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RISS 인기검색어
- 검색키워드
- 저자 : Stefan Hartl (검색결과 2 건)
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Pearls and Pitfalls of Pulsed Field Ablation
Stefan Hartl,Nico Reinsch,Anna Füting,Kars Neven 대한심장학회 2023 Korean Circulation Journal Vol.53 No.5
Pulsed field ablation (PFA) was recently rediscovered as an emerging treatment modality for the ablation of cardiac arrhythmias. Ultra-short high voltage pulses are leading to irreversible electroporation of cardiac cells subsequently resulting in cell death. Current literature of PFA for pulmonary vein isolation (PVI) consistently reported excellent acute and long-term efficacy along with a very low adverse event rate. The undeniable benefit of the novel ablation technique is that cardiac cells are more susceptible to electrical fields whereas surrounding structures such as the pulmonary veins, the phrenic nerve or the esophagus are not, or if at all, minimally affected, which results in a favorable safety profile that is expected to be superior to the current standard of care without compromising efficacy. Nevertheless, the exact mechanisms of electroporation are not yet entirely understood on a cellular basis and pulsed electrical field protocols of different manufactures are not comparable among one another and require their own validation for each indication. Importantly, randomized controlled trials and comparative data to current standard of care modalities, such as radiofrequency- or cryoballoon ablation, are still missing. This review focuses on the “pearls” and “pitfalls” of PFA, a technology that has the potential to become the future leading energy source for PVI and beyond.
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Inhibitor of MYC identified in a Kröhnke pyridine library
Hart, Jonathan R.,Garner, Amanda L.,Yu, Jing,Ito, Yoshihiro,Sun, Minghao,Ueno, Lynn,Rhee, Jin-Kyu,Baksh, Michael M.,Stefan, Eduard,Hartl, Markus,Bister, Klaus,Vogt, Peter K.,Janda, Kim D. National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.34
<P>In a fluorescence polarization screen for the MYC–MAX interaction, we have identified a novel small-molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The <I>K</I><SUB>d</SUB> of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM, as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC–MAX complex formation in the cell, as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-amplified human cancer cells.</P>
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