Supplementary document for broadband achromatic and wide field of view metalens-doublet by inverse design - 6913574.pdf

additional results for three metalenses result

Supplementary document for An achromatic and wide field of view metalens based on the harmonic diffraction and quadratic phase - 6118468.pdf

supplemental documen

Stereochemically Active Lone Pairs and Nonlinear Optical Properties of Two-Dimensional Multilayered Tin and Germanium Iodide Perovskites

Two-dimensional (2D) metal halide perovskites are promising tunable semiconductors. Previous studies have focused on Pb-based structures, whereas the multilayered Sn- and Ge-based analogues are largely unexplored, even though they potentially exhibit more diverse structural chemistry and properties associated with the more polarizable ns2 lone-pair electrons. Herein, we report the synthesis and structures of 2D tin iodide perovskites (BA)2(A)Sn2I7, where BA = n-butylammonium and A = methylammonium, formamidinium, dimethylammonium, guanidinium, or acetamidinium, and those of 2D germanium iodide perovskites (BA)2(A)Ge2I7, where A = methylammonium or formamidinium. By comparing these structures along with their Pb counterparts, we establish correlations between the effect of group IV-cation’s lone-pair stereochemical activity on the perovskite crystal structures and the resulting semiconducting properties such as bandgaps and carrier–phonon interactions and nonlinear optical properties. We find that the strength of carrier–phonon interaction increases with increasing lone-pair activity, leading to a more prominent photoluminescence tail on the low-energy side. Moreover, (BA)2(A)Ge2I7 exhibit strong second harmonic generation with second-order nonlinear coefficients of ∼10 pm V–1 that are at least 10 times those of Sn counterparts and 100 times those of Pb counterparts. We also report the third-order two-photon absorption coefficients of (BA)2(A)Sn2I7 to be ∼10 cm MW–1, which are one order of magnitude larger than those of the Pb counterparts and traditional inorganic semiconductors. These results not only highlight the role of lone-pair activity in linking the compositions and physical properties of 2D halide perovskites but also demonstrate 2D tin and germanium iodide perovskites as promising lead-free alternatives for nonlinear optoelectronic devices

Praziquantel Synergistically Enhances Paclitaxel Efficacy to Inhibit Cancer Cell Growth

<div><p>The major challenges we are facing in cancer therapy with paclitaxel (PTX) are the drug resistance and severe side effects. Massive efforts have been made to overcome these clinical challenges by combining PTX with other drugs. In this study, we reported the first preclinical data that praziquantel (PZQ), an anti-parasite agent, could greatly enhance the anticancer efficacy of PTX in various cancer cell lines, including PTX-resistant cell lines. Based on the combination index value, we demonstrated that PZQ synergistically enhanced PTX-induced cell growth inhibition. The co-treatment of PZQ and PTX also induced significant mitotic arrest and activated the apoptotic cascade. Moreover, PZQ combined with PTX resulted in a more pronounced inhibition of tumor growth compared with either drug alone in a mouse xenograft model. We tried to investigate the possible mechanisms of this synergistic efficacy induced by PZQ and PTX, and we found that the co-treatment of the two drugs could markedly decrease expression of X-linked inhibitor of apoptosis protein (XIAP), an anti-apoptotic protein. Our data further demonstrated that down-regulation of XIAP was required for the synergistic interaction between PZQ and PTX. Together, this study suggested that the combination of PZQ and PTX may represent a novel and effective anticancer strategy for optimizing PTX therapy.</p> </div

Apoptosis induced by the co-treatment of PZQ and PTX may result from the mitotic arrest induced by this treatment.

<p>(A) After DLD-1 cells were co-treated with 20 µM PZQ and 10 nM PTX for indicated time points, the G2/M and Sub-G1 fractions were determined by flow cytometry. (B) DLD-1 cells were treated with a combination of PZQ (20 µM) and PTX (10 nM) with or without 12.5 µM roscovitine for 12 h, and then cell cycle was analyzed by flow cytometry. (C) DLD-1 cells were treated as in (B), and mitotic index was determined. After DLD-1 were treated with a combination of PZQ (20 µM) and PTX (10 nM) in the presence or absence of 12.5 µM roscovitine for 48 h, Apoptosis was assessed by flow cytometry analysis of Sub-G1 population (D) and Western analysis of cle-PARP level (E). All Values are shown as mean±SEM from three separate experiments.</p

PZQ enhances PTX-induced apoptosis in various cancer cell lines.

<p>(A) The indicated cell lines were treated as in Fig. 1A, and apoptosis was examined by Western analysis of the cleaved PARP (cle-PARP) level. (B) DLD-1 and H1299 cells were treated with 20 µM PZQ alone, 10 nM PTX alone, or the combination for 48 h. Then sub-G1 fraction was determined by flow cytometry. (C) DLD-1 cells were treated with 20 µM PZQ and 10 nM PTX in the absence or presence of 20 µM caspase inhibitor zVAD-fmk for 48 h, and the expression of caspase 3 and cle-PARP were examined by Western blot. (D) After DLD-1 cells were treated as in C, the percentage of apoptotic cells was determined by DAPI staining. All Values represent mean±SEM from three separate experiments.</p

The co-treatment of PZQ and PTX could suppress XIAP protein.

<p>(A) DLD-1 cells were treated with 20 µM PZQ alone, 10 nM PTX alone, or the combination for 24 h. Then expression of Bcl-XL, Bcl-2, Survivin, XIAP, Bim, Puma, Noxa, Bax and Bak were monitored by Western blot. (B) After exposure of DLD-1 cells to a combination of 20 µM PZQ and 10 nM PTX in the presence or absence of 20 µM zVAD-fmk for 24 h, expression of XIAP was determined by Western blot. (C) H1299 cells were treated with 20 µM PZQ alone, 10 nM PTX alone, or the combination for 24 h, after which expression of XIAP was examined. (D) After DLD-1 cells were treated as in (A), total RNA was isolated and XIAP mRNA was quantified by real-time RT-PCR. Following normalization to GAPDH mRNA, the XIAP mRNA expression values for each condition were relative to vehicle-treated control cells. (E) DLD-1 cells were treated with a combination of 20 µM PZQ and 10 nM PTX in the absence or presence of 10 µM MG132 for 24 h, and then expression of XIAP was monitored by Western blot. Values represent mean±SEM from three separate experiments.</p

The co-treatment of PZQ and PTX could induce mitotic arrest.

<p>(A) DLD-1 cells were treated with 10 nM or 20 nM PTX in the absence or presence of 20 µM PZQ for 12 h, and cell cycle was analyzed by flow cytometry. The results are representative of three independent experiments. After DLD-1 cells were treated as above, mitotic index was determined as described in “<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0051721#s2" target="_blank">Materials and Methods</a>” (B), and expression level of phospho-histone H3 (Ser-10) (P-H3) was monitored by Western blot (C). Values represent mean±SEM from three separate experiments.</p

XIAP plays an important role in the synergistic cytotoxicity of PZQ and PTX.

<p>(A) Western blot showed XIAP expression in DLD-1 cells at 24 h after transfection with pcDNA3-myc-XIAP or control vector. (B) 24 h after transfection with pcDNA3-myc-XIAP and control vector, DLD-1 cells were treated with 20 µM PZQ alone, 10 nM PTX alone or the combination for 48 h, and then cell viability was determined by MTT assay. (C) 24 h after transfection with pcDNA3-myc-XIAP and control vector, DLD-1 cells were treated with a combination of 20 µM PZQ and 10 nM PTX. Then the sub-G1 fraction was determined by flow cytometry. (D) DLD-1 cells were infected with a lentivirus encoding control shRNA or XIAP shRNA for 48 h, and expression of XIAP was analyzed by Western blot. (E) DLD-1 cells were infected with a lentivirus encoding control shRNA or XIAP shRNA for 48 h, and then treated with 20 µM PZQ alone, 10 nM PTX alone or the combination for 48 h. The cell viability was determined by MTT assay. All Values are shown as mean±SEM from three separate experiments.</p

PZQ synergistically enhances PTX-induced growth inhibition of cancer cells.

<p>(A) The cell viability was determined by MTT assay after various cancer cell lines were treated with PZQ alone, PTX alone or combined both drugs at concentrations and time points as indicated following: HeLa, ZR7530, DLD-1 and H1299 cells were treated with 20 µM PZQ alone, 10 nM PTX alone, or combined both for 48 h; Bcap37 and SPC-A-1 cells were treated with 30 µM PZQ, 5 nM PTX alone, or both for 48 h; Ltep-a-2 cells were treated with 30 µM PZQ alone, 5 nM PTX alone, or both for 60 h. (B) DLD-1 were treated with the indicated concentrations of PTX in the absence or presence of 20 or 40 µM PZQ for 48 h. Cell viability was then determined by MTT assay. (C) DLD-1 and H1299 cells were treated with 20 µM PZQ alone, 10 nM PTX alone, or the combination for 10 days. Colonies were then stained with crystal violet and counted. (D) DLD-1 and H1299 cells were treated with various concentrations of PZQ and PTX at a fixed ratio (2000∶1) for 48 h. After cell viability was determined in each condition, the combination index (CI) was calculated as described in “<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0051721#s2" target="_blank">Materials and Methods</a>.” CI values<1.0 suggest a synergistic interaction between the two drugs. All Values represent mean±SEM from three separate experiments.</p