Results 91 to 100 of about 263,601 (301)

Life Expectancy at Current Rates vs. Current Conditions

open access: yesDemographic Research, 2002
Life expectancy is overestimated if mortality is declining and underestimated if mortality is increasing. This is the fundamental claim made by Bongaarts and Feeney (2002) in their article "How Long Do We Live?", where they base their claim on arguments ...
doaj  

Adenosine‐to‐inosine editing of miR‐200b‐3p is associated with the progression of high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
A‐to‐I editing of miRNAs, particularly miR‐200b‐3p, contributes to HGSOC progression by enhancing cancer cell proliferation, migration and 3D growth. The edited form is linked to poorer patient survival and the identification of novel molecular targets.
Magdalena Niemira   +14 more
wiley   +1 more source

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 more
wiley   +1 more source

Gamma-Gompertz life expectancy at birth

open access: yesDemographic Research, 2013
BACKGROUND The gamma-Gompertz multiplicative frailty model is the most common parametric modelapplied to human mortality data at adult and old ages. The resulting life expectancy hasbeen calculated so far only numerically.
Trifon I. Missov
doaj  

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

Kidney Disease, Income, and Life Expectancy [PDF]

open access: bronze, 2016
Joshua M. Lang, Michael G. Shlipak
openalex   +1 more source

Life expectancy and years of life lost in chronic obstructive pulmonary disease: Findings from the NHANES III Follow-up Study

open access: yesInternational Journal of COPD, 2009
Robert M Shavelle1, David R Paculdo1, Scott J Kush1, David M Mannino2, David J Strauss11Life Expectancy Project, San Francisco, CA, USA; 2Pulmonary Epidemiology Research Laboratory, University of Kentucky School of Medicine, Division of Pulmonary and ...
Robert M Shavelle   +4 more
doaj  

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

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