Results 121 to 130 of about 17,499,756 (289)

Non-orthogonal Multiple Access (NOMA) with Asynchronous Interference Cancellation [PDF]

open access: yes, 2015
Non-orthogonal multiple access (NOMA) allows allocating one carrier to more than one user at the same time in one cell. It is a promising technology to provide high throughput due to carrier reuse within a cell.
Haci, Huseyin
core  

Castration‐resistant prostate cancer cells are addicted to the high activity of cyclin‐dependent kinase 2

open access: yesMolecular Oncology, EarlyView.
We show that emergence of castration‐resistant prostate (CRPC) is associated with significant upregulation of cyclins that positively regulate cyclin‐dependent kinase 2 (CDK2) and concomitant downregulation of CDK4 cyclins. This renders CRPC cells dependent on the high activity of CDK2, and CDK2 inhibitors synergistically sensitize CRPC cells to both ...
Joyeeta Chatterjee   +3 more
wiley   +1 more source

Adaptive channel reservation multiple access protocol based on differentiated traffic guarantee

open access: yesXibei Gongye Daxue Xuebao
Ad Hoc network is widely used because of its distributed flexibility, in which nodes may generate different types of traffic, and some high-priority traffic requires lower delay and other Quality of service (QoS) requirements.
LIU Ze, LI Bo, YANG Mao, YAN Zhongjiang
doaj   +1 more source

Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation

open access: yesMolecular Oncology, EarlyView.
Partial inhibition of focal adhesion kinase (FAK) can paradoxically promote tumor growth, rather than simply producing a weaker antitumor effect than that observed with strong FAK suppression. In breast cancer and melanoma models, targeting p110δ PI3K, particularly in macrophages, counteracted these tumor‐promoting effects, highlighting the importance ...
Lydia Xenou   +4 more
wiley   +1 more source

Federated learning-based user access strategy and energy consumption optimization in cell-free massive MIMO network

open access: yesTongxin xuebao, 2023
To solve the problem that how users choose access points in cell-free massive multiple-input multiple-output (CF-mMIMO) network, a prioritized access strategy for poorer users based on channel coefficient ranking was proposed.First, users were evaluated ...
Yuanyuan YAO   +5 more
doaj  

Unraveling the epigenetic code in cancer cell–tumor microenvironment crosstalk

open access: yesMolecular Oncology, EarlyView.
Epigenetic regulation is a key driver of cancer development and progression. Diverse epigenetic alterations in cancer cells and components of the tumor microenvironment (TME) orchestrate their communication through multiple mechanisms. We discuss how the epigenetic code coordinates bidirectional cancer cell–TME crosstalk to promote cancer progression ...
Ji Hoon Park, Mi‐Young Kim
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular Oncology, EarlyView.
Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad   +2 more
wiley   +1 more source

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

open access: yesMolecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault   +12 more
wiley   +1 more source

Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation

open access: yesMolecular Oncology, EarlyView.
How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim   +11 more
wiley   +1 more source

Coding for the Multiple-Access Adder Channel

open access: yesElectronic Notes in Discrete Mathematics, 2005
The coding problem for the multiple-access adder channel is considered, both for the case of permanent user activity and partial user activity. For permanent user activity, Khachatrian [10] has written an excellent survey for general, symmetric and non-symmetric rates.
openaire   +2 more sources

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