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  • 1
    Electronic Resource
    Electronic Resource
    Asymptomatic neurogenic bladder in juvenile diabetics (1971)
    Springer
    Diabetologia 7 (1971), S. 168-172 
    Details
    ISSN: 1432-0428
    Keywords: Neurogenic bladder ; juvenile diabetes ; cystometry ; impotence ; neuropathy ; intravesical pressures ; vesical capacity ; bioelectric test ; residue urinary ; first matinal micturition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le présent travail concerne une investigation sur les troubles de la vessie chez 31 diabétiques jeunes. Il a été démontré que: 1. La lésion prédominante est une lésion de neuropathie. — 2. Des signes vésicaux tels que la capacité accrue et l'atonie mesurées par cystométrie, ont été démontrés dans 27 cas sur les 31 (87%). — 3. 4 cas avaient une hypertrophie du col. — 4. Le symptome le plus frappant était l'important volume de la première urine du matin. Ceci a été indiqué par les patients. Ils ne se plaignaient d'aucun trouble urologique. — 5. On trouve une haute fréquence d'impuissance chez les diabétiques ayant une vessie neurogène. — 6. Les causes possibles de telles lésions et la valeur de certaines mesures thérapeutiques sont discutées.
    Abstract: Zusammenfassung Es wird über Blasenstörungen bei 31 jugendlichen Diabetikern berichtet. Es konnte gezeigt werden, daß: 1. die Neuropathie die vorherrschende Störung darstellt; 2. bei 27 von 31 Fällen (87%) eine Blasenbeteiligung (gesteigerte Kapazität und zytometrisch nachweisbare Atonie) vorlag; — 3. bei 4 Fällen eine Blasenhalshypertrophie bestand; — 4. hervorstechendes Symptom war die große Harnmenge bei der ersten morgendlichen Blasenentleerung, über das die Patienten auf Anfrage berichteten. Sie äußerten keine urologischen Beschwerden; — 5. Bei vielen Diabetikern mit einer neurogenen Blasenstörung ist eine Impotenz festzustellen; — 6. Die für diese Läsionen in Frage kommenden Ursachen und der Wert einiger therapeutischer Maßnahmen werden diskutiert.
    Notes: Summary The present report concerns investigation of bladder disturbances in 31 juvenile diabetics. It was shown that: 1. The predominant lesion is one of neuropathy. — 2. Vesical involvement such as increased capacity and atony was demonstrated by cystometry in 27 out of the 31 cases (87%). — 3. 4 cases had neck hypertrophy. — 4. The most striking symptom was a large volume of first morning urine. This information was elicited from the patients. They had no urological complaints. — 5. A high incidence of impotence was seen in diabetics with neurogenic bladder. — 6. The possible causes of such lesions and the value of certain therapeutic measures was discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01212549
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  • 2
    Electronic Resource
    Electronic Resource
    Highly conserved and disease-specific patterns of carboxyterminally truncated Aβ peptides 1–37/38/39 in addition to 1–40/42 in Alzheimer's disease and in patients with chronic neuroinflammation (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 81 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Human lumbar CSF patterns of Aβ peptides were analysed by urea-based β-amyloid sodium dodecyl sulphate polyacrylamide gel electrophoresis with western immunoblot (Aβ-SDS–PAGE/immunoblot). A highly conserved pattern of carboxyterminally truncated Aβ1–37/38/39 was found in addition to Aβ1–40 and Aβ1–42. Remarkably, Aβ1–38 was present at a higher concentration than Aβ1–42, being the second prominent Aβ peptide species in CSF. Patients with Alzheimer's disease (AD, n = 12) and patients with chronic inflammatory CNS disease (CID, n = 10) were differentiated by unique CSF Aβ peptide patterns from patients with other neuropsychiatric diseases (OND, n = 37). This became evident only when we investigated the amount of Aβ peptides relative to their total Aβ peptide concentration (Aβ1–x%, fractional Aβ peptide pattern), which may reflect disease-specific γ-secretase activities. Remarkably, patients with AD and CID shared elevated Aβ1–38% values, whereas otherwise the patterns were distinct, allowing separation of AD from CID or OND patients without overlap. The presence of one or two ApoE ε4 alleles resulted in an overall reduction of CSF Aβ peptides, which was pronounced for Aβ1–42. The severity of dementia was significantly correlated to the fractional Aβ peptide pattern but not to the absolute Aβ peptide concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.00818.x
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  • 3
    Electronic Resource
    Electronic Resource
    Flupirtine shows functional NMDA receptor antagonism by enhancing Mg2+ block via activation of voltage independent potassium channels (1999)
    Springer
    Journal of neural transmission 106 (1999), S. 857-867 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Potassium channel ; inwardly rectifying potassium channel ; GIRK ; flupirtine ; N-methyl-D-aspartate receptor antagonist ; patch clamp ; superior colliculus culture.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The spectrum of action of flupirtine includes analgesia, muscle relaxation and neuroprotection. N-methyl-D-aspartate (NMDA) receptor antagonism has been discussed as a possible mechanism of action of this compound with little direct evidence. The objective of the present study was to develop a plausible model to explain flupirtine's spectrum of action. A four-stage strategy was selected for this purpose: Firstly, the serum concentration of flupirtine under therapeutic conditions was determined on the basis of the current literature. The second stage involved assessing the known in-vitro effects in light of the therapeutic active concentration. Using whole cell patch clamp recordings from cultured rat superior colliculus neurones interactions between flupirtine and NMDA receptors were assessed. Only very high concentrations of flupirtine antagonized inward currents to NMDA (200 μM) at −70 mV with an lC50 against steady-state responses of 182.1 ± 12.1 μM. The effects of flupirtine were voltage-independent and not associated with receptor desensitization making actions within the NMDA receptor channel or at the glycine modulatory site unlikely. NMDA receptor antagonism probably has little relevance for the clinical efficacy of flupirtine as the concentrations needed were far higher than those achieved in clinical practice. However, the activation of a G-protein-regulated inwardly rectifying K+ channel was identified as an interesting molecular target site of flupirtine. In the next stage, the central nervous spectrum of action of experimental K+ channel openers (PCO) was considered. As far as they have been studied, experimental K+ channel openers display a spectrum of action comparable to that of flupirtine. In the final stage, a global model was developed in which flupirtine stabilizes the resting membrane potential by activating inwardly rectifying K+ channels, thus indirectly inhibiting the activation of NMDA receptors. The model presented here reconciles the known functional NMDA receptor antagonism of flupirtine with the activation of K+ channels that occurs at therapeutic concentrations, thus providing an understanding of flupirtine's spectrum of action. This makes flupirtine the prototype of a clinically applicable substance group with analgesic, muscle-relaxant and neuroprotective properties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050206
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    Paper (German National Licenses)
    Fulltext
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