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  • 2000-2004  (26)
  • 1995-1999  (87)
  • 1
    Unknown
    Unterschleißheim : Microsoft Press
    Call number: 05-MAT-20:54
    Keywords: EDV / Windowtechnik
    Pages: various pagings
    ISBN: 3-86063-854-8
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    05-MAT-20:54 departmental collection or stack – please contact the library
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  • 2
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    German Medical Science; Düsseldorf, Köln
    In:  68. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 90. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie und 45. Tagung des Berufsverbandes der Fachärzte für Orthopädie; 20041019-20041023; Berlin; DOC04dguK4-1840 /20041019/
    Publication Date: 2004-10-20
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
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    German Medical Science; Düsseldorf, Köln
    In:  Patientenbeteiligung bei medizinischen Entscheidungen; 2. Tagung des Förderschwerpunktes "Der Patient als Partner im medizinischen Entscheidungsprozess"; 20040325-20040327; Freiburg; DOC04pat20 /20040615/
    Publication Date: 2004-06-15
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 4
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    German Medical Science; Düsseldorf, Köln
    In:  Patientenbeteiligung bei medizinischen Entscheidungen; 2. Tagung des Förderschwerpunktes "Der Patient als Partner im medizinischen Entscheidungsprozess"; 20040325-20040327; Freiburg; DOC04pat21 /20040615/
    Publication Date: 2004-06-15
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
    ISSN: 1432-0983
    Keywords: Key wordsPodospora anserina ; Genome analysis ; Repetitive sequences ; Minisatellite
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A genomic DNA fragment, PaGT7-5, of Podospora anserina was cloned that contains three different repetitive sequence motifs including a minisatellite with an unusual structure. This element, PaMin1, consists of ten copies of a 16 bp repeat unit with five GT dinucleotide repeats. Adjacent to PaMin1, a short poly(GT) stretch and four repeats of a 12 bp sequence were identified. Six alleles which differ in the number of the minisatellite unit were demonstrated in 18 different P. anserina strains. The flanking sequences of PaMin1 did not display any sequence alterations. A PCR analysis of total DNA from cultures of different age revealed no sequence changes, indicating that this repetitive DNA remains stable during aging. Southern-blot hybridization experiments of DNA from different strains detected only minor fragment length polymorphisms in the immediate vicinity of PaMin1. In contrast, major polymorphisms were observed at a greater distance from the locus indicating that this locus can be used as an informative probe to discriminate between different P. anserina strains.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1106
    Keywords: Key words Vestibular compensation ; Linear vestibulo-ocular reflex ; Angular vestibulo-ocular reflex ; Optokinetic nystagmus ; Optokinetic afternystagmus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Static and dynamic otolith, horizontal vestibular and optokinetic ocular reflexes were investigated in pigmented rats 1–6 and more months after unilateral vestibular nerve (UVN) section. Evoked responses were compared with published data from control rats studied under identical conditions. Static lateral tilt of UVN rats in the light evoked a vertical deviation in static eye position that was as large as in controls. In darkness, the evoked responses in UVN rats 6 months after the lesion were consistently smaller than in controls. Linear horizontal acceleration in darkness evoked vertical and torsional response components in UVN rats that were parallel-shifted towards lower gains and larger phase lags. Off-vertical axis rotation on a platform provoked responses that differed markedly from those recorded in intact rats with respect to the bias velocity component. These results suggest a permanent deficiency in the static and dynamic otolith-ocular reflex performance of UVN rats. Ocular responses to horizontal table velocity steps in darkness exhibited a direction-specific asymmetry in UVN rats. Step responses evoked by acceleration towards the intact side were larger in gain and longer in duration than responses evoked by acceleration towards the operated side. When compared with control data, responses to either side were reduced in UVN rats and the velocity store mechanism was barely activated by velocity steps towards the operated side. Responses evoked by horizontal optokinetic stimulation with constant pattern velocities were below control values in either direction. Slow-phase eye velocity saturated at much lower values than in intact rats, particularly during pattern motion towards the intact side. The duration of the optokinetic afternystagmus was asymmetrically reduced with respect to control data. Practically identical reductions in duration were found for vestibulo-ocular responses in the opposite directions. Behaving animals exhibited no obvious impairment in their spontaneous locomotory or exploratory activities. However, each UVN rat was impaired, even 2 years after the lesion, in its postural reaction to being lifted by the tail in the air. This observation suggests the presence of a permanent deficit in static and dynamic otolith-spinal reflexes that may be substituted on the ground by proprioceptive inputs.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  The NK gene complex on mouse chromosome 6 and its human homologue on chromosome 12 encode type II transmembrane proteins with a C-type lectin domain which trigger or inhibit target cell lysis by NK cells (NKR-P1, Ly49, NKG2, CD94) or function as cellular activators of various hematopoietic cells (CD69). We herein report the cDNA cloning of a new molecule, designated activation-induced C-type lectin (AICL), whose gene maps to the human NK gene complex proximal to the CD69 gene. AICL is a 149-amino acid (aa) polypeptide with a short cytoplasmic part of seven aa and a C-type lectin domain separated from the transmembrane region by only nine aa. The highest sequence similarity is found to the C-type lectin domains of CD69 and the chicken lectin 17.5. The presence of AICL transcripts in different cell types of hematopoietic origin, a rapid increase of gene transcription during lymphocyte activation, and a short half-life of the mRNA characterize AICL as a new, broadly expressed activation antigen.
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  • 8
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Hämorrhagische Transformation ; Intrazerebrale Blutung ; Thrombolyse ; Basalmembran ; Zerebrale Mikrogefäße ; Key words Intracerebral hemorrhage ; Thrombolysis ; Basal lamina ; Cerebral microvasculature
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The role of cerebral hemorrhagic transformation, either as clinically silent hemorrhagic infarction or disastreous parenchymal hemorrhage, is crucial for any risk/benefit analysis of thrombolysis. Especially, thrombolysis in acute ischemic stroke increases the risk of severe, life-threatening hemorrhagic complications up to 10 times compared to untreated controls. In this paper, previous proposed concepts for the development of intracerebral hemorrhage and hemorrhagic transformation are presented. The role of the cerebral microvasculature will be emphasized. In experimental focal cerebral ischemia a significant loss of basal lamina components of the cerebral microvessels has been demonstrated. This loss in vessel wall integrity is associated with the development of petechial hemorrhage. The mechanisms for this microvascular damage may include the plasmin-generated laminin degradation, matrix metalloproteinases activation, and the transmigration of leukocytes through the vessel wall. The attenuation of the microvascular integrity loss with subsequent reduction in hemorrhage is theoretically possible 1) by an improvement in the definition of an individual time window of therapy (by means of imaging techniques), 2) by a biochemical quantification of the basal lamina damage to avoid dangerous interventions, and 3) by pharmacological strategies to protect the basal lamina during thrombolysis.
    Notes: Zusammenfassung Die Bedeutung hämorrhagischer Transformationen, entweder als klinisch stumme hämorrhagische Infarkte oder als klinisch auffällige bis lebensbedrohliche parenchymatöse Blutungen, ist entscheidend für die Beurteilung des Risiko-Nutzen-Verhältnisses der Thrombolyse, aber auch anderer gerinnungshemmender Therapien, wie der Antikoagulation, beim Hirninfarkt. Insbesondere kann die Thrombolyse das Risiko schwerer Blutungskomplikationen verglichen mit unbehandelten Hirninfarktpatienten bis zu 10fach erhöhen. Verschiedene Konzepte der Entwicklung intrazerebraler Blutungen und hämorrhagischer Transformationen werden vorgestellt. Die Rolle der zerebralen Mikrogefäßstrombahn wird betont. Es konnte in experimentellen Untersuchungen der fokalen zerebralen Ischämie ein signifikanter Verlust von Basalmembranbestandteilen der zerebralen Mikrogefäße nachgewiesen werden. Dieser Verlust von Basalmembranstrukturen, der zu einer deutlichen Integritätsminderung der Gefäßwand führte, war auch signifikant mit der Entwicklung petechialer Blutungen in der Umgebung zerstörter Gefäße verbunden. Mechanismen für die mikrovaskuläre Schädigung können die Plasmin-vermittelte Laminindegradation, die Aktivierung von Matrixmetalloproteinasen, sowie die Transmigration von Leukozyten durch die Gefäßwand sein. Eine mögliche Verbesserung der mikrovaskulären Integrität mit nachfolgender Reduktion der Blutungsrate ist theoretisch über verschiedene Wege möglich: 1. Durch eine Verbesserung der Definition des individuellen Zeitfensters zur Behandlung, z.B. durch neue Kernspintechniken 2. durch den biochemischen Nachweis der Basalmembranschädigung, insbesondere um Patienten mit starken Basalmembranschädigungen von einer Intervention auszuschließen, und 3. durch pharmakologische Behandlungsmöglichkeiten zum Schutz der Basalmembran während der Thrombolyse.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Der Chirurg 70 (1999), S. 1149-1155 
    ISSN: 1433-0385
    Keywords: Key words: Heparin-induced thrombocytopenia type II ; Thromboembolic complications ; Anticoagulation ; Prophylaxis. ; Schlüsselwörter: Heparin-induzierte Thrombozytopenie Typ II ; thromboembolische Komplikationen ; Antikoagulation ; Prophylaxe.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Die Heparin-induzierte Thrombozytopenie Typ II (HIT Typ II) ist eine immunologisch vermittelte und im weiteren Verlauf durch thromboembolische Komplikationen klinisch relevante Medikamentennebenwirkung bei Heparinexposition mit einer Inzidenz von 1–3 %, einer Letalität von ca. 20 % sowie bleibenden Schäden in weiteren 20 %. Bei Heparintherapie oder -prophylaxe sind regelmäßige Kontrollen der Thrombozytenzahlen erforderlich. Der bei dieser Erkrankung auftretende Thrombozytenabfall geht meist den thromboembolischen Komplikationen im venösen und arteriellen Gefäßsystem voraus. Bei Verdacht auf HIT Typ II ist jegliche weitere Heparinexposition sofort zu unterbrechen und die weiterhin notwendige antikoagulatorische Therapie zu beginnen. Die hierzu zugelassenen Medikamente werden ausführlich dargestellt. Gleichzeitig ist sofort die Diagnose durch ein Laborverfahren inkl. Austestung der Kreuzreaktivität mit Danaparoid zu bestätigen. Die weitere Therapie ist abhängig von der Klinik. Bei klinischer Relevanz dieses Krankheitsbilds muß zunehmend über prophylaktische Maßnahmen wie strenge Indikationsstellung, der Einsatz von niedermolekularem Heparin (auch bei der Thrombosetherapie) sowie frühzeitiges Umsetzen auf orale Antikoagulantien nachgedacht werden.
    Notes: Summary. Heparin-induced thrombocytopenia type II (HIT type II) is an immunoglobulin-mediated, drug-induced side effect for heparin-treated patients with thromboembolic complications. With an incidence of 1–3 %, mortality of 20 % it and permanent disability for another 20 % is a clinically relevant disorder. With heparin treatment or prophylaxis frequent platelet count monitoring is necessary. With HIT type II the thrombocytopenia is often a harbinger of thromboembolic complications in the venous or arterial system. If HIT type II is suspected, further heparin exposure is to be stopped immediately and another anticoagulant therapy should be started. The two anticoagulant options in Germany are discussed. At the same time the diagnosis should be confirmed by laboratory testing, including testing for cross-reactivity with danaparoid. Further therapy depends on the symptoms. In the case of clinical relevance of this disorder we should think about prophylaxis: strict indications for perioperative prophylaxis only use of low-molecular-weight heparin (LMWH) for routine prophylaxis, use of LMWH for thrombosis treatment and early change to cumarine.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Hämolytisch-urämisches Syndrom ; Thrombotisch-thrombozytopenische Purpura ; Transkranielle Dopplersonographie ; Vasospasmen ; Key words Haemolytic uremic syndrome ; Thrombotic-thrombopenic purpura ; Vasospasms ; TCD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Cerebral involvement is typical for thrombotic microangiopathies like haemolytic uremic syndrome (HUS) and thrombotic-thrombopenic purpura (Moschcowitz disease or TTP). Symptoms are irritation, restless behaviour, disorientation, disturbance of consciousness, seizures, and focal neurological deficits. The lack of typical imaging changes or pathological observations may explain the unknown pathophysiological cascade leading to the neurological symptoms. We describe the development of HUS/TTP in a 52-year-old woman after acute pneumonia caused by Diplococcus pneumoniae. The patient showed an increasing psycho-organic syndrome with disorientation, followed by severe loss of consciousness and coma. Initially, computed tomography showed slight diffuse brain oedema, which was not found in later follow-up images. Magnetic resonance imaging was normal. The TCD examination revealed general velocity increases and vasospasms (especially MCA, ACA and PCA bilateral and BA). The reduction in blood flow velocities in the basal arteries was accompanied by a marked clinical improvement. The development of vasospasms may be an explanation for the neurological deficits in HUS/TTP. The origin of the vasospasms may be found in disturbed prostacyclin production, increased serotonin or platelet factor IV release, and leucocyte activation with consecutive endothelial damage.
    Notes: Zusammenfassung Mikroangiopathische hämolytische Anämien (thrombotisch-thrombozytopenische Purpura = TTP oder Moschcowitz-Syndrom, hämolytisch-urämisches Syndrom = HUS) gehen oft mit Beteiligungen des zentralen Nervensystemes einher. Typische Symptome sind Gereiztheit, Ruhelosigkeit, Verwirrtheitszustände, Bewußtseinstrübungen, Krampfanfälle oder fokalneurologische Ausfälle. Teilweise fehlende bildmorphologische und pathologisch-histologische Korrelate erschweren die Klärung der Pathogenese. Wir berichten über eine 52 jährige Patienten mit HUS/TTP aufgrund einer Pneumokokkensepsis. Sie entwickelte ein akutes hirnorganisches Psychosyndrom mit progredienter Bewußtseinsstörung bis zum Koma. Die initiale kraniale Computertomographie zeigte eine diskrete, allgemeine Hirnschwellung, welche sich unabhängig von der klinischen Verschlechterung zurückbildete. Die kraniale Kernspintomographie war unauffällig. In der transkraniellen Dopplersonographie fanden sich generalisierte Flußgeschwindigkeitssteigerungen (A. cerebri media, anterior und posterior beidseits sowie A. basilaris). Der ursächliche Zusammenhang zwischen Flußgeschwindigkeitssteigerungen und Bewußtseinsstörungen wird durch die Beobachtung wahrscheinlich gemacht, daß die klinische Besserung analog der Rückbildung der Flußgeschwindigkeitssteigerungen erfolgte. Bei HUS/TTP können Vasospasmen die Ursache neurologischer Ausfälle darstellen. Pathophysiologisch werden ein gestörter Prostacyclinstoffwechsel, eine Erhöhung von Serotonin und Plättchenfaktor IV und eine Leukozytenaktivierung als Ursachen diskutiert.
    Type of Medium: Electronic Resource
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