The Life Style Index (LSI; Plutchik, Kellerman, & Conte, 1979 ) was designed to assess defense mechanisms, assuming that their use is related to specific affective states and diagnostic concepts. We aimed to assess the psychometric properties of its Greek version and its relation to psychopathological symptoms. The LSI was back-translated into Greek and was administered to 1,261 participants. Six factors were identified, 5 of them largely corresponding to the original version's defenses (compensation, denial, projection, reaction formation, and repression). The sixth factor, named regressive emotionality, included mainly the original scale's regression and displacement factors. Test-retest reliabilities, internal consistencies, and construct validity were quite satisfactory. Most defenses were able to discriminate psychiatric patients from healthy participants and were associated with specific psychopathological symptoms in a theoretically expected mode, further supporting the validity of the Greek version. Our findings suggest that the LSI, based on both psychoevolutionary and psychoanalytic theory, can provide a solid ground for assessing ego defense mechanisms.
Depressive symptomatology is common in pediatric patients with NCS. Our findings call for additional investigation in larger controlled clinical interventional studies that will enhance understanding of the possible pathophysiological association between depressive symptomatology and NCS in pediatric populations.
A perifusion system based on ovine pituitary tissue explants was used to investigate the effects of follicular fluid (hFF) and serum from superovulated women on pituitary responsiveness to gonadotrophin-releasing hormone (GnRH). The specific aims of the study were to determine both if gonadotrophin surge-attenuating factor (GnSAF) bioactivity is present in the peripheral circulation as well as in the follicles of superovulated women and if GnSAF suppresses GnRH self-priming in vitro. Two pulses of GnRH, 1 h apart, produced marked peaks in LH secreted from control chambers, with GnRH self-priming evident in the significant difference between the first (134.4 +/- 1.7 - 232.1 +/- 24.0% of basal secretion) and second (183.9 +/- 15.8 - 313.9 +/- 14.0% of basal secretion) LH peaks. Both follicular fluid and serum pooled from two different groups of women produced marked suppression of the first (unprimed) and second (primed) LH peaks. The hFF reduced the first LH peak to 69.6 +/- 7.8 and 60.2 +/- 9.7% and the second LH peak to 57.4 +/- 6.7 and 42.6 +/- 6.5% of control LH secretion. Overall, the serum reduced the first and second LH peaks to 76.8 +/- 4.2 and 62.9 +/- 3.6% of control respectively. These results demonstrated that GnSAF bioactivity suppresses GnRH self-priming, and is present in both the peripheral circulation and hFF. The same material administered to dispersed ovine pituitary monolayers produced similar marked suppression of GnRH-induced LH secretion, with approximately 50-fold less GnSAF bioactivity in serum compared with hFF. Combined doses of oestradiol and progesterone, or hFF from large follicles containing little GnSAF, produced stimulation of GnRH-induced LH secretion and GnRH self-priming (second peaks 78.1 +/- 38.9 and 27.4 +/- 15.7% respectively higher than first peaks). Thus, in conclusion, GnSAF in hFF and serum markedly attenuated both unprimed and primed pituitary response to GnRH, virtually abolishing the GnRH self-priming effect.
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