch deutliche Zeichen für Aktivität der Zellelemente. Die lichtmikroskopisch nur angedeutete Eisenablagerung im Deckepithel der Glomerula konnte elektronenmikroskopisch bestätigt werden. — Das Gesamtbild entspricht einem typischen Goodpasture-Syndrom.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 46 (1968), S. 874-881 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary This is a report on two children with the hemolytic-uremic syndrome (Gasser). Case 1 had an unusual course with recurrent exacerbations. During the last episode coagulation studies indicated intravascular coagulation. Therapy with corticosteroids and heparin was without success. The post mortem examination revealed fibrin clots in the glomerular capillaries of the kidneys and a focal glomerulitis which had progressed in several stages. Case 2 developed hyporesorptive hydrocephalus — possibly due to meningeal fibrin clots. The current concepts of pathogenesis and therapy of the hemolytic-uremic syndrome are discussed.
    Notes: Zusammenfassung Es wird über zwei Kinder mit hämolytisch-urämischem Syndrom (Gasser) berichtet. Fall 1 war durch einen ungewöhnlichen schubweisen Verlauf gekennzeichnet. Im letzten Schub zeigte der Gerinnungsstatus eine Verbrauchscoagulopathie an. Die Therapie mit Corticoiden und zuletzt mit Heparin war erfolglos. Pathologisch-anatomisch fanden sich Fibringerinnsel in den Glomerulumcapillaren beider Nieren und eine in mehreren Schüben abgelaufene Herdglomerulitis. Bei Fall 2 entwickelte sich — möglicherweise infolge meningealer Thrombenbildung — ein Hydrocephalus hyporesorptivus. Die derzeitigen Vorstellungen über die Pathogenese des Krankheitsbildes und die therapeutischen Möglichkeiten werden dargelegt.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 45 (1967), S. 295-299 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Clinico-pathological description of a uremic case of glycogen storage disease in a 16 year old girl with contracted kidneys and retarded growth. Furhtermore the girl showed an increased tendency to hemorrhage, which was explained by a functional lesion of the platelets. The kidney contraction was of the tubular-interstitial type with heavy thickening of the tubular basement membranes. This lesion seems to be the consequence of an increased permeability of the tubular epithelium damaged by extremely severe glycogen storage. Similar cases of kidney damage in glycogen storage disease could not be found in the literature.
    Notes: Zusammenfassung Klinisch-pathologisch-anatomische Beschreibung eines Falles von Urämie bei Schrumpfniere auf dem Boden einer Glykogenspeicherkrankheit bei 16 jährigem Mädchen mit Minderwuchs. Daneben bestand eine erhöhte Blutungsneigung, welche auf eine Funktionsstörung der Plättchen zurückgeführt wird. Bei der Schrumpfniere handelt es sich um eine tubulär-interstitielle Form mit ausgesprochen schwerer Verdickung der tubulären Basalmembranen, was als Folge einer Permeabilitätsstörung der speichergeschädigten Tubulusepithelien aufgefaßt wird. Entsprechende Fälle bei Glykogenose konnten im Schrifttum nicht gefunden werden.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1440
    Keywords: Whipple's disease ; Chronic interstitial nephritis ; Granulomas ; Boeck's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Report is given on a 68-year-old man who suffered primarily from progressive weight loss and repeated episodes of fever and arthralgia. Later, liver dysfunction and renal insufficiency developed. Liver and kidney biopsics disclosed granulomatous hepatitis and nephritis. Because of the morphologic and clinical findings, the diagnosis of Boeck's disease was made. Shortly before death, diarrhea developed. Autopsy revealed a massive systemic involvement in Whipple's disease proven by light and electron microscopy and immunofluorescence. Tuberculoid and epitheloid cell granulomas and isolated giant cells were found in addition to the biopsy findings in skeleton muscles, the small intestine, lymphnodes and bronchi. At autopsy, the kidney showed chronic interstitial nephritis. The literature of kidney involvement in Whipple's disease is reviewed. This is the first case with granulomatous interstitial nephritis and chronic renal insufficiency in an inadequately treated Whipple's disease.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Reported is the case of a patient who suffered from chronic haemolytic anaemia with paroxysmal nocturnal haemoglobinuria for 25 years. Over this period he received more than 360 blood transfusions (mostly washed red cells), equivalent to a total volume of more than 184 liters of whole blood. During the course of his illness he developed an increasing fibrosis of the bone marrow. During the last 4 years of his life, haemoglobinuria diminished. It finally seized 9 months prior to his death. At the same time the patient's red cells gave a negative response to the acid-serum-test, which had always been positiv in previous years. In analogy to similar observations of other authors, it is suggested that the increasing fibrosis of the bone marrow led to a deminution of the pathological population of red cells specific for the disease. During the last year of his life, the patient developed uraemia which became the immediate cause of his death. At autopsy most organs showed haemosiderosis, presumably due to blood transfusions. Most striking was the finding of very small and scarred kidneys with diffuse interstitial fibrosis and only slight deposition of haemosiderin. This was interpreted as the final stage of a renal complication of an unrecognised haemolytic transfusion reaction.
    Notes: Zusammenfassung Es wird über einen Patienten berichtet, der 25 Jahre lang an einer chronischen hämolytischen Anämie mit paroxysmaler nächtlicher Hämoglobinurie litt und während dieser Zeit über 360 Bluttransfusionen (größtenteils gewaschene Erythrocyten) erhielt, entsprechend einer Vollblutmenge von über 184 Litern. Im Laufe der Jahre entwickelte sich eine zunehmende Knochenmarksfibrose. In den letzten 4 Lebensjahren wurde die Hämoglobinurie schwächer und hörte während der letzten 9 Monate völlig auf. Gleichzeitig ergaben die Patientenerythrocyten im Gegensatz zu den früheren Jahren keinen positiven Säure-Serum-Test mehr. In Analogie zu einigen ähnlichen Beobachtungen anderer Autoren wird diskutiert, daß mit der zunehmenden Markfibrose die Produktion der krankheitsspezifischen abnormen Erythrocytenpopulation versiegte. Während des letzten Lebensjahres entwickelte sich außerdem eine progrediente Urämie, an der der Patient starb. Pathologisch-anatomisch fand sich in den meisten Organen eine ausgeprägte Transfusionshämosiderose. Im Mittelpunkt des autoptischen Befundes standen relativ eisenarme hochgradige beiderseitige Schrumpfnieren mit diffuser interstitieller Fibrose, die als Endzustand einer Chromoproteinniere nach wahrscheinlich unbemerkt verlaufenem Bluttransfusionszwischenfall gedeutet werden.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 388 (1980), S. 155-165 
    ISSN: 1432-2307
    Keywords: Schönlein-Henoch's disease ; Glomerulonephritis ; Glomerular basement membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In glomerulonephritis accompanying the Schönlein-Henoch syndrome (SHS) a characteristic subepithelial basement membrane change is present in 85% of cases. The subepithelial change is a reaction to subepithelial deposits and consists of a garland or dome-like new formation of thin densa lamellae. This change is much more frequent in SHS than in IgA-nephritis or idiopathic glomerulonephritis or any other systemic disease. Furthermore, subepithelial deposits (50% of cases) are nearly as frequent as subendothelial deposits (65%) and more often present than formerly assumed.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 351 (1970), S. 99-121 
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird auf das häufige Vorkommen einer idiopathischen Fibroelastose speziell in den Nierenarterien hingewiesen. Die Veränderung kann zu einer leichten Riffelung der Innenfläche sowie zu sekundärer adaptativer Intimafibrose und vereinzelt auch zu Elastica interna- und -externa-Defekten führen. Sie beruht einerseits auf einer Degeneration der Mediamyocyten, welche bis zu Nekrose gehen kann, andererseits auf einem Funktionswandel dieser Zellen, wodurch es zu vermehrter Sekretion von Grundsubstanz und Aus-differenzierung von Kollagen und Elastin kommt. Sehr selten werden Aneurysmata durch Rupturbildung beobachtet. Eine Beziehung zur Druckerhöhung (Hypertonie) bzw. Druckreduktion (Ostienstenose) konnte nicht gefunden werden. Die Veränderung beginnt im zweiten Dezenium und nimmt an Stärke mit höherem Alter dauernd zu. Sie scheint uns nicht identisch zu sein mit der sog. fibromuskulären Dysplasie. Pathogenetisch bestehen keine Anhaltspunkte für eine primäre Insudation von Plasmabestandteilen aus dem Lumen oder für eine primäre Degeneration der Elastica interna. Die fast ausschließliche Beschränkung dieses Prozesses auf die Nierenarterien läßt daran denken, daß die hier besonders häufig zu vermutenden spastischen Zustände durch Summation zur beschriebenen Myocytenveränderung führen (Schockzustände etc.).
    Notes: Summary Idiopathic fibroelastosis is a frequent lesion of renal arteries. Thereby, the inner vascular wall may become finely ondulated. Secondary adaptive fibrosis of the intima and in some instances lesions of the inner and outer elastic layers may occur. Aneurysma formation as a consequence of ruptures is found very rarely. Idiopathic fibroelastosis is the result of two main mechanisms: 1. degeneration of smooth muscle cells of the tunica media, 2. a change in functional properties of these muscle cells leading to an increased secretion of ground substance containing collagen and elastic fibers. The process cannot be related with alterations of high blood pressure, e.g. hypertension or low pressure due to stenosis of an ostium. Idiopathic fibroelastosis becomes manifest in the second decade of life and shows an increase in severity with age of the patient. The disease most likely has to be differentiated from fibromuscular dysplasia. Pathogenesis of idiopathic fibroelastosis is not yet clarified. The possibilities of either a primary insudation of constituents of blood plasm from the vascular lumen or a degeneration of the internal tunica elastica cannot be supported. The preferential involvement of kidney vessels suggests that repeated vascular spasms which are supposed to occur most frequently in renal vessels (e.g. shock) could be contributory in the alteration of muscle cells described.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Virchows Archiv 354 (1971), S. 336-348 
    ISSN: 1432-2307
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Klinisch ist das Zusammentreffen von Ikterus und akuter Niereninsuffizienz mit Erhöhung von Serumbilirubin, Transaminasen und Fibrinogen, sowie Thrombocytopenie und normaler Prothrombinzeit charakteristisch für Morbus Weil. Die Leberbiopsie am 13. Tag zeigt spärliche Herde mit Leberzellnekrose, umgeben von Leukocyteninfilatration und mesenchymaler Proliferation, daneben intrahepatische Cholostase. Die Nierenbiopsie am 17. Tag ergibt ein akutes interstitielles entzündliches Ödem und elektronenmikroskopisch eine Glomerulonephrose mit lockerer, feingranulärer Verdickung der Lamina rara interna. Letztere Veränderung ist nach 4 1/2 Monaten noch nicht völlig restituiert. Glomeruläres und intertubuläres Endothel lassen nach 2 1/2 Wochen schwere, reparatorisch-proliferative Veränderungen erkennen. Die Glomerulonephrose und das interstitielle Ödem werden als eine Folge der direkten Endothelläsion durch die Leptospiren, die Anurie als Folge des interstitiellen Ödems und des Kreislaufkollapses aufgefaßt.
    Notes: Summary Clinically, the coincidence of jaundice and acute renal failure with elevation of serum bilirubin, transaminases and fibrinogen, as well as thrombocytopenia and normal prothrombin time are characteristic for Morbus Weil. Liver biopsy, 13 days after onset of the disease, showed scattered foci of liver cell necrosis with surrounding leucocytic infiltration and mesenchymal proliferation as well as intrahepatic cholostasis. Kidney biopsy 17 days after the onset of the disease showed an acute interstitial inflammatory edema, and electronmicroscopically, a glomerulonephrosis with a loose, finely granular thickening of the lamina rara interna. The latter lesion is not completely restituted after 4 1/2 months. Glomerular and intertubular endothelial cells show severe reparatory-proliferative alterations after 2 1/2 weeks. The glomerulonephrosis as well as the interstitial edema are considered as consequence of the direct lesion of endothelial cells by leptospirae, the anuria is considered as consequence of the interstitial edema as well as of the circulatory collapse.
    Type of Medium: Electronic Resource
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