Single-walled carbon nanotube as hole transport layer in perovskite solar cell: Efficiency enhancement

We propose a new hole transport layer (HTL) in a perovskite solar cell (PSC) using single-walled carbon nanotube (SWCNT) achieving a power conversion efficiency (PCE) up to 19.98%, for the first time. Owing to its exceptional quantum properties, this one-dimensional (1D) element is utilized in order to facilitate hole transport inside the cell structure. Using (6, 5) SWCNT as the HTL and the MAPbI3 perovskite material on top of it as the main adsorbent layer, while colloidal quantum dots (CQDs) of lead sulfide (PbS-CQDs) with excellent absorption in the wavelength range of 500–1100 nm fills the space around the SWCNTs in each unit cell as the second adsorbent layer, we achieved excellent performance. Also, we observe a 49.7% increase compared to when the space around the HTL is filled with perovskite material. The proposed PSC arrangement, due to its brilliant electrical and mechanical properties besides excellent stability of SWCNTs, gives significantly superior cell stability in addition to a high PCE. Finally, we hope that utilizing this novel structure can be extended in the industry along with solving problem of perovskite stability

Molecular mechanisms mediating relapse following ivosidenib monotherapy in IDH1-mutant relapsed or refractory AML

Baseline mutations are associated with response ( JAK2 ) or resistance ( NRAS , PTPN11 ) to ivosidenib monotherapy in m IDH1 R/R AML. 2-HG restoration via novel IDH1 second-site and IDH2 mutations, and non- IDH –related pathways, are identified at relapse. Isocitrate dehydrogenase ( IDH ) 1 and 2 mutations result in overproduction of D-2-hydroxyglutarate (2-HG) and impaired cellular differentiation. Ivosidenib, a targeted mutant IDH1 (mIDH1) enzyme inhibitor, can restore normal differentiation and results in clinical responses in a subset of patients with m IDH1 relapsed/refractory (R/R) acute myeloid leukemia (AML). We explored mechanisms of ivosidenib resistance in 174 patients with confirmed m IDH1 R/R AML from a phase 1 trial. Receptor tyrosine kinase (RTK) pathway mutations were associated with primary resistance to ivosidenib. Multiple mechanisms contributed to acquired resistance, particularly outgrowth of RTK pathway mutations and 2-HG–restoring mutations (second-site IDH1 mutations, IDH2 mutations). Observation of multiple concurrent mechanisms in individual patients underscores the complex biology of resistance and has important implications for rational combination therapy design. This trial was registered at www.clinicaltrials.gov as #NCT0207483