Dose-dependent differences in the development of reserpine-induced oral dyskinesia in rats: support for a model of tardive dyskinesia

1994 ◽  
Vol 116 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Janet L. Neisewander ◽  
Edward Castañeda ◽  
Debra A. Davis
Keyword(s):  
Tardive Dyskinesia ◽  
Oral Dyskinesia ◽  
Dose Dependent

Electromyographic Assessment of Dimethylaminoethanol (Deanol) in Treatment of Tardive Dyskinesia

1979 ◽  
Vol 45 (2) ◽  
pp. 415-419 ◽  
Author(s):  
Daniel J. Lonowski ◽  
F. E. Sterling ◽  
Hugh A. King
Keyword(s):  
Tardive Dyskinesia ◽  
Control Subject ◽  
Normal Control ◽  
Psychological Functioning ◽  
Rating Scales ◽  
Emg Activity ◽  
Normal Control Subject ◽  
Slight Improvement ◽  
Oral Dyskinesia ◽  
Reversal Design

An ABAB reversal design with matched placebo was employed to assess the acetylcholine precursor, deanol, in the treatment of tardive dyskinesia. Oral dyskinesia was monitored by electromyography in four patients with tardive dyskinesia. A battery of psychological rating scales was also utilized to determine effects of deanol on psychological functioning. Improvement ranged from 35 to 70% dyskinetic symptom reduction in three patients given deanol. The decrease in symptomatology, however, did not reach the level of oral EMG activity observed in a normal control subject. Psychological functioning was generally unaffected, but slight improvement was seen in two subjects.

Oral dyskinesia in brain-damaged rats withdrawn from a neuroleptic: Implication for models of tardive dyskinesia

1980 ◽  
Vol 69 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Robert B. Glassman ◽  
Harriet N. Glassman
Keyword(s):  
Tardive Dyskinesia ◽  
Oral Dyskinesia

Tardive Dyskinesia in Elderly Patients

1992 ◽  
Author(s):  
R. Yassa ◽  
C. Natase ◽  
D. Dupont ◽  
M. Thibeau
Keyword(s):  
Elderly Patients ◽  
Tardive Dyskinesia

Increased Expression of u-PA and u-PAR on Monocytes by LDL and Lp(a) Lipoproteins – Consequences for Plasmin Generation and Monocyte Adhesion

1999 ◽  
Vol 81 (04) ◽  
pp. 594-560 ◽  
Author(s):  
Florence Ganné ◽  
Marc Vasse ◽  
Jean-Louis Beaudeu ◽  
Jacqueline Peynet ◽  
Arnaud François ◽  
...  
Keyword(s):  
Fold Increase ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Atheromatous Plaque ◽  
Monocyte Adhesion ◽  
Blood Monocytes ◽  
Proteolytic Cascade ◽  
Ecm Degradation ◽  
Dose Dependent Increase ◽  
Dose Dependent

SummaryMonocyte-derived foam cells figure prominently in rupture-prone regions of atherosclerotic plaque. As urokinase/urokinase-receptor (u-PA/u-PAR) is the trigger of a proteolytic cascade responsible for ECM degradation, we have examined the effect of atherogenic lipoproteins on monocyte surface expression of u-PAR and u-PA. Peripheral blood monocytes, isolated from 10 healthy volunteers, were incubated with 10 to 200 µg/ml of native or oxidised (ox-) atherogenous lipoproteins for 18 h and cell surface expression of u-PA and u-PAR was analysed by flow cytometry. Both LDL and Lp(a) induced a dose-dependent increase in u-PA (1.6-fold increase with 200 μg/ml of ox-LDL) and u-PAR [1.7-fold increase with 200 μg/ml of ox-Lp(a)]. There is a great variability of the response among the donors, some of them remaining non-responders (absence of increase of u-PA or u-PAR) even at 200 μg/ml of lipoproteins. In positive responders, enhanced u-PA/u-PAR is associated with a significant increase of plasmin generation (1.9-fold increase with 200 μg/ml of ox-LDL), as determined by an amidolytic assay. Furthermore, monocyte adhesion to vitronectin and fibrinogen was significantly enhanced by the lipoproteins [respectively 2-fold and 1.7-fold increase with 200 μg/ml of ox-Lp(a)], due to the increase of u-PAR and ICAM-1, which are receptors for vitronectin and fibrinogen. These data suggest that atherogenous lipoproteins could contribute to the development of atheromatous plaque by increasing monocyte adhesion and trigger plaque weakening by inducing ECM degradation.

Sign in / Sign up

Export Citation Format

Share Document