Openness predicts cognitive functioning in bipolar disorder.

OBJECTIVES: Openness to experience (O) is a well-established personality factor and is associated with cognitive performance. Little is known about the personality-cognitive relationship in bipolar disorder, an illness with significant variability in mood. Cognitive evaluation is essential in psychopathology assessment as it may reflect underlying disease processes and psychosocial functional capacity. Screening using a proxy personality variable may identify those in need of comprehensive cognitive testing. We hypothesized that O and measures of cognition would associate in both the Bipolar Disorder (BD) and healthy control (HC) samples, whereas neuroticism and extraversion would correlate with cognition only in the BD sample. METHODS: Data from a longitudinal study of BD were used to study the association between personality factors and cognitive measures of attention, executive functioning, memory and fine motor skills. Regression analyses were used to determine the variables that account for the association between personality and cognition. RESULTS: Aspects of O explained significant cognitive variance (~5%) in both groups; this persisted when demographic variables (including BD versus HC status) were considered. Neuroticism and extraversion did not consistently correlate with cognitive performance in either group. LIMITATIONS: There were more females in the HC group who were slightly younger compared to the BD group. We lack direct measures of positive affect, and there is a reliance on a single measure of personality. CONCLUSIONS: BD Individuals scoring low on self-reported Openness are potential candidates for more comprehensive cognitive assessments (which represent a limited resource).

ECOLOGICALLY VALID LONG-TERM MOOD MONITORING OF INDIVIDUALS WITH BIPOLAR DISORDER USING SPEECH.

Speech patterns are modulated by the emotional and neurophysiological state of the speaker. There exists a growing body of work that computationally examines this modulation in patients suffering from depression, autism, and post-traumatic stress disorder. However, the majority of the work in this area focuses on the analysis of structured speech collected in controlled environments. Here we expand on the existing literature by examining bipolar disorder (BP). BP is characterized by mood transitions, varying from a healthy euthymic state to states characterized by mania or depression. The speech patterns associated with these mood states provide a unique opportunity to study the modulations characteristic of mood variation. We describe methodology to collect unstructured speech continuously and unobtrusively via the recording of day-to-day cellular phone conversations. Our pilot investigation suggests that manic and depressive mood states can be recognized from this speech data, providing new insight into the feasibility of unobtrusive, unstructured, and continuous speech-based wellness monitoring for individuals with BP.

17ß-Estradiol inhibits phosphorylation of stromal interaction molecule 1 (STIM1) protein: implication for store-operated calcium entry and chronic lung diseases.

Sex plays a significant role in the development of lung diseases including asthma, cancer, chronic bronchitis, and cystic fibrosis. In cystic fibrosis, 17ß-estradiol (E2) may inhibit store-operated Ca(2+) entry (SOCE) to impinge upon airway secretions, leaving females at greater risk of contracting lung infections. Stromal interaction molecule 1 (STIM1)-mediated SOCE is essential for cell homeostasis and regulates numerous processes including cell proliferation, smooth muscle contraction, and secretion. E2 can signal nongenomically to modulate Ca(2+) signaling, but little is known of the underlying mechanisms. We found that E2 exposure inhibited STIM1 translocation in airway epithelia, preventing SOCE. This correlated with a decrease in STIM1-STIM1 FRET and STIM1 mobility in E2-exposed HEK293T cells co-expressing estrogen receptor α. We also examined the role of STIM1 phosphorylation in E2-mediated inhibition of STIM1 mobility. STIM1 is basally phosphorylated at serine 575, which is required for SOCE. Exposure to E2 significantly decreased STIM1 serine phosphorylation. Mutating serine 575 to an alanine blocked STIM1 phosphorylation, reduced basal STIM1 mobility, and rendered STIM1 insensitive to E2. These data indicate that E2 can signal nongenomically by inhibiting basal phosphorylation of STIM1, leading to a reduction in SOCE.