Results 151 to 160 of about 2,917,992 (321)

Citywalk in Chinese Metropolises: A Multidimensional Framework for Evaluating Urban Walking Environments

open access: yesBuildings
Citywalk, a recently emerging form of leisure-oriented mobility, reflects increasing public interest in healthier lifestyles and more immersive urban experiences in Chinese metropolises.
Qiang Wang, Pengfei Ma, Zijin Zhou
doaj   +1 more source

On block designs with repeated blocks

open access: yesDiscrete Mathematics, 1992
This paper is concerned with balanced incomplete block designs in which repeated blocks are allowed. If \({\mathcal D}\) is such a \((v,k,\lambda)\)- design (using the standard notation), let \(b^*\) denote the number of distinct blocks. Let \(BIBD(v,k,\lambda| b^*)\) denote the family of all such designs \({\mathcal D}\). Fixing the number of points \(
openaire   +1 more source

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

open access: yesMolecular Oncology, EarlyView.
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz   +15 more
wiley   +1 more source

Block Design with Common Reference Samples Enables Robust Large-Scale Label-Free Quantitative Proteome Profiling. [PDF]

open access: yesJ Proteome Res, 2020
Zhang T   +9 more
europepmc   +1 more source

Cytoplasmic p21 promotes stemness of colon cancer cells via activation of the NFκB pathway

open access: yesMolecular Oncology, EarlyView.
Cytoplasmic p21 promotes colorectal cancer stem cell (CSC) features by destabilizing the NFκB–IκB complex, activating NFκB signaling, and upregulating BCL‐xL and COX2. In contrast to nuclear p21, cytoplasmic p21 enhances spheroid formation and stemness transcription factor CD133.
Arnatchai Maiuthed   +10 more
wiley   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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