D-cycloserine Inhibits Amygdala Responses During Repeated Presentations of Faces

CNS Spectrums ◽  
2007 ◽  
Vol 12 (8) ◽  
pp. 600-605 ◽  
Author(s):  
Jennifer C. Britton ◽  
Andrea L. Gold ◽  
Eric J. Feczko ◽  
Scott L. Rauch ◽  
Danielle Williams ◽  
...  

ABSTRACTIntroduction: Recently, human studies using exposure therapy to treat anxiety have demonstrated that pretreatment with D-cycloserine (DCS) enhances fear reduction in anxiety disorders. However, the underlying brain mechanisms mediating this fear reduction have yet to be determined.Methods: The effects of orally administered DCS on amygdala activity during the processing of repeated facial expressions were examined in this double-blind study. Fourteen healthy males (30.0±8.7 years of age) randomly received DCS 500 mg or placebo prior to 3.0 Tesla functional magnetic resonance imaging acquisition. All participants viewed four separate runs, consisting of a single block of a repeated facial expression (happy or fearful) bracketed by fixation blocks.Results: Anatomic region-of-interest analyses showed that the placebo group exhibited amygdala activation and response habituation, while the DCS group displayed blunted amygdala responses to emotional faces across the experiment, whereby habituation was not detected.Conclusion: This finding may have relevance for testing treatments of anxiety and depression.

Author(s):  
Alicja Urbaniak ◽  
Anna Skarpańska-Stejnborn

Abstract. The aim of the study was to review recent findings on the use of POM supplements in athletes of various disciplines and physically active participants. Eleven articles published between 2010 and 2018 were included, where the total number of investigated subjects was 176. Male participants constituted the majority of the group (n = 155), as compared to females (n = 21). 45% of research described was conducted on athletes, whereas the remaining studies were based on highly active participants. Randomised, crossover, double-blind study designs constituted the majority of the experimental designs used. POM supplementation varied in terms of form (pills/juice), dosage (50 ml–500 ml) and time of intervention (7 days–2 months) between studies. Among the reviewed articles, POM supplementation had an effect on the improvement of the following: whole body strength; feeling of vitality; acute and delayed muscle fatigue and soreness; increase in vessel diameter; blood flow and serum level of TAC; reduction in the rate of increase for HR, SBP, CK and LDH; support in the recovery of post-training CK, LDH, CRP and ASAT to their baseline levels; reduction of MMP2, MMP9, hsCRP and MDA; and increased activity of antioxidant enzymes (glutathione peroxidase and superoxide dismutase). In the majority of reviewed articles POM supplementation had a positive effect on a variety of parameters studied and the authors recommended it as a supplement for athletes and physically active bodies.


1987 ◽  
Vol 57 (03) ◽  
pp. 326-328 ◽  
Author(s):  
Ph Vague ◽  
I Juhan-Vague ◽  
M C Alessi ◽  
C Badier ◽  
J Valadier

SummaryWe have previously observed a positive correlation between Plasminogen Activator Inhibition capacity (PA Inhibition), Body Mass Index (BMI) and plasma insulin levels in a population of non diabetic subjects. The anti diabetic biguanide Metformin which decreases insulin resistance has been reported to increase the blood fibrinolytic activity. Therefore we have studied the effect of Metformin on PA Inhibition levels in obese subjects with normal glucose tolerance. Eighteen obese women (O) (BMI: 31.4 ± 1.13, m ± S.E.M.) were compared to age matched controls (C) (BMI: 20.2 ± 0.8) and randomized to a 15 days treatment by Metformin (M) (1.7 g/day) or placebo (P) in a double blind study while on a weight maintaining diet. O compared to C had higher levels (m ± S.E.M.) of PA Inhibition (9 ± 1.8 IU/ml, versus 2.88 ± 0.29 p <0.01), lower euglobulin fibrinolytic activity (EFA) (4.95 ±1.17 mm versus 9 ± 0.29 p <0.05), higher plasma insulin (24.1 ±2.1. uU/ml), versus 12 ± 1 p <0.01) and triglyceride (1.32 ± 0.16 mmol/1, versus 0.8 ± 0.08 p <0.05). After 15 days of treatment, in group M a significant decrease in PA Inhibition (5.51 ± 1.4, versus 9.48 ±2.1 p <0.05) in plasma insulin (18.5 ±0.1, versus 24.5 ± 3.5, p <0.05) and plasma triglyceride (1.08 ± 0.1, versus 1.47 ± 0.3 p <0.05) and an increase in EFA (6.50 ± 0.28, versus 5.25 ± 0.35 p <0.05) were observed. No significant variation was observed in group P.


1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.


Sign in / Sign up

Export Citation Format

Share Document