A Simple Approach to Fourth Generation Effects in B→Xsℓ+ℓ−B\to X_s \ell^+ \ell^- Decay

In a scenario in which fourth generation fermions exist, we study effects of new physics on the differential decay width, forward-backward asymmetry $A_{\text{FB}}$ and integrated branching ratio for $B\to X_s \ell^+ \ell^-$ decay with $(\ell=e,\mu)$. Prediction of the new physics on the mentioned quantities essentially differs from the Standard Model results, in certain regions of the parameter space, enhancement of new physics on the above mentioned physical quantities can yield values as large as two times of the SM predictions, whence present limits of experimental measurements of branching ratio is spanned, contraints of the new physics can be extracted. For the fourth generation CKM factor $V_{t^\prime b}^\ast V_{t^\prime s}$ we use $\pm 10^{-2}$ and $\pm 10^{-3}$ ranges, take into consideration the possibility of a complex phase where it may bring sizable contributions, obtained no significant dependency on the imaginary part of the new CKM factor. For the above mentioned quantities with a new family, deviations from the SM are promising, can be used as a probe of new physics.Comment: 9 pages aps forma

B&#8594;K&#956;<SUP>+</SUP>&#956;<SUP>-</SUP>: light higgs and fourth generation

We examine the current limit on the branching ratio for B&#8594;K&#956;+&#956;- and the theoretical predictions for B&#8594;KH&#8594;K&#956;+&#956;- in three- and four-generation models. It is shown that for a heavy top quark mt60 GeV a light Higgs, mH &#8804; 3.5 GeV, is disfavoured in a three-generation model. We also find that the existence of a light Higgs constrains the four-generation model quite strongly through the above process

Convergent Akt activation drives acquired EGFR inhibitor resistance in lung cancer

Non-small-cell lung cancer patients with activating epidermal growth factor receptor (EGFR) mutations typically benefit from EGFR tyrosine kinase inhibitor treatment. However, virtually all patients succumb to acquired EGFR tyrosine kinase inhibitor resistance that occurs via diverse mechanisms. The diversity and unpredictability of EGFR tyrosine kinase inhibitor resistance mechanisms presents a challenge for developing new treatments to overcome EGFR tyrosine kinase inhibitor resistance. Here, we show that Akt activation is a convergent feature of acquired EGFR tyrosine kinase inhibitor resistance, across a spectrum of diverse, established upstream resistance mechanisms. Combined treatment with an EGFR tyrosine kinase inhibitor and Akt inhibitor causes apoptosis and synergistic growth inhibition in multiple EGFR tyrosine kinase inhibitor-resistant non-small-cell lung cancer models. Moreover, phospho-Akt levels are increased in most clinical specimens obtained from EGFR-mutant non-small-cell lung cancer patients with acquired EGFR tyrosine kinase inhibitor resistance. Our findings provide a rationale for clinical trials testing Akt and EGFR inhibitor co-treatment in patients with elevated phospho-Akt levels to therapeutically combat the heterogeneity of EGFR tyrosine kinase inhibitor resistance mechanisms.EGFR-mutant non-small cell lung cancer are often resistant to EGFR tyrosine kinase inhibitor treatment. In this study, the authors show that resistant tumors display high Akt activation and that a combined treatment with AKT inhibitors causes synergistic tumour growth inhibition in vitro and in vivo