Positive Emotion Dysregulation in Posttraumatic Stress Disorder.

Although PTSD is associated with both emotion regulation (ER) difficulties and persistent difficulties experiencing positive emotions, research concerning positive ER in PTSD is still scarce. We aimed to clarify whether PTSD patients show dysfunctional responses to positive emotions and whether positive ER is associated with PTSD symptom severity. PTSD patients (N = 59) were compared to healthy controls (HC, N = 58) with respect to their self-reported regulation of positive and negative emotions. We used the Responses to Positive Affect Questionnaire to assess positive ER and the Difficulties in Emotion Regulation Scale and Response Styles Questionnaire to assess negative ER. PTSD patients showed deficient negative as well as deficient positive ER as compared to HC. Both dampening of positive emotions as well as positive rumination were associated with self-reported symptom severity. Furthermore, dampening contributed to the prediction of PTSD symptom severity beyond depressive symptoms and negative rumination. This study supports and expands previous findings of dysfunctional positive ER in PTSD. Further research is needed to clarify whether deficits in positive ER contribute to the onset and maintenance of PTSD. If so, therapeutic approaches should aim to help PTSD patients build up adequate skills to handle positive emotions in PTSD.

Hb S-San Martin: a new sickling hemoglobin with two amino acid substitutions [ß6(A3)Glu→Val;ß105(G7)Leu→Pro] in an Argentinean family.

A new sickling hemoglobin (Hb) detected in an Argentinean family from San Martín, Buenos Aires, Argentina, is hereby described. Two mutations were identified on the same ß-globin gene resulting in a new variant named Hb San Martin. One mutation was found on exon 1, corresponding to Hb S [ß6Glu→Val, GAG>GTG] and the second one on exon 3 at ß105(G7)Leu→Pro, CTC>CCC. The replacement of leucine by proline will likely impair the structure breaking helix G and causing instability of the molecule and the clinical manifestations typical of unstable Hbs. The mutation at ß105 seemed to be a de novo one in our patients, arising on a previously mutated gene, due to the fact that Hb S is the most frequent structural variant.