Corporations: When May a Montana Corporation Collect on Its Subscription Contracts?

Corporations: When May a Montana Corporation Collect on its Subscription Contracts

Corporations: When May a Montana Corporation Collect on Its Subscription Contracts?

Corporations: When May a Montana Corporation Collect on its Subscription Contracts

The construction of a non-verbal vocational interest inventory for use at the high school and adult levels

Thesis (M.A.)--Boston Universit

Gain control in molecular information processing: Lessons from neuroscience

Statistical properties of environments experienced by biological signaling systems in the real world change, which necessitate adaptive responses to achieve high fidelity information transmission. One form of such adaptive response is gain control. Here we argue that a certain simple mechanism of gain control, understood well in the context of systems neuroscience, also works for molecular signaling. The mechanism allows to transmit more than one bit (on or off) of information about the signal independently of the signal variance. It does not require additional molecular circuitry beyond that already present in many molecular systems, and, in particular, it does not depend on existence of feedback loops. The mechanism provides a potential explanation for abundance of ultrasensitive response curves in biological regulatory networks.Comment: 10 pages, 5 figure

Molecular cloning of the cDNA encoding pp36, a tyrosine-phosphorylated adaptor protein selectively expressed by T cells and natural killer cells.

Activation of T and natural killer (NK) cells leads to the tyrosine phosphorylation of pp36 and to its association with several signaling molecules, including phospholipase Cgamma-1 and Grb2. Microsequencing of peptides derived from purified rat pp36 protein led to the cloning, in rat and man, of cDNA encoding a T- and NK cell-specific protein with several putative Src homology 2 domain-binding motifs. A rabbit antiserum directed against a peptide sequence from the cloned rat molecule recognized tyrosine phosphorylated pp36 from pervanadate-treated rat thymocytes. When expressed in 293T human fibroblast cells and tyrosine-phosphorylated, pp36 associated with phospholipase Cgamma-1 and Grb2. Studies with GST-Grb2 fusion proteins demonstrated that the association was specific for the Src homology 2 domain of Grb-2. Molecular cloning of the gene encoding pp36 should facilitate studies examining the role of this adaptor protein in proximal signaling events during T and NK cell activation

High scale impact in alignment and decoupling in two-Higgs doublet models

The two-Higgs doublet model (2HDM) provides an excellent benchmark to study physics beyond the Standard Model (SM). In this work we discuss how the behaviour of the model at high energy scales causes it to have a scalar with properties very similar to those of the SM -- which means the 2HDM can be seen to naturally favor a decoupling or alignment limit. For a type II 2HDM, we show that requiring the model to be theoretically valid up to a scale of 1 TeV, by studying the renormalization group equations (RGE) of the parameters of the model, causes a significant reduction in the allowed magnitude of the quartic couplings. This, combined with $B$-physics bounds, forces the model to be naturally decoupled. As a consequence, any non-decoupling limits in type II, like the wrong-sign scenario, are excluded. On the contrary, even with the very constraining limits for the Higgs couplings from the LHC, the type I model can deviate substantially from alignment. An RGE analysis similar to that made for type II shows, however, that requiring a single scalar to be heavier than about 500 GeV would be sufficient for the model to be decoupled. Finally, we show that not only a 2HDM where the lightest of the CP-even scalars is the 125 GeV one does not require new physics to be stable up to the Planck scale but this is also true when the heavy CP-even Higgs is the 125 GeV and the theory has no decoupling limit for the type I model.Comment: 28 pages, 19 figure