Results 211 to 220 of about 7,026,646 (351)
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
The nature of cultural competency and its constructs in health sciences: Insights from qualitative research in Iran. [PDF]
Sargazi S, Yamani N, Najimi A.
europepmc +1 more source
Research Digest - July 2017 [PDF]
Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine in St. Louis
core +1 more source
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert +13 more
wiley +1 more source
Personalised learning in higher education for health sciences: a scoping review. [PDF]
Ali M, Wahab IA, Huri HZ, Yusoff MS.
europepmc +1 more source
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser +14 more
wiley +1 more source
Early detection of at-risk health sciences students: a machine learning-based predictive study using midterm grades. [PDF]
Al Hashmi RAM, Ozturk I, Elmehdi HM.
europepmc +1 more source
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source

