Results 101 to 110 of about 226,605 (286)

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

Molecular 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, Soheil Akbari, Ceyda Caliskan, Canan Celiker, Ozden Oz, Leman Binokay, Gökhan Karakulah, Serif Senturk, Esra Erdal   +8 more
wiley   +1 more source

Intravenous Dantrolene Does Not Exhibit Calcium Channel Blocking Effects on the Cardiac Conduction System in Humans [PDF]

, 1991
M. Kentsch, Norbert Roewer, Klaus-Peter Kunze, Karl‐Heinz Kück   +3 more
openalex   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

Molecular Oncology, EarlyView.
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, Jan Niklas Schäfer, Shraga Nahum Goldberg, Philipp Maximilian Kazmierczak, Moritz Nikolaus Gröper, Philipp Franz Linden, Elif Öcal, Tanja Burkard, Stefanie Corradini, Najib Ben Khaled, Moritz Wildgruber, Max Seidensticker, Jens Ricke, Matthias Stechele, Marianna Alunni‐Fabbroni   +14 more
wiley   +1 more source

His–Purkinje Conduction System Pacing: State of the Art in 2020

Arrhythmia & Electrophysiology Review, 2020
doaj   +1 more source

A histopathologic study of the conduction system in an elderly patient with partial atrial standstill.

, 1987
Hironori Ezaki, Shin-ichiro Ohkawa, Akihiko Miyagawa, Keiji Ueda, Masaya Sugiura   +4 more
openalex   +2 more sources

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
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, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source

Isolation and characterization of myosin heavy chain isozymes of the bovine conduction system. [PDF]

, 1987
Issei Komuro, K. Nomoto, Taku Sugiyama, Masahiko Kurabayashi, Fumimaro Takaku, Y Yazaki   +5 more
openalex   +1 more source

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

Molecular 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, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source

Predictors, clinical impact, and management strategies for conduction abnormalities after transcatheter aortic valve replacement: an updated review

Frontiers in Cardiovascular Medicine
Transcatheter aortic valve replacement (TAVR) has increasingly become a safe, feasible, and widely accepted alternative surgical treatment for patients with severe symptomatic aortic stenosis. However, the incidence of conduction abnormalities associated
Qingyun Yu, Qingan Fu, Yunlei Xia, Yanqing Wu   +3 more
doaj   +1 more source

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

Molecular 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, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source