Antipsychotic adherence and emergency department utilization among patients with schizophrenia.

This retrospective cohort study evaluated the relationship between antipsychotic medication adherence and emergency department (ED) utilization for 7851 Medicaid patients with schizophrenia enrolled in Community Care of North Carolina (CCNC). Claims and pharmacy data from January to December 2015 were collected. Medication adherence was approximated using the medication possession ratio (MPR). Negative binomial regressions estimated the effect of antipsychotic adherence on rates of medical and psychiatric ED visits. The results demonstrated a statistically significant negative relationship between antipsychotic adherence and medical ED utilization. Non- and partially adherent patients (MPR < 0.80) had 1.61 times the rate of medical ED visits as fully adherent patients (MPR ≥ 0.80) (95% CI: 1.50-1.74, p-value < 0.001). The relationship between adherence and psychiatric utilization was small and not statistically significant. The most common diagnostic categories of ED visits were injuries and poisonings (16%), ill-defined symptoms (14%), and musculoskeletal conditions (12%). This study demonstrates a clear association between antipsychotic adherence and medical ED utilization, suggesting an important link between psychiatric management and medical utilization in patients with schizophrenia.

The relation of brain oscillations to attentional networks.

Previous studies have suggested the relation of particular frequency bands such as theta (4-8 Hz), alpha (8-14 Hz), beta (14-30 Hz), or gamma (>30 Hz) to cognitive functions. However, there has been controversy over which bands are specifically related to attention. We used the attention network test to separate three anatomically defined brain networks that carry out the functions of alerting, orienting, and executive control of attention. High-density scalp electrical recording was performed to record synchronous oscillatory activity and power spectrum analyses based on functional magnetic resonance imaging constrained dipole modeling were conducted for each attentional network. We found that each attentional network has a distinct set of oscillations related to its activity. The alerting network showed a specific decrease in theta-, alpha-, and beta-band activity 200-450 ms after a warning signal. The orienting network showed an increase in gamma-band activity at approximately 200 ms after a spatial cue, indicating the location of a target. The executive control network revealed a complex pattern when a target was surrounded with incongruent flankers compared with congruent flankers. There was an early (<400 ms) increase in gamma-band activity, a later (>400 ms) decrease in beta- and low gamma-band activity after the target onset, and a decrease of all frequency bands before response followed by an increase after the response. These data demonstrate that attention is not related to any single frequency band but that each network has a distinct oscillatory activity and time course.

Imatinib improves but may not fully reverse the poor prognosis of patients with CML with derivative chromosome 9 deletions.

Deletions of the derivative chromosome 9 occur in a subset of patients with Philadelphia chromosome-positive chronic myeloid leukemia (CML) and are associated with a poor prognosis on standard drug therapy. However, it is currently unknown if the presence of deletions influences the response to imatinib, an Abl-specific tyrosine kinase inhibitor, that has recently shown excellent hematologic and cytogenetic responses in patients with CML. We, therefore, compared hematologic and cytogenetic responses with imatinib in 397 patients with CML, and survival and progression in 354 of these patients, according to deletion status and disease phase. We found no difference in survival between patients with and without deletions, contrasting with previous reports in cohorts with a lower proportion of patients treated with imatinib. However, the time to disease progression on imatinib treatment was significantly shorter for patients with deletions, both in chronic phase (P =.02) and advanced phases (P =.02). Moreover, both in chronic phase and more advanced phases of CML, hematologic and cytogenetic responses were uniformly lower in patients with deletions, with significant differences seen for hematologic response (P =.04), for major cytogenetic response (P =.008) in chronic phase, and for hematologic response in advanced phases (P =.007) of CML. This finding suggests that differences in survival may become apparent with longer follow-up.

Derivative chromosome 9 deletions in chronic myeloid leukemia: poor prognosis is not associated with loss of ABL-BCR expression, elevated BCR-ABL levels, or karyotypic instability.

Deletions of the derivative chromosome 9 have recently been reported in chronic myeloid leukemia. These deletions are large, occur at the time of the Philadelphia (Ph) translocation, span the translocation breakpoint, and represent a powerful prognostic indicator. However, the molecular mechanisms responsible for the poor prognosis associated with deletions are obscure, and several possible models are investigated here. First, we demonstrate that all derivative chromosome 9 deletions detected by fluorescence in situ hybridization were associated with an absence of ABL-BCR expression. However, loss of ABL-BCR expression also occurred without an overt deletion, suggesting the existence of other mechanisms by which ABL-BCR transcription can be abolished. Furthermore, analysis of survival in 160 patients demonstrated that loss of ABL-BCR expression, in contrast to deletion status, was not an indicator of poor prognosis. Second, we addressed the possibility that concomitant small deletions of the Ph chromosome modulate BCR-ABL transcription. Real-time reverse-transcription polymerase chain reaction was used to demonstrate that derivative chromosome 9 deletions were not accompanied by altered levels of BCR-ABL transcripts. Third, deletions may represent a consequence of genetic instability within the target cell at the time of the Ph translocation, with the poor prognosis reflecting a predisposition to subsequent additional genetic alterations. However, patients with deletions do not exhibit an increased frequency of secondary cytogenetic changes following disease progression. Taken together, these data support a model in which deletions of the derivative chromosome 9 result in rapid disease progression as a result of the loss of one or more genes within the deleted region.