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  • Human cerebral cortex  (2)
  • Multimorbidity  (2)
  • Systemic inflammatory response syndrome  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of ranitidine in geriatric patients with multiple diseases
    Amsterdam : Elsevier
    Archives of Gerontology and Geriatrics 8 (1989), S. 139-150 
    Details
    ISSN: 0167-4943
    Keywords: Age ; Laboratory parameters ; Multimorbidity ; Pharmacokinetics ; Ranitidine
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-4943(89)90058-7
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  • 2
    Electronic Resource
    Electronic Resource
    Pharmakokinetik und Pharmakodynamik von Theophyllin bei multimorbiden geriatrischen Patienten (1987)
    Springer
    Journal of molecular medicine 65 (1987), S. 551-557 
    Details
    ISSN: 1432-1440
    Keywords: Theophylline ; Age ; Multimorbidity ; Pharmacokinetics ; Pharmacodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pharmacokinetics of theophylline (200 mg i.v.) were determined in 20 geriatric patients with multiple diseases. Serum concentrations were fitted to an open 2-compartment model. Percent changes in venous pCO2 and pO2 were used as parameters of the pharmacodynamic action. Total clearance was decreased and elimination half-life of theophylline was found to be prolonged in the elderly patients compared with data of a study with young healthy volunteers. The stronger the pharmacodynamic action of theophylline (percent change of venous pCO2 after 30 min), the faster was its elimination and the lower were measured concentrations after 2, 6, and 12 h.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01727621
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  • 3
    Electronic Resource
    Electronic Resource
    Cortical and striatal neurone number in Huntington's disease (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 320-333 
    Details
    ISSN: 1432-0533
    Keywords: Key words Huntington's disease ; Human cerebral cortex ; Striatum ; Neurone number ; Stereology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five age- and sex-matched control cases. Serial 500-μm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36 – 72 years) was 5.97×109±320×106, the average number of small striatal neurones was 82×106±15.8×106. The left striatum (caudatum, putamen, and accumbens) contained a mean of 273×106±53×106 glial cells (oligodendrocytes, astrocytes and unclassifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36 – 75 years) was diminished by about 33  % to 3.99×109±218×106 nerve cells (P≤ 0.012, Mann-Whitney U-test). The mean number of small striatal neurones decreased tremendously to 9.72 × 106± 3.64×106 ( – 88  %). The decrease in total glial cells was less pronounced (193 × 106±26 × 106) but the mean glial index, the numerical ratio of glial cells per neurone, increased from 3.35 to 22.59 in Huntington's disease. Qualitatively, neuronal loss was most pronounced in supragranular layers of primary sensory areas (Brodmann's areae 3,1,2; area 17, area 41). Layer IIIc pyramidal cells were preferentially lost in association areas of the temporal, frontal, and parietal lobes, whereas spared layer IV granule cells formed a conspicuous band between layer III and V in these fields. Methodological issues are discussed in context with previous investigations and similarities and differences of laminar and lobar nerve cell loss in Huntington's disease are compared with nerve cell degeneration in other neuropsychiatric diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310376
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Pathophysiologie der Sepsis Aktuelle Konzepte (1996)
    Springer
    Der Anaesthesist 45 (1996), S. 312-322 
    Details
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Sepsis ; systemic inflammatory response syndrome (SIRS) ; Zytokine ; Endotoxin ; Stickstoffmonoxid (NO) ; Endothelin-1 ; Zell-Zell-Kommunikation ; Streßgene ; Apoptose ; Key words Sepsis ; Systemic inflammatory response syndrome ; SIRS ; Cytokines ; Endotoxin ; Nitric oxide ; Endothelin-1 ; Intercellular communication ; Stress genes ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Clinical manifestations of sepsis, such as systemic inflammatory response and multiple organ dysfunction syndrome, are considered to be the results of a decompensated host defense response. If tissue injury is sufficiently severe to overwhelm local defense mechanisms, systemic activation of these essentially protective mechanisms may lead to autodestructive „host defense failure disease.“ This is not always caused by invading bacteria; sterile inflammation such as results from multiple trauma or pancreatitis can initiate a similar response. Evidence suggests that the activation of the macrophage/monocyte system that underlies the systemic inflammatory response may reflect one facet of a more generalized dysregulation of intercellular communication, as well as a dysfunction of such subcellular processes as signal transduction or stress gene expression. Alterations in signal transduction or stress gene expression can affect the host defense response to subsequent stressful events in either a negative or a positive sense. In particular, the sequential induction of acute phase and heat shock response may initiate programmed cell death, reflecting a potential molecular mechanism for the development of multiple organ dysfunction syndrome. The development of anti-inflammatory treatment strategies seems to be hampered by the discrepancy between locally protective and systemically deterimental properties of the host defense response.
    Notes: Zusammenfassung Sepsisbegriff und pathophysiologische Konzepte der Sepsis haben in den letzten Jahren einen tiefgreifenden Wandel erfahren. Im Zentrum der pathogenetischen Vorstellungen zur Entwicklung eines septischen (Mehr-) Organversagens steht heute die Fehlregulation potentiell protektiver Defensivsysteme des septischen Patienten im Sinne einer „host defense failure disease“. Initialer Auslöser der pathophysiologischen Sequenz von Ereignissen, die letztlich zur systemischen Entzündungsreaktion und Organschädigung führt, scheint die Aktivierung des unspezifischen Immunsystems mit exzessiver Produktion von Entzündungsmediatoren zu sein. Neben bakteriellen Toxinen kommen auch abakterielle Insulte wie Polytrauma oder Pankreatitis als Auslöser eines vergleichbaren Symptomenkomplexes mit Überstimulation der Monozyten und Makrophagen in Frage. Die Aktivierung des Monozyten-Makrophagensystems scheint dabei eine Facette einer generalisierten Störung der Zell-Zellkommunikation und subzellulärer Funktionen wie Signaltransduktion und Streßgenexpression zu sein. Veränderungen der Signaltransduktion wie der Genexpression können die Reaktion des Organismus auf nachfolgende Streßereignisse positiv wie negativ beeinflussen. Dieses als „priming“ bezeichnete Phänomen beeinflußt nach heutigem Verständnis wesentlich die Entwicklung eines eventuellen Organversagens („double hit“-Modell der Sepsis). Die Diskrepanz zwischen lokal protektiven Wirkungen und systemischen Auswirkungen einer Aktivierung der Defensivsysteme stellt ein besonderes Hindernis für die Entwicklung antiinflammatorischer oder immunmodulatorischer Therapien dar.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001010050266
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Cortical and striatal neurone number in Huntington's disease (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 320-333 
    Details
    ISSN: 1432-0533
    Keywords: Huntington's disease ; Human cerebral cortex ; Striatum ; Neurone number ; Stereology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The total cortical and striatal neurone and glial numbers were estimated in five cases of Huntington's disease (three males, two females) and five age-and sex-matched control cases. Serial 500-μm-thick gallocyanin-stained frontal sections through the left hemisphere were analysed using Cavalieri's principle for volume and the optical disector for cell density estimations. The average cortical neurone number of five controls (mean age 53±13 years, range 36–72 years) was 5.97×109±320×106, the average number of small striatal neurones was 82×106±15.8×106. The left striatum (caudatum, putamen, and accumbens) contained a mean of 273×106±53×106 glial cells (oligodendrocytes, astrocytes and unclassifiable glial profiles). The mean cortical neurone number in Huntington's disease patients (mean age 49±14 years, range 36–75 years) was diminished by about 33% to 3.99×109±218×106 nerve cells (P≦0.012, Mann-Whitney U-test). The mean number of small striatal neurones decreased tremendously to 9.72×106±3.64×106 (−88%). The decrease in total glial cells was less pronounced (193×106±26×106) but the mean glial index, the numerical ratio of glial cells per neurone, increased from 3.35 to 22.59 in Huntington's disease. Qualitatively, neuronal loss was most pronounced in supragranular layers of primary sensory areas (Brodmann's areae 3,1,2; area 17, area 41). Layer IIIc pyramidal cells were preferentially lost in association areas of the temporal, frontal, and parietal lobes, whereas spared layer IV granule cells formed a conspicuous band between layer III and V in these fields. Methodological issues are discussed in context with previous investigations and similarities and differences of laminar and lobar nerve cell loss in Huntington's disease are compared with nerve cell degeneration in other neuropsychiatric diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310376
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Mixed agonistic-antagonistic cytokine response in whole blood from patients undergoing abdominal aortic aneurysm repair (1999)
    Springer
    Intensive care medicine 25 (1999), S. 279-287 
    Details
    ISSN: 1432-1238
    Keywords: Key words Abdominal aortic aneurysm ; Cytokines ; Systemic inflammatory response syndrome ; Ischemia-reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To characterize the impact of abdominal aortic aneurysm repair (AAAR) on spontaneous as well as lipopolysaccharide (LPS)-induced gene expression of pro- and anti-inflammatory cytokines. Design: Prospective, controlled in vivo / ex vivo study. Setting: University hospital. Patients and interventions: Whole blood from 14 consecutive patients undergoing AAAR withdrawn prior to surgery (T1), at the end of ischemia (T2), 90 min after declamping (T3) and on the first postoperative day (T4) was cultured in the absence or presence of LPS. Five patients undergoing elective inguinal hernia repair served as controls. Measurements and results: While tumor necrosis factor (TNF), Interleukin (IL)-1 and IL-10 plasma concentrations did not increase significantly, IL-6 was elevated at each time point, as compared with T1. Despite the spontaneous release of trace amounts of IL-6, the ability of cultured whole blood to mount a cytokine response in vitro to LPS was impaired for all cytokines studied at T2 (TNF –62 %, IL-1 –51 %, IL-6 –20 %, IL-10 –51 %). The stimulated IL-6 response was restored early after declamping (T3: + 56 %) and enhanced 1 day after operation (T4: + 144 %). In contrast, stimulated TNF and IL-1 responses remained depressed at T3 (TNF –48 %, IL-1 –64 %) and T4 (TNF –40 %, IL-1 –24 %). A biphasic pattern was observed for IL-10 with initial depression at T3 (-51 %) and restoration at T4 ( + 40 %). Among the different cytokines monitored, only impaired TNF responsiveness at early reperfusion (T3) correlated with the postoperative course, as reflected by APACHE II. Cytokine response to LPS was maintained or even increased during and after surgery in the whole blood from patients undergoing hernia repair. Conclusions: Despite consistent development of clinical signs of systemic inflammatory response syndrome (SIRS) and spontaneous release of IL-6 abdominal aortic aneurysm repair produces a state of impaired pro-inflammatory cytokine response upon a subsequent in vitro Gram-negative stimulus. This early impairment of TNF responsiveness seems to correlate with an unfavorable postoperative course.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050836
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    Paper (German National Licenses)
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