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The loss of organic components from perovskites has inevitably triggered a series of undesirable results, including ion migration, increased defects, and organic vapors, which severely limit the performance of perovskite solar cells (PSCs) and impede their progress toward commercial applications. To circumvent this issue, we report a novel covalent bonding strategy by employing bis-diazirine (BD) molecules to covalently bond organic cations of perovskites. Experimental and ab initiosimulation results confirmed the efficacy of BD molecules to strongly immobilize the organic cations and eventually enhance the thermal, illumination, and electrical bias resistance properties of perovskites. Consequently, highly efficient (24.36% efficiency, certified 24.02%) and ultra-stable PSCs were realized, which retained 98.6% of their initial efficiency even after 1,000 h of operational tests.

The 2D/3D heterojunction structure emerges as a viable approach for enhancing the efficiency and stability of perovskite photovoltaics. However, the formation of an accumulative low-dimensional 2D perovskite (n=1) cladding layer often impedes carrier transport due to the insulating nature and high quantum confinement, and there is a paucity of detailed understanding regarding its surface phase control. This study introduces a Dion-Jacobson (DJ) phase 2D perovskite, employing decane-1,10-diammonium diiodide (DDADI) to interface with 3D perovskite, leveraging long-chain diammonium cations for structural stability and defect passivation on the 3D FAPbI3perovskite surface. In addition, a novel PbI2-assisted phase control (PAPC) technique is proposed to mitigate the quantum confinement effects of the 2D layer, especially reducing the formation of the highly confined insulating n=1 phase. X-ray scattering analysis confirms the method's efficacy in promoting the formation of an n=2 phase, facilitating cascading HOMO levels and improving hole carrier transport. The optimized 2D/3D perovskite solar cell (PSC) achieve an exemplary efficiency of 25.16 %, with a notable open-circuit voltage of 1.192 V, and retain 92.9 % of its initial efficiency after 1000 hours in a nitrogen atmosphere, signifying a strategic advancement in 2D/3D PSC construction.

The unsteady lift characteristics of a double-delta wing were studied using both experimental and numerical approaches, which were also compared with a single-delta wing with the same main wing sweep angle. It was found that by increasing the reduced frequency of pitching, the hysteresis effect of lift was magnified. Moreover, in the high reduced frequency case k= 0.48, the difference between the lift coefficients of single- and double-delta wings became rather subtle. The wing surface pressure distribution results indicated the flow phenomenon of dramatic lift losses was due to the effect of lower surface suction during the wing being pitched downstroke. It was observed that, as the reduced frequency became sufficiently high, the virtual camber effect induced by pitching could dominate the flow field, which would mitigate the impact of wing geometry on the lift characteristics.

This work investigates the turbulent decaying behaviors downstream of a propeller in the core-flow region. Both axial and tangential velocity fluctuations behind a two-bladed propeller were measured using a stationary hot-wire probe. Unexpectedly, the complex near-wake core-flow of the propeller is found to show a similar decay characteristic of homogeneous turbulence, such as grid turbulence. The decay of turbulence intensity is found to be dominated by the level of periodic velocity fluctuations, showing a similar behavior of the homogenous and isotropic turbulence. This turbulent decaying behavior of the core-flow can be adopted for future turbulent modeling techniques.

Micro aerial vehicles are currently receiving growing interest because of their broad applications in many fields. In their flight tests, the onset of unwanted large amplitude roll oscillations was reported, which resulted in difficulties with flight control, and this has become one of the major challenges of current micro aerial vehicles design. In this review type of article, the low Reynolds number flow characteristics of a low-aspect-ratio wing are reviewed, and the self-induced roll oscillations are discussed with special attention being payed to the interaction between the three-dimensional flow structure and wing in reciprocatively rolling motion. The roll attenuation methods are introduced via flow control approaches, which can suppress the roll oscillations effectively by manipulating the leading-edge flow separation and tip vortices of the low-aspect-ratio wings.

Wind tunnel tests of five propellers with different blade tip widths are carried at pitch angles between 20.5° and 40°. The aerodynamic performance are provided, which can be treated as a supplement of the high altitude airship propeller database. The influences of the blade planform and advance ratio on both power coefficient and propulsive efficiency are analyzed. It is found that at advance ratio below 0.8, the propeller with narrow tip has higher efficiency but limited power coefficient. While at advance ratio above 0.8, the propeller with wider tip has the advantages of higher power coefficient and acceptable efficiency. The variation of the propulsive efficiency with planform and advance ratio is dominated by the radial distributions of the airflow angle and interference angle.

Oncogenic transformation of hematopoietic stem cells by chimeric fusion kinases causing constitutive activation of FGFR1 leads to a stem cell leukemia/lymphoma (SCLL) syndrome, accompanied by widespread dysregulation of gene activity. We now show that FGFR1 activation is associated with upregulation of MYC and pharmacological suppression of FGFR1 activation leads to downregulation of MYC and suppression of MYC target genes. Luciferase reporter assays demonstrate that FGFR1 can directly regulate MYC expression and this effect is enhanced in the presence of chimeric FGFR1 kinases. In SCLL cells, a truncated form of FGFR1 is generated by granzyme B cleavage of the chimeric kinases, producing a nucleus-restricted derivative that can bind MYC regulatory regions. Mutation of the granzyme B cleavage site prevents relocation to the nucleus but does not suppress MYC activation, suggesting additional mechanisms of MYC activation in the presence of cytoplasm-restricted chimeric kinases. We show that one of these mechanisms involves activating cytoplasmic STAT5, which upregulates MYC independent of the truncated FGFR1 kinase. Targeting MYC function using shRNA knockdown and 10054-F8 in SCLL cells leads to inhibition of cell proliferation and synergizes with the BGJ398 FGFR1 inhibitor, suggesting a combination therapy that could be used in the treatment of SCLL.

MicroRNAs (miRNAs) have pathogenic roles in the development of a variety of leukemias. Here we identify miRNAs that have important roles in the development of B lymphomas resulting from the expression of the chimeric BCR-FGFR1 kinase. The miR-17/92 cluster was particularly implicated and forced expression resulted in increased cell proliferation, while inhibiting its function using miRNA sponges reduced cell growth and induced apoptosis. Cells treated with the potent BGJ389 FGFR1 inhibitor led to miR-17/92 downregulation, suggesting regulation by FGFR1. Transient luciferase reporter assays and qRT-PCR detection of endogenous miR-17/92 expression in stable transduced cell lines demonstrated that BCR-FGFR1 can regulate miR-17/92 expression. This positive association of miR-17/92 with BCR-FGFR1 was also confirmed in primary mouse SCLL tissues and primary human CLL samples. miR-17/92 promotes cell proliferation and survival by targeting CDKN1A and PTEN in B-lymphoma cell lines and primary tumors. An inverse correlation in expression levels was seen between miR-17/92 and both CDKN1A and PTEN in two cohorts of CLL patients. Finally, in vivo engraftment studies demonstrated that manipulation of miR-17/92 was sufficient to affect BCR-FGFR1-driven leukemogenesis. Overall, our results define miR-17/92 as a downstream effector of FGFR1 in BCR-FGFR1-driven B-cell lymphoblastic leukemia.

ABSTRACTLTR retrotransposons are repetitive DNA elements comprising ∼10% of the human genome. They are silenced by hypermethylation of cytosines in CpG dinucleotides and are considered parasitic DNA serving no useful function for the host genome. However, hypermethylated LTRs contain enhancer and promoter sequences and can promote tissue-specific transcription of cis-linked genes. To resolve the apparent paradox of hypermethylated LTRs possessing transcriptional activities, we studied the ERV-9 LTR retrotransposon located at the 5′ border of the transcriptionally active β-globingene locus in human erythroid progenitor and erythroleukemia K562 cells. We found that the ERV-9 LTR, containing 65 CpGs in 1.7 kb DNA, was hypermethylated (with > 90% methylated CpGs). Hypermethylated LTR possessed transcriptional enhancer activity, since in vivodeletion of the LTR by CRISPR-cas9 suppressed transcription of the globin genes by > 50%. ChIP-qPCR and ChIP-seq studies showed that the hypermethylated LTR enhancer spanning recurrent CCAATCG and GATA motifs associated respectively with key transcription factors (TFs) NF-Y and GATA-1 and -2 at reduced levels, compared with the unmethylated LTR in transfected LTR-reporter gene plasmids. Electrophoretic mobility shift assays with methylated LTR enhancer probe showed that the methylated probe bound both NF-Y and GATA-1 and -2 with lower affinities than the unmethylated enhancer probe. Thus, hypermethylation drastically reduced, but did not totally abolish, the binding affinities of the enhancer motifs to the key TFs to assemble the LTR-pol II transcription complex that activated transcription of cis-linked genes at reduced efficiency.

Polyethylene naphthalate (PEN) has been widely employed in highly desired flexible perovskite solar cells (F-PSCs) because of its better chemical stability and higher temperature tolerance. However, the naphthalene ring in the PEN induces poor transmittance in the ultraviolet (UV) region below 380nm, which significantly lowers the power conversion efficiency (PCE) of F-PSCs. Here, a novel strategy is adopted by introducing UV–visible downshifting material before the PEN substrate to increase the spectral response under the UV region. The PCE of modified F-PSCs increases from 22.19% to 22.81% and retains the same stability as that of the control device. The optimized device shows improved photocurrent due to the enhanced spectral response in the UV region. Interestingly, the humidity resistance characteristic of the device had also improved because of the hydrophobicity of downshifting materials. This novel strategy is distinguishable where downshifting material has been externally employed without altering the internal device architecture, which is also broadly applicable to other types of flexible solar cells.

Preferred crystalline orientation at the surface of quasi-2D organic–inorganic halide perovskites is crucial to promote vertical carrier transport and interface carrier extraction, which further contribute to device efficiency and stability in photovoltaic applications. However, loose unoriented and defective surfaces are inevitably formed in the crystallization process, especially with the introduction of bulky organic cations into the quasi-2D perovskites. Here, a facile and effective surface polishing method using a natural-friendly green solvent, 2,2,2-trifluoroethanol, is proposed to reconstruct the surface. After solvent polishing, the randomly oriented phases containing trap sites on the surface are successfully removed, and the compact vertical-oriented phases underneath are revealed with less defectiveness and better smoothness, which greatly facilitates carrier transport and interfacial charge extraction. Consequently, the green solvent polished devices show a boosting efficiency of 18.38% with a high open-circuit voltage of 1.21 V. The devices also show improved storage and operational stability.

No relevant conflicts of interest to declare.

Stem cell leukemia/lymphoma syndrome (SCLL) develops as a result of the ligand-independent, constitutive activation of FGFR1 kinase as a result of chromosome translocations that lead to chimeric FGFR1 kinases. This disorder typically presents as a chronic myeloproliferative disease accompanied by B-cell and T-cell lymphomas with rapid progression to AML. The BCR-FGFR1 variant of SCLL is relatively rare, with only ~20 cases reported to date but is perhaps one of the more aggressive forms of the disease. While the BCR-FGFR1 rearrangement clearly activates the FGFR1 kinase domain through oligomerization, which is also the case for the other FGFR1 chimeric kinases. The more aggressive progression of BCR-FGFR1-driven disease, however, may be a result of the effects of unique domains within the BCR component of the chimeric protein.

MicroRNAs have pathogenic roles in the development of various types of leukemia. Here we identify miRNAs that have important roles in the development of stem cell leukemia/lymphoma syndrome (SCLL) resulting from the expression of the chimeric BCR-FGFR1 kinase. Comparison of BBC2 cells, a murine pre-B-cell lymphoma models of SCLL, with FACS sorted normal murine splenic CD19+ B cells, led to identification of 191 upregulated and 59 downregulated in BBC2 cells. We next investigated which of these miRNAs directly respond to FGFR1 through inhibition of FGFR1 signaling with BGJ398 in BBC2 cells, and finally defined 46 core miRNAs, with 33 activated in BBC2 downregulated by BGJ398, and 13 suppressed upregulated by BGJ398.

No relevant conflicts of interest to declare.

Long noncoding RNAs (lncRNAs) regulate diverse cellular processes in development, differentiation and malignancy. In human cells, over 80% of the lncRNAs contain retrotransposon sequences transcribed from Alu, L1 and LTR retrotransposons, which comprise ~40% of the human genome. The functional significance of the retrotransposon lncRNAs is largely unknown. The human genome contains ~4000 copies of the ERV-9 LTR retrotransposon, which exhibits strong enhancer activity and initiates synthesis of ERV-9 lncRNAs in erythroid progenitor cells. Recently, we discovered that depletion of the ERV-9 lncRNAs in human erythroid progenitor cells cultured ex vivo from peripheral blood CD34+ cells inhibited ex vivo erythropoiesis. Whole genome RNA sequencing (RNA-seq) found that depletion of ERV-9 lncRNAs significantly suppressed transcription of 608 genes including ~50 key erythroid genes. We hypothesize that the ERV-9 lncRNAs together with the ERV-9 LTR act in cis to regulate transcription of these key erythroid genes and other genes to set up a transcriptional network that promotes erythropoiesis.