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001-es BibID:BIBFORM024644
Első szerző:Sziklai István (fül-orr-gégész)
Cím:Tinnitus control by dopamine agonist pramipexole in presbycusis patients : a randomized, placebo-controlled, double-blind study / Sziklai I., Szilvássy J., Szilvássy Z.
Dátum:2011
ISSN:0023-852X
Megjegyzések:Since the concept of tinnitus dopaminergic pathway emerged, studies have been proposed to investigate if dopaminergic agents influence tinnitus. We hypothesized that pramipexole, an agonist on D2/D3 receptors, may antagonize tinnitus in the presbycusis patients (in the frequency range of 250 to 8,000 Hz) in a dose schedule accepted for the treatment of Parkinson's disease in elderly people. STUDY DESIGN: We designed a randomized, prospective, placebo-controlled and double-blind trial. METHODS: Forty presbycusis patients aged 50 years or older with subjective tinnitus were randomized to two groups (20 patients in both). Patients in the drug group took pramipexole over a period of 4 weeks according to a treatment schedule as follows: week 1, 0.088 mg t.i.d.; week 2, 0.18 mg t.i.d.; week 3, 0.7 mg t.i.d.; week 4, 0.18 mg t.i.d. over 3 days and 0.088 mg t.i.d. the rest of the week. Patients in the second group received placebo. Determination of subjective grading of tinnitus perception, the tinnitus handicap inventory (THI) questionnaire and electrocochleography (ECOG) examinations served as the end points. Subjective audiometry was used to produce secondary data. A significant improvement in tinnitus annoyance is found in the group treated with pramipexole versus placebo with respect to inhibition of tinnitus and a decrease of tinnitus loudness greater than 30 dB. However, neither ECOG nor subjective pure-tone threshold audiometry revealed any change in hearing threshold in response to either pramipexole or placebo. CONCLUSIONS: Pramipexole is an effective agent against subjective tinnitus associated with presbycusis at a dose schedule used for the treatment of Parkinson's disease. The drug did not change hearing threshold.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Laryngoscope. - 121 : 4 (2011), p. 888-893. -
További szerzők:Szilvássy Judit (1960-2022) (fül- orr- gégész) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM020459
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Impaired bronchomotor responses to field stimulation in guinea-pigs with cisplatin-induced neuropathy / Judith Szilvássy, Istvan Sziklai, Tamas Racz, Peter Horvath, Gyorgy Rabloczky, Zoltan Szilvassy
Dátum:2000
Megjegyzések:AbstractPre-treatment with cisplatin (3 mg/kg) i.p. once a day over 6 days induced sensory neuropathy as confirmed by femoral nerve conduction velocity test and significantly decreased contractions induced by electrical field stimulation (100 stimuli, 20 V, 0.1 ms, 20 Hz) in isolated main bronchial rings from guinea-pigs. The field stimulation-induced non-adrenergic, non-cholinergic (NANC) relaxations, however, were amplified in rings from animals with cisplatin neuropathy. The NANC relaxation response was completely blocked by 30 microM N(G)-nitro-L-arginine methyl ester in preparations from both control and cisplatin-treated animals. Superoxide dismutase (40 units/ml) was without effect on NANC relaxation in control rings, however, it substantially decreased NANC relaxation in preparations from animals with cisplatin neuropathy. These results show that cisplatin-induced sensory neuropathy is accompanied by attenuation of neural bronchoconstriction and an enhanced NANC relaxation. The latter is in part attained by an increased peripheral superoxide production.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Impaired bronchomotor responses
bronchomotor responses
field stimulation
cisplatin-induced neuropathy
Megjelenés:European Journal of Pharmacology. - 403 : 3 (2000), p. 259-265. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Rácz Tamás (1961-) (fül-orr-gégész) Horváth Péter Rablóczky György Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM020438
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Feeble bronchomotor responses in diabetic rats in association with decreased sensory neuropeptide release / Judit Szilvássy, Istvan Sziklai, Peter Horvath, Maria Szilasi, József Németh, Péter Kovács, Zoltán Szilvássy
Dátum:2002
Megjegyzések:AbstractType I diabetes is associated with a low incidence of asthma. We tested whether a decrease in sensory neuropeptide release is associated with an attenuated bronchoconstrictive response to field stimulation (FS; 100 stimuli, 20 V, 0.1 ms, 20 Hz) in streptozotocin (STZ)-induced diabetes. The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. Preparations were from either normal rats or those pretreated with 50 mg/kg STZ iv 8 wk before experiment. A group of STZ-treated animals was supplied with insulin delivery (4 IU/day sc) implants between 4 and 8 wk. A subgroup was formed to study the effect of capsaicin desensitization. The atropine-resistant contraction was attenuated by diabetes without capsaicin-sensitive relaxation response. Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. Insulin supplementation restored neuropeptide release in rings from STZ-treated rats. The results show that the decreased FS-induced contractions occurred with a decrease in sensory neuropeptide release in STZ-diabetic rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
bronchomotor responses
decreased sensory
neuropeptide
Megjelenés:American Journal of Physiology. - 282 : 5 (2002), p. 1023-1030. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Horváth Péter Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Németh József (Pécs) Kovács Péter (1939-) (farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM020269
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Neurogenic insulin resistance in guinea-pigs with cisplatin-induced neuropathy / Judit Szilvássy, István Sziklai, Réka Sári, József Németh, Barna Peitl, Robert Porszasz, János Lonovics, Zoltán Szilvássy
Dátum:2006
Megjegyzések:The aim of the present work was to study whether neurotoxicity produced by cisplatin modified tissue insulin sensitivity in guinea-pigs. One week after selective sensory denervation of the anterior hepatic plexus by means of perineurial 2% capsaicin treatment, hyperinsulinaemic euglycaemic glucose clamp were performed to estimate insulin sensitivity in male guinea-pigs. The guinea-pigs underwent regional sensory denervation of the anterior hepatic plexus exhibited insulin resistance, whereas systemic capsaicin desensitization increased insulin sensitivity. Intraportal administration of L-nitro-arginine methyl ester (L-NAME decreased, whereas capsaicin increased insulin sensitivity. Neither atropine nor acetylcholine produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological maneuvers modified the resulting insulin resistant state. Cisplatin pretreatment induced sensory neuropathy and decreased insulin sensitivity. Insulin sensitivity did not change after either regional or systemic capsaicin desensitization in the cisplatin-treated animals. CGRP(8-37), a nonselective calcitonin gene-related peptide (CGRP) antagonist (50 microg/kg i.v.), significantly increased insulin sensitivity in normal animals but only a tendency to insulin sensitization was seen after cisplatin treatment. Cisplatin treatment, similar to regional capsaicin desensitization of the anterior hepatic plexus, produced a significant decrease in insulin-stimulated uptake of 2-deoxy-D [L-14C] glucose in cardiac and gastrocnemius muscle with no effect on percentage suppression of endogenous glucose production by hyperinsulinaemia. We conclude that the majority of cisplatin-induced insulin resistance is related to functional deterioration of the hepatic insulin sensitizing substance (HISS) mechanism.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic insulin
insulin resistance
cisplatin-induced
neuropathy
Megjelenés:European Journal of Pharmacology. - 531 : 1-3 (2006), p. 217-225. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lonovics János (Szeged) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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