Results 131 to 140 of about 70,917 (350)
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
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
Electrophysiological features of complete AV block within the His bundle. [PDF]
Priya Gupta +2 more
openalex +1 more source
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
Measurements of sinus impulse conduction from electrogram of bundle of His.
S. Bekheit +3 more
semanticscholar +1 more source
This study integrates transcriptomic profiling of matched tumor and healthy tissues from 32 colorectal cancer patients with functional validation in patient‐derived organoids, revealing dysregulated metabolic programs driven by overexpressed xCT (SLC7A11) and SLC3A2, identifying an oncogenic cystine/glutamate transporter signature linked to ...
Marco Strecker +16 more
wiley +1 more source
This study characterizes the responses of primary acute myeloid leukemia (AML) patient samples to the MCL‐1 inhibitor MIK665. The results revealed that monocytic differentiation is associated with MIK665 sensitivity. Conversely, elevated ABCB1 expression is a potential biomarker of resistance to the treatment, which can be overcome by the combination ...
Joseph Saad +17 more
wiley +1 more source
Aggressive prostate cancer is associated with pericyte dysfunction
Tumor‐produced TGF‐β drives pericyte dysfunction in prostate cancer. This dysfunction is characterized by downregulation of some canonical pericyte markers (i.e., DES, CSPG4, and ACTA2) while maintaining the expression of others (i.e., PDGFRB, NOTCH3, and RGS5).
Anabel Martinez‐Romero +11 more
wiley +1 more source

