Library

feed icon rss

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Age  (2)
  • Prophylaxeresistenz  (2)
  • Striatum  (2)
  • Systemic inflammatory response syndrome  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Archives of Gerontology and Geriatrics 8 (1989), S. 139-150 
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 551-557 
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Thyroxin ; Schilddrüsenhormone ; Therapieresistente Depression ; Prophylaxeresistenz ; Major Depression ; Bipolare Störungen ; Key words Thyroxine ; Thyroid hormones ; Therapy- resistant depression ; Prophylaxis-resistance ; Major depression ; Bipolar disorde
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The following review summarizes current knowledge on the treatment of therapy-resistant patients with affective disorders with supraphysiological doses of thyroxine (T4). Several groups have reported independently of each other that administration of 200–500 µg T4/day has excellent effects in 50–65% of patients a) with bipolar disorder, with or without „rapid cycling” course, who were previously resistant to all prophylactic drugs and b) in the treatment of therapy-resistant depression. T4 is effective only in combination with an antidepressant or a prophylactic drug. Side effects are minimal, even when T4 is administered over several years. These results now justify to recommend high dose T4-augmentation as „last-resort” treatment also beyond research purposes, i. e. in psychiatric wards and in private practice. Recommendations for clinical applications are given and hypotheses on possible mechanisms underlying the efficacy of T4 treatment are discussed.
    Notes: Zusammenfassung Die nachfolgende Übersicht faßt die bisherigen Erfahrungen mit einer hochdosierten Thyroxin(T4)-Behandlung bei therapie- und prophylaxeresistenten Patienten mit affektiven Psychosen zusammen. Mehrere voneinander unabhängige Arbeitsgruppen berichteten in offenen Studie über ausgezeichnete prophylaktische bzw. therapeutische Ergebnisse einer Behandlung mit „supraphysiologischen” Dosen von T4 (200 bis 500 µg pro Tag) bei 50 bis 65% aller bislang prophylaxeresistenten bipolaren Patienten mit oder ohne Rapid-cycling-Verlauf sowie bei bisher therapieresistenten Depressionen. T4 ist nur bei gleichzeitiger Medikation eines Antidepressivums bzw. Phasenprophylaktikums wirksam. Die Nebenwirkungen sind – auch bei Langzeitbehandlung – in fast allen Fällen minimal. Diese Ergebnisse rechtfertigen, die hochdosierte T4-Behandlung als „Mittel der letzten Wahl” bei therapie- und prophylaxeresistenten Patienten mit affektiven Psychosen in Zukunft auch außerhalb der Forschung, d. h. auf den Stationen Psychiatrischer Abteilungen sowie in Nervenarztpraxen durchzuführen. Praktische Empfehlungen zur Durchführung dieser Behandlung werden gegeben und die möglichen Wirkungsmechanismen diskutiert.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Der Nervenarzt 70 (1999), S. 587-599 
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Bipolare Störung ; Rapid Cycling ; Prophylaxeresistenz ; Langzeitbehandlung ; Lithium ; Antikonvulsiva ; Thyroxin ; Kalzium-Antagonisten ; Key words Bipolar disorder ; Rapid cycling ; Resistance to prophylaxis ; Long-term-treatment ; Lithium ; Anticonvulsants ; Thyroxine ; Calcium channel blockers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Lithium is still regarded as the first choice substance in the prophylactic treatment of bipolar disorder. However, approximately one third of patients with a „classic” course of bipolar affective disorder do not adequately respond to lithium prophylaxis. The introduction of carbamazepine and valproic acid allowed a more differential syndrome- and course-orientated approach to the prophylactic treatment of bipolar disorder for the first time. However, about 10 to 20 percent of patients still remain refractory to standard regimes. Therefore, criteria for resistance to prophylactic treatment have to be further established. It has been suggested that at least two adequate trials of more than 12 months duration with sufficient drug blood levels have to be performed before refractoriness should be assumed. A severe subtype of affective disorder with poor response to lithium and other treatment approaches is a rapid cycling course which is characterised by at least four affective episodes per year. Here we present an overview of the currently available alternatives for prophylactic treatment, i.e. anticonvulsants, combination treatment, adjunctive thyroxine, calcium channel blockers, and more experimental approaches for treating refractory bipolar disorder patients. Suggestions for optimizing the prophylactic treatment of bipolar disorder are summarized in an algorithm.
    Notes: Zusammenfassung Für die Prophylaxe der manisch-depressiven (bipolaren) Erkrankung gilt Lithium weltweit weiterhin als Mittel der ersten Wahl. Etwa ein Drittel der Patienten mit der „klassischen” Verlaufsform der Erkrankung spricht jedoch nicht zufriedenstellend auf eine Lithiumprophylaxe an. Die Einführung der beiden Antikonvulsiva Carbamazepin und Valproat erlaubt erstmals zwar eine differentiellere Verlaufsform- und syndromorientierte Phasenprophylaxe, ein Teil der Patienten – etwa 10–20% – bleibt jedoch refraktär auf die gängige Rezidivprophylaxe. Die Prophylaxeresistenz ist ein bislang in der Literatur nicht genau definierter Begriff. Als klinisch-pragmatische Definition wird das Nichtansprechen auf mindestens zwei verschiedene, adäquat durchgeführte Behandlungsversuche – jeweils über mindestens 12 Monate bei ausreichenden Serumspiegeln der Phasenprophylaktika – vorgeschlagen. Eine spezielle Form einer Prophylaxeresistenz findet sich bei Patienten mit Rapid Cycling, einer malignen Verlaufsform mit mindestens 4 affektiven Episoden in den vergangenen 12 Monaten, die in der Regel auf Lithium, aber auch auf andere Substanzen häufig nicht anspricht. Der Beitrag gibt einen Überblick über die derzeitigen Alternativen in der Prophylaxe zu Lithium in der Rezidivprophylaxe bipolarer Störungen (u.a. Antikonvulsiva, Zweifach- und Dreifachkombinationen, adjuvante Thyroxin-Therapie, Kalzium-Antagonisten und experimentelle Verfahren) und stellt die Möglichkeiten der Prophylaxeoptimierung anhand eines Algorithmus dar.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Der Anaesthesist 45 (1996), S. 312-322 
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...