School-based counseling using systematic feedback: A cohort study evaluating outcomes and predictors of change

The outcomes of school-based counseling incorporating the Partners for Change Outcome Monitoring System (PCOMS) were evaluated using a cohort design, with multilevel modeling to identify predictors of change. Participants were 288 7-11 year olds experiencing social, emotional or behavioral difficulties. The intervention was associated with significant reductions in psychological distress, with a pre-post effect size (d) of 1.49 on the primary outcome measure and 88.7% clinical improvement. Greater improvements were found for disabled children, older children, and where CBT methods were used. The findings provide support for the use of systematic feedback in therapy with children.

The Polish Competition Authority Publishes its Annual Report for 2012

In May 2013 the President of the Office of Competition and Consumer Protection (UOKiK), the Polish Competition Authority, published its Annual Report for 2012. This piece provides an overview of the reported activities within the competition law & policy domain, and comments on some of them.

Comparison of adaptive beamforming and orthogonal STBC with outdated feedback

We compare the achievable performance of adaptive beamforming (A-BF) and adaptive orthogonal space time block coding (A-OSTBC) with outdated channel feedback. We extend our single user setup to multiuser diversity systems employing adaptive modulation, and illustrate the impact of feedback delay on the multiuser diversity gain with either A-OSTBC or A-BF. Using closed-form expressions for spectral efficiency and average BER of a multiuser diversity system derived in this paper, we prove that the A-BF scheme outperforms the A-OSTBC scheme with no feedback delay. However, when the feedback delay is large, the A-OSTBC scheme achieves better performance due to the reduced diversity advantage of A-BF. We observe that more transmit antennas bring higher spectral efficiency for BF. With small feedback delay, this becomes inverted using OSTBC, due to the effect of channel-hardening. Interestingly, however, we show that A-OSTBC with multiple users enjoys improved spectral efficiency when the number of transmit antennas is increased and the feedback delay is significant

Impact of oncogenic driver mutations on feedback between the PI3K and MEK pathways in cancer cells

Inhibition of the PI3K (phosphoinositide 3-kinase)/Akt/mTORC1 (mammalian target of rapamycin complex 1) and Ras/MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK pathways for cancer therapy has been pursued for over a decade with limited success. Emerging data have indicated that only discrete subsets of cancer patients have favourable responses to these inhibitors. This is due to genetic mutations that confer drug insensitivity and compensatory mechanisms. Therefore understanding of the feedback mechanisms that occur with respect to specific genetic mutations may aid identification of novel biomarkers that predict patient response. In the present paper, we show that feedback between the PI3K/Akt/mTORC1 and Ras/MEK/ERK pathways is cell-line-specific and highly dependent on the activating mutation of K-Ras or overexpression c-Met. We found that cell lines exhibited differential signalling and apoptotic responses to PD184352, a specific MEK inhibitor, and PI103, a second-generation class I PI3K inhibitor. We reveal that feedback from the PI3K/Akt/mTORC1 to the Ras/MEK/ERK pathway is present in cancer cells harbouring either K-Ras activating mutations or amplification of c-Met but not the wild-type counterparts. Moreover, we demonstrate that inhibition of protein phosphatase activity by OA (okadaic acid) restored PI103-mediated feedback in wild-type cells. Together, our results demonstrate a novel mechanism for feedback between the PI3K/Akt/mTORC1 and the Ras/MEK/ERK pathways that only occurs in K-Ras mutant and c-Met amplified cells but not the isogenic wild-type cells through a mechanism that may involve inhibition of a specific endogenous phosphatase(s) activity. We conclude that monitoring K-Ras and c-Met status are important biomarkers for determining the efficacy of PI103 and other PI3K/Akt inhibitors in cancer therapy.