Ears of the Armadillo: Global Health Research and Neglected Diseases in Texas

Neglected tropical diseases (NTDs) have\ud been recently identified as significant public\ud health problems in Texas and elsewhere in\ud the American South. A one-day forum on the\ud landscape of research and development and\ud the hidden burden of NTDs in Texas\ud explored the next steps to coordinate advocacy,\ud public health, and research into a\ud cogent health policy framework for the\ud American NTDs. It also highlighted how\ud U.S.-funded global health research can serve\ud to combat these health disparities in the\ud United States, in addition to benefiting\ud communities abroad

Application of artificial neural networks to the evaluation of the ultimate strength of uniaxially compressed welded stiffened aluminium plates

peer reviewedA series of elastoplastic large-deflection finite element analyses is performed on stiffened aluminium plates with flat-bar stiffeners under in-plane longitudinal compression loads. Then, the closed-form ultimate compressive strength formula is derived for stiffened aluminium plates by regression analysis. Finally, artificial neural network methodology is applied to predict the ultimate strength of uniaxially compressed stiffened aluminium plates. It is found that artificial neural network models can produce a more accurate prediction of the ultimate strength of the stiffened aluminium plates than can the existing empirical formula

Cross-talk between Chk1 and Chk2 in double-mutant thymocytes

Chk1 is a checkpoint kinase and an important regulator of mammalian cell division. Because null mutation of Chk1 in mice is embryonic lethal, we used the Cre-loxP system and the Lck promoter to generate conditional mutant mice in which Chk1 was deleted only in the T lineage. In the absence of Chk1, the transition of CD4(−)CD8(−) double-negative (DN) thymocytes to CD4(+)CD8(+) double-positive (DP) cells was blocked due to an increase in apoptosis at the DN2 and DN3 stages. Strikingly, loss of Chk1 activated the checkpoint kinase Chk2 as well as the tumor suppressor p53 in these thymocytes. However, the developmental defects caused by Chk1 deletion were not rescued by p53 inactivation. Significantly, even though Chk1 deletion is highly lethal in proliferating tissues, we succeeded in using in vivo methods to generate Chk1/Chk2 double-knockout T cells. Analysis of these T cells revealed an interesting interaction between Chk1 and Chk2 functions that partially rescued the apoptosis of the double-mutant cells. Thus, Chk1 is both critical for the survival of proliferating cells and engages in cross-talk with the Chk2 checkpoint kinase pathway. These factors have implications for the targeting of Chk1 as an anticancer therapy