Abstract
We study a softly-broken supersymmetric model whose gauge symmetry is that of the standard model (SM) gauge group times an extra Abelian symmetry U(1)'. We call this gauge-extended model U(1)' model, and we study a U(1)' model with a secluded sector such that neutrinos acquire Dirac masses via higher-dimensional terms allowed by the U(1)' invariance. In this model the mu term of the minimal supersymmetric model (MSSM) is dynamically induced by the vacuum expectation value of a singlet scalar. In addition, the model contains exotic particles necessary for anomaly cancellation, and extra singlet bosons for achieving correct Z'/Z mass hierarchy. The neutrinos are charged under U(1)', and thus, their production and decay channels differ from those in the MSSM in strength and topology. We implement the model into standard packages and perform a detailed analysis of sneutrino production and decay at the Large Hadron Collider, for various mass scenarios, concentrating on three types of signals: (1) 0lep+ MET,(2) 2lep+MET, and (3) 4lep + MET. We compare the results with those of the MSSM whenever possible, and analyze the SM background for each signal. The sneutrino production and decays provide clear signatures enabling distinction of the U(1)' model from the MSSM at the LHC.
Highlights
Mechanical loads can regulate cell proliferation and differentiation at various stages of development and homeostasis
The composition of an extracellular matrix that is stiffer, and cells that are softer than a healthy tissue suggests that breast cancer cells may be protected from mechanical loads in a manner that is similar to the event of “stress shielding” seen in orthopedic biomaterial applications [30,31]
During 19 days of culture a steady increase was observed in sham control MDA-MB-231 cells as measured with Trypan Blue cell counts
Summary
Mechanical loads can regulate cell proliferation and differentiation at various stages of development and homeostasis. Since no universal treatment is available for cancer other than remedies that kill rapidly dividing cells at the expense of life quality [2,3,4,5], prevention strategies are often emphasized for the practice of healthy lifestyle choices such as following a healthy diet, minimizing sun Mechanical loads are omnipresent in all tissues and they act as an important modulator of cellular machinery during an organism’s development and homeostasis [17,18,19,20] Cellular decisions such as growth, migration and differentiation are dependent on mechanical loads, and the absence of these loads induces catabolism and malformation in many tissue types. Even though cancer cells are known to be responsive to mechanical cues [32,33], if they are protected from global loads within stiffer tumors, potential regulatory effects of these loads on cancer cells may not be able to potentiate in the first place
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