In the absence/presence of S8, the one-pot assembly of [Et4N][Tp*WS3] [1; Tp* = hydridotris(3,5-dimethylpyrazol-1-yl)borate] with [Cu(MeCN)4]PF6 and bis- or tetraphosphine ligands 1,2-bis(diphenylphosphino)ethane (dppe), 1,3-bis(diphenylphosphino)propane (dppp), 1,4-bis(diphenylphosphino)butane (dppb), and N,N,N',N'-tetrakis(diphenylphosphinomethyl)ethylenediamine (dppeda) produces six W-Cu-S clusters, namely, [(Tp*WS3Cu2Cl)2(dppe)] (2), [Tp*WS3Cu4(dppp)2(μ4-Cl)(μ-Cl)]PF6·MeCN (3·MeCN), [(Tp*WS3Cu3)2(μ4-Cl)(μ-Cl)2(dpppS2)] (4), [(Tp*WS3Cu2Cl)2(dppbS2)]·2MeCN·2H2O (5·2MeCN·2H2O), [(Tp*WS3Cu3Cl2)2(dppbS2)] (6), and [(Tp*WS3Cu3)2(Ph2PS2)3(μ6-Cl)0.5](PF6)0.5·0.75CH2Cl2 (7·0.75CH2Cl2). Compounds 2-7 are characterized by elemental analysis, IR, UV-vis, (1)H and (31)P{(1)H} NMR, electrospray ionization mass spectrometry, and X-ray crystallography. For 2, the dppe ligand bridges a pair of butterfly-shaped [Tp*WS3Cu2] cores to form a double-butterfly-shaped structure. For 4, the dppp ligand is susceptible toward S association and forms an in situ generated dpppS2 ligand, supporting an octanuclear double-half-open-cubane structure and contrasting an analogous system wherein a pentanuclear motorcycle-shaped cationic cluster 3 is formed with the absence of S8. A longer dppb ligand readily converts to S-based ligands in 5 and 6, subsequently serving as bridges between a pair of a butterfly-shaped (5) and nest-shaped (6) clusters. Further use of a tetraphosphine ligand, dppeda, in the cluster formation, with the presence of S8, leads to an unexpected ligand degradation to give the [Ph2PS2](-) anions. Three [Ph2PS2](-) anions juxtapose a pair of nest-shaped cluster cores to yield an octanuclear cluster, 7, featuring a cage to encapsulate μ6-Cl(-). The third-order nonlinear-optical (NLO) properties of 2-7 in N,N-dimethylformamide, investigated using a Z-scan technique at 532 nm, show that 2-6 have a reverse saturable absorption, while 7 has a notable saturable absorption. All of 2-7 exhibit a self-focusing effect with hyperpolarizability γ values in the range of 4.71 × 10(-30)-1.02 × 10(-29) esu, which are 440-1000 times higher than that of 1. The formation of 4-7 from 1 through the in situ thiolation of phosphine ligands presents a new approach to the design and assembly of the W-Cu-S clusters with interesting structural arrays and better NLO properties.

Six analogous two-dimensional (2D) [Tp*WSCu]-based (Tp* = hydridotris(3,5-dimethylpyrazol-1-yl)borate) networks, namely, {[(Tp*WSCu)L](μ-N)} (2: L = 5-methyltetrazolate (Mtta); 3a: L = 5-ethyltetrazolate (Etta)) and {[(Tp*WSCu)L]BF} (3b: L = Etta; 4: L = 5-propyltetrazolate (Ptta); 5: L = 5-butyltetrazolate (Btta); 6: L = 5-pentyltetrazolate (Petta)) were synthesized by reactions of [EtN][Tp*WS] (1), [Cu(CHCN)]BF, NaN, and NHBF in different nitrile solvents (CH(CH)CN, n = 0, 1, 2, 3, and 4) under solvothermal conditions. In the structures of 2-6, each alkyl tetrazolate L as a bridging ligand was generated in situ from the "click" reaction between azide and nitrile. These 2D (6,3) networks support two types of voids wherein the pendant alkyl groups are accommodated. A tetrahedron cage-like cluster [Tp*W(μ-S)(μ-S')Cu] (7) was also formed in some of the above reactions and can be readily separated by solvent extraction. The proportion of 7 increased with the elongation of the alkyl chains and finally became the exclusive product when heptylnitrile was employed. Further use of CuCN as a surrogate for [Cu(CHCN)]BF with the aim of introducing additional CN bridges into the network led us to isolate a tetrazolate-free compound, {[EtN]{(Tp*WSCu)[Cu(CN)]}·2PhCHCN} (8·2PhCHCN), a unique 2D network that features {(Tp*WSCu)[Cu(CN)]}, {(Tp*WSCu)[Cu(CN)][Cu(CN)]}, and {(Tp*WSCu)[Cu(CN)]} ring subunits. Compounds 5-8 are soluble in DMF and exhibit a reverse saturable absorption and self-focusing third-order nonlinear optical (NLO) effect at 532 nm with hyperpolarizability γ values in the range of 4.43 × 10 to 5.40 × 10 esu, which are 400-500 times larger than that of their precursor 1. The results provide an interesting insight into the synergetic synthetic strategy related to the assembly of the [Tp*WSCu] cluster core, the "click" formation of the tetrazolate ligands, and the construction of the [Tp*WSCu] cluster-based 2D networks.

High-density lipoprotein cholesterol (HDL-C) has an inverse association with the incidence of lung cancer. However, whether it can be used as a predictive factor in advanced lung adenocarcinoma patients treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) still remains undefined. This research aimed at studying the relationship of serum HDL-C baseline level and HDL-C kinetics to EGFR mutation, the efficacy of EGFR-TKI, and the predictive value of PFS. The presence of mutation rate in the 192 patients with lung adenocarcinoma was compared within stratified groups. Levels of baseline HDL-C and kinetics of HDL-C were analyzed retrospectively in patients treated with EGFR-TKI harboring EGFR mutation. Univariate and multivariate analyses were performed to investigate the prognostic value of HDL-C. EGFR mutation rate of HDL-C high-level group was significantly higher than that of low-level group (59.0% vs 35.6%, P=0.001). Multivariate logistic analysis showed that high-level HDL-C was an independent predictive factor for EGFR gene mutation (P=0.005; odds ratio =0.417; 95% confidence interval [CI], 0.227–0.768). Patients with a low level of HDL-C before therapy showed a progression of disease in most cases (P<0.001). According to HDL-C kinetics, patients who received EGFR-TKI treatment harboring EGFR mutation were divided into four groups. Univariate analysis showed that patients in nondecreased group had longer progression-free survival (P<0.001; hazard ratio =0.003; 95% CI, 0.001–0.018). Multivariate Cox proportional hazards model analyses showed the same result (P<0.001; hazard ratio =0.003; 95% CI, 0.001–0.018). Current results suggest that HDL-C seems to be a good independent predictive biomarker for advanced lung adenocarcinoma patients treated with the first-line EGFR-TKI. Roles of this biomarker include indicating EGFR mutation, assessing the efficacy of EGFR-TKI, and predicting the progression-free survival.