Results 141 to 150 of about 69,564 (313)

Fatigue Crack Growth in Complex Stress Fields [PDF]

open access: yes, 2008
Fatigue crack growth has been traditionally modelled using LEFM through the use of the Paris law. This requires an accurate method for stress intensity factor (K) calculation. Weight functions have been developed for one-dimensional cracks (e.g.
Chahardehi A, Chahardehi, Amir Ebrahim
core  

Acoustic Emission during Crack Growth in FM94 Epoxy

open access: yes, 2016
Acoustic emission data generated during mode I quasi-static and fatigue crack growth in an aluminium-2024-T3/FM94 epoxy/aluminium-2024-T3 adhesive bond. The objective was to investigate when and how crack growth occurs during a single fatigue load cycle.
Zarouchas, D.S. (Dimitrios)   +1 more
core   +1 more source

Small RNA pathways in mammalian oocytes

open access: yesFEBS Open Bio, EarlyView.
Three distinct small RNA pathways operate in mammalian oocytes: RNAi interference (RNAi), the microRNA (miRNA) pathway, and the PIWI‐associated RNA (piRNA) pathway. These pathways use small RNAs to guide sequence‐specific repression and contribute to oocyte biology by targeting genes and mobile elements or appear insignificant since different ...
Petr Svoboda, Josef Pasulka
wiley   +1 more source

Fatigue failure analysis of pin-loaded lugs

open access: yesFracture and Structural Integrity, 2015
In the present paper, mathematical models are proposed in order to analyze the strength of pinloaded lugs with semi-elliptical crack and through-the-thickness crack.
Slobodanka Boljanovic, Stevan Maksimovic
doaj  

Molecular characterization of covRS mutations in M1UK Streptococcus pyogenes

open access: yesFEBS Open Bio, EarlyView.
Group A Streptococcus (GAS) acquires covRS mutations driving a hypervirulent bacterial state, frequently associated with invasive disease‐like necrotizing fasciitis. We demonstrate that the newly emerged M1UK GAS lineage can also acquire these mutations.
Jarrad Pritchard   +12 more
wiley   +1 more source

Hyperosmotic stress‐induced redistribution of pre‐mRNA cleavage factor I subunits is associated with shifts in alternative polyadenylation

open access: yesFEBS Open Bio, EarlyView.
Hyperosmotic stress triggers the relocation of the CFIm complex from the nucleus to the cytoplasm. This shift creates a nuclear ‘stoichiometric bottleneck’, limiting CFIm availability for mRNA processing. Consequently, specific mRNAs like NUDT21 and DICER1 undergo targeted 3′UTR shortening, demonstrating how spatial protein dynamics drive rapid ...
Hitomi Soumiya   +2 more
wiley   +1 more source

FRACTURE PARAMETER AND FATIGUE CRACK GROWTH RATE MODEL FOR COMMERCIAL PURE TITANIUM UNDER DIFFERENT CRACK TIP PLASTIC STATES

open access: yesJixie qiangdu
It's an important task that choosing appropriate fracture parameters and predicting the fatigue crack growth rate accurately considering the different degrees of plastic deformation at the crack tip.The relation between crack tip fracture parameters and ...
doaj  

Effects of IGFBP4 deficiency on human preadipocyte proliferation and differentiation through the IGF1R/AKT pathway

open access: yesFEBS Open Bio, EarlyView.
IGFBP4 knockdown (KD) impairs preadipocyte proliferation and is associated with IGF1R protein downregulation and attenuated AKT phosphorylation. The mechanisms by which IGFBP4 KD influences the IGF1R/AKT signaling pathway involve newly synthesized proteins and lysosomal degradation pathways. Created in BioRender.
Yujia Guo   +6 more
wiley   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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