28,839 research outputs found
Pilot Power Allocation Through User Grouping in Multi-Cell Massive MIMO Systems
In this paper, we propose a relative channel estimation error (RCEE) metric,
and derive closed-form expressions for its expectation and
the achievable uplink rate holding for any number of base station antennas ,
with the least squares (LS) and minimum mean squared error (MMSE) estimation
methods. It is found that RCEE and converge to the same
constant value when , resulting in the pilot power
allocation (PPA) is substantially simplified and a PPA algorithm is proposed to
minimize the average per user with a total pilot power
budget in multi-cell massive multiple-input multiple-output systems.
Numerical results show that the PPA algorithm brings considerable gains for the
LS estimation compared with equal PPA (EPPA), while the gains are only
significant with large frequency reuse factor (FRF) for the MMSE estimation.
Moreover, for large FRF and large , the performance of the LS approaches to
the performance of the MMSE, which means that simple LS estimation method is a
very viable when co-channel interference is small. For the achievable uplink
rate, the PPA scheme delivers almost the same average achievable uplink rate
and improves the minimum achievable uplink rate compared with the EPPA scheme.Comment: 30 pages, 5 figures, submitted to IEEE Transactions on Communication
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The Rbm38-p63 feedback loop is critical for tumor suppression and longevity.
The RNA-binding protein Rbm38 is a target of p63 tumor suppressor and can in-turn repress p63 expression via mRNA stability. Thus, Rbm38 and p63 form a negative feedback loop. To investigate the biological significance of the Rbm38-p63 loop in vivo, a cohort of WT, Rbm38-/-, TAp63+/-, and Rbm38-/-;TAp63+/- mice were generated and monitored throughout their lifespan. While mice deficient in Rbm38 or TAp63 alone died mostly from spontaneous tumors, compound Rbm38-/-;TAp63+/- mice had an extended lifespan along with reduced tumor incidence. We also found that loss-of-Rbm38 markedly decreased the percentage of liver steatosis in TAp63+/- mice. Moreover, we found that Rbm38 deficiency extends the lifespan of tumor-free TAp63+/- mice along with reduced expression of senescence-associated biomarkers. Consistent with this, Rbm38-/-;TAp63+/- MEFs were resistant, whereas Rbm38-/- or TAp63+/- MEFs were prone, to cellular senescence. Importantly, we showed that the levels of inflammatory cytokines (IL17D and Tnfsf15) were significantly reduced by Rbm38 deficiency in senescence-resistant Rbm38-/-;TAp63+/- mouse livers and MEFs. Together, our data suggest that Rbm38 and p63 function as intergenic suppressors in aging and tumorigenesis and that the Rbm38-p63 loop may be explored for enhancing longevity and cancer management
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