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To summarize a 10-year, single-institution experience with ethanol embolization of nasal arteriovenous malformations (NAVMs) in 52 patients.The present work was a retrospective study of 52 patients (aged between 1 and 67 years) with NAVMs who were treated with ethanol embolization between August 2009 and August 2019. The diagnosis of NAVMs was established based on clinical and imaging studies including ultrasound, computer tomography angiography, and digital subtract angiography. Embolization techniques used in the current study included transarterial, direct puncture, and a combination of both. The clinical and angiographic features, treatment methods, clinical outcomes, and complications were assessed within the mean period of 55.2 months (range, 1-119 months) after the last embolization.The total number of embolization sessions (140 embolization procedures in 52 pts) included transarterial approach (1 pt), direct puncture (2 pt), and a combination of transarterial and direct puncture (49 pts). There was a positive correlation between nidus size and treatment sessions (r = 0.780, P = 0.0005) and the amount of ethanol injected (r = 0.840, P = 0.0004). Results of the current study showed that the therapeutic outcomes were complete response in two patients (3.8%) without recurrence throughout the follow-up period (range, 1-119 months; mean, 55.2 months), and partial response in 50 patients (96.2%). A total of seven patients (13.5%) experienced one or more complications, including skin necrosis in one patient (1.9%), transient hemoglobinuria in five patients (9.6%), and skin blister in five patients (9.6%).The reported single-institution experience evidently indicated that ethanol embolotherapy has the potential to successfully devascularize NAVMs and also significantly improve symptoms and signs. Further, it was evident that the use of a combination of transarterial and direct puncture techniques has the potential to increase the rate of therapeutic response in patients with NAVMs.

A facile strategy toward the synthesis of theranostic curcumin–tryptanthrin–Zn(ii) complexes for cancer-specific therapy is demonstrated.

RhQ can be used to target DNA as a highly anticancer therapeutic and fluorescence imaging agent. Importantly, RhQ exhibited significantly more potency than RhS and cisplatin.

Nickel(ii) oxyquinoline–bipyridine complexes inhibit cell growth in A549 and A549/DDP tumor cells via mitophagy pathways.

In recent years, the ecological environment along highways in Tibetan Plateau has been severely affected due to the rapid construction of highways. In order to solve the problems of multiple indicators and inconsistent criteria in the ecological impact assessment of highways, and to scientifically screen assessment indicators, the paper proposes a multi-round indicator screening method, which combines literature analysis, expert rating, and statistical analysis. Based on this screening method, normalized difference vegetation index, land surface temperature, elevation, and normalized difference soil index are screened out. Combined with multiple linear regression, an ecological impact assessment model is established and applied to ecological impact assessment of Gonghe-Yushu Expressway. The results show that the expressway construction is the first driving force for the deterioration of the ecological environment along the roadside, and its interference range on the desert grassland ecosystem is greater than that on the agroforestry system. The ecological environment within 150 m on both sides of the expressway should be protected.

Six new lanthanide(III) complexes, namely [GdIII(QL1)3(BL1)] (Gd1), [GdIII(QL1)3(BL2)] (Gd2), [LuIII(QL2)2(BL3)(NO3)] (Lu1), [LuIII(QL2)2(BL2)(NO3)] (Lu2), [YbIII(QL3)2(BL2)(NO3)] (Yb1), and [YbIII(QL4)2(BL2)(NO3)] (Yb2) coordinated with 5,7-dibromo-8-quinolinol (H-QL1), 5,5′-dimethyl-2,2′-bipyridyl (BL1), 4,4′-di-tert-butyl-2,2′-bipyridine (BL2), 5,7-dibromo-2-methylquinolin-8-ol (H-QL2), 2,2′-bipyridine (BL3), 5,7-dichloro-8-hydroxyquinoline (H-QL3), and 5,7-dichloro-8-hydroxy-2-methylquinoline (H-QL4), were prepared. The LnIII complexes Gd1, Gd2, Lu1, Lu2, Yb1 and Yb2 showed high cytotoxicity toward cervical (HeLa), ovarian (SK-OV-3) and lung (NCI-H460) cancer cells with IC50 values from 0.18 ± 0.14 to 8.02 ± 1.71 μM. In addition, Yb1 and Yb2 impaired mitochondrial functions, decreased mitochondrial membrane potential, and altered the levels of mitochondrial related-proteins. The apoptosis-inducing capability was in the order of Yb2 > Yb1. Such observed differences in biological activities could be caused by the electronic effect of the methyl group of H-QL4 in Yb2.

We herein designed two new PtIV prodrugs of oxoplatin (cis,cis,cis-[PtCl2(NH3)2(OH)2]), [PtIVCl2(NH3)2(O2C-FA)2] (Pt-2) and [PtIVCl2(NH3)2(O2C-RH)2] (Pt-3), by conjugating with ferulic acid (FA-COOH) and rhein (RH-COOH) which have well-known biological activities. Three other Pt(iv) complexes of [PtIVCl2(NH3)2(O2C-BA)2] (Pt-1), [PtIVCl2(NH3)2(O2C-CA)2] (Pt-4) and [PtIVCl2(NH3)2(O2C-TCA)2] (Pt-5) (where BA-COOH = benzoic acid, CA-COOH = crotonic acid and TCA-COOH = trans-cinnamic acid) were also prepared for the comparative study. Like most PtIV prodrug complexes, the cytotoxicity of Pt-3 containing the biologically active rhein (RH-COOH) ligand against lung carcinoma (A549 and A549/DDP) cells was higher than those of Pt-1, Pt-2, Pt-4, cisplatin and Pt-5. Moreover, the cytotoxicity of Pt-3 in HL-7702 normal cells was lower than those of PtIV derivatives bearing BA-COOH, FA-COOH, TCA-COOH and CA-COOH ligands. The highly efficacious Pt-2 and Pt-3 were found to accumulate strongly in the A549/DDP cells, with the prodrug Pt-3 showing highest levels of penetration into the mitochondria. The prodrug Pt-3 effectively entered the A549/DDP cells and caused mitochondrial damage, significantly greater than Pt-2. In addition, the prodrug Pt-3 exhibited higher antitumor efficacy (inhibition rates (IR) = 67.45%) than Pt-2 (28.12%) and cisplatin (33.05%) in the A549/DDP xenograft mouse model. Thus, the prodrug Pt-3 containing the rhein (RH-COOH) ligand is a promising candidate drug targeting the mitochondria.

Four mononuclear cyclometalated iridium(III) complexes, namely, [Ir(FQ)(L1)2] (Ir-1), [Ir(FQ)(L2)2] (Ir-2), [Ir(FQ)(L3)2] (Ir-3) and [Ir(FQ)(L4)2]·2CH3OH (Ir-4) using 5-fluoro-8-quinolinol (H-FQ)-based ligands and [(C^N)2IrCl(μ-Cl)]2 precursor have been first synthesised. The two most effective complexes (containing 7,8-benzoquinoline (H-L3) and 1-phenylpyrazole (H-L4)), Ir-3 and Ir-4, kill HeLa cells in the nanomole range, with the IC50 values of 0.170 ± 0.05 and 0.035 ± 0.002 μM, respectively, indicating that they could potentially inhibit HeLa tumour populations at a lower concentration. Encouragingly, Ir-3 and Ir-4 induce HeLa apoptosis, as indicated by the clear changes in the apoptosis-associated proteins; both accumulate to a high extent in the mitochondrial fraction; promote mitochondrial membrane (MMP) depolarisation and loss of MMP; and trigger caspase-mediated mitochondrial dysfunction apoptosis pathways. To the best of our knowledge, this study is the first to synthesize cyclometalated iridium(III)-5-fluoro-8-quinolinol complexes that can function as mitochondrion-targeting anticancer drugs.

Novel red Zn(ii) complex-based fluorescent probes featuring cryptolepine-curcumin derivatives, namely, [Zn(BQ)Cl2] (BQ-Zn) and [Zn(BQ)(Cur)]Cl (BQCur-Zn), were developed for the simple and fluorescent label-free detection of apoptosis, an important biological process. The probes could synergistically promote mitochondrion-mediated apoptosis and enhance tumor therapeutic effects in vitro and vivo.

Compared with 1–9, 10–13 displayed stronger cytotoxic activities against the tested A549/DDP cells. 11 and 13 could induce apoptosis and autophagy in A549/DDP cells and exhibited pronounced and selective activity against A549/DDP xenografts in vivo.

Objectives: To summarize the clinical characteristics and investigate the efficacy of ethanol embolotherapy in the treatment of chest well arteriovenous malformation (AVM). Treatment-associated complications were also explored. Materials and Methods: Between March 2017 and August 2021, 32 consecutive patients (mean age, 23.7 years; age range, 5–54 years) who underwent ethanol embolotherapy for chest well AVMs under general anesthesia were included in this study. Embolization was performed through a direct puncture, transarterial catheterization, or a combination of the 2 procedures. The mean follow-up duration after the last treatment was 18.0 months (range, 3–42 months). The degree of devascularization on follow-up (assessed using angiography or computed tomography), and the clinical signs and symptoms of AVMs were evaluated as the therapeutic outcomes. The major and minor complications associated with the procedures were recorded. Results: A total of 103 embolization procedures (mean, 3.2; range, 2–7) comprising 101 ethanol embolization and 2 coil embolizations were performed on 32 patients with chest wall AVMs. The AVM nidus was accessed through the transarterial approach alone in 4 patients, by direct puncture in 11, and a combined procedure in 17 patients. Overall, more than 80% of the procedures were performed using the combined approach. Complete AVM devascularization was achieved in 12 (37.5%) patients. Moreover, 76% to 99% AVM was achieved in 18 patients (56.3%), and 50% to 75% in 2 patients (6.3%). Bleeding, pain, heart failure, and cosmetic deformities were the indications for treatment. For 3 patients (3/32, 9.4%) who had bleeding, the treatment stopped the hemorrhage. Complete pain relief was reported in 8 patients (8/32, 25.0%), whereas complete relief from congestive heart failure post-embolization was observed in 5 of the 6 patients with congestive heart failure (5/6, 83.3%). Complete correction of cosmesis deformities after embolization was achieved in 10 patients (10/32, 31.3%). Two patients who underwent surgery to correct persistent deformity after embolization only showed insignificant improvement. In addition, 6 (18.8%) patients developed 13 complications including blister, necrosis, hemothorax, transient hemoglobinuria, and transient pulmonary artery hypertension. Conclusions: Ethanol embolotherapy is a safe and effective procedure for chest well AVMs. Surgery is required for some patients with residual cosmesis deformity. Clinical Impact Currently, there is no standard treatment for chest well AVMs due to their rarity and high heterogeneity. The present study shows that thanol embolotherapy is a safe and clinically effective treatment procedure for the chest well AVMs. Transarterial embolization in combination with direct puncture embolization can reach the AVM nidus. Ethanol embolotherapy can achieve complete obliteration of the AVM nidus in the majority of patients. Surgery may still be needed to correct cosmetic deformity after embolization. The present study provides valuable evidence to inform clinical decision-making.

Experiments of a steel sphere oblique impact with a rubber cushion have been proceeded to research the variation laws of the specific energy at interface. The contact surfaces above and under the rubber cushion can be recorded with a thin carbon paper. The parameters of deformation volume and specific energy are analyzed by the developed formulas in different cases of the impact angle, cushion thickness, drop height and sphere diameter. It is found that the deformation volume and related geometrical sizes decrease approximately exponentially with the impact angle, and the volume of the tangential moving part reaches a maximum at 50° or 60°. The variation laws of the specific energy absorption/dissipation in normal are similar to that of the axis length. The tangential specific energy can be divided into three main phases, the first two appear the states of slow increase and plateau, between of them a fluctuating peak exists at 30–40°. In final phase, the energy absorption shows sharp increase, but the energy dissipation first increases and then decreases. In addition, they increase linearly with the drop height and sphere diameter, and an optimum cushion thickness of 4 or 5 mm in the given cases.

Berberine and jatrorrhizine are major bioactive components that are emerging as potential anti-cancer drugs. However, no zinc(II) - berberine/jatrorrhizine - curcumin compounds have been reported in the literature to date. Therefore, the molecular mechanisms associated with their cytotoxicity remain unexplored. To investigate the potential mitochondria-targeting ability, anti-neoplastic activity, and utility in cell imaging of berberine and jatrorrhizine derivates, four novel zinc(II) complexes, [Zn(Ber)(H

CeO2 is an important energy storage material that can be used in solid fuel cells. Adding citric acid can improve the particle distribution of the pyrolytic preparation of CeO2 inside the reactor. Through Fluent, this paper investigated the pyrolysis preparation of CeO2 with the addition of citric acid by adopting the Eulerian multiphase flow model, component transportation model, and standard k-ε turbulence model. The experimental and simulation results suggest that the addition of citric acid can alter the pressure, temperature, and component distributions inside the reactor. When the mass fraction of O2 is 0.3, the concentration distribution effect of the CeO2 component is optimal and its conversation rate is the highest. When the mass fraction of citric acid is 0.04, the concentration distribution effect of the CeO2 component is the best, as witnessed by the high CeO2 concentration at the exit. It was found that an O2 content of 30 wt % and citric acid content of 4 wt % were optimal operating conditions for this technology.

Two new platinum(II) complexes with naphthalene imide derivatives as the ligands, [Pt(3a)Cl]Cl (3a-Pt) and [Pt(3b)Cl]Cl (3b-Pt), where 3a = 5‑(3‑(bis(pyridin‑2‑ylmethyl)amino)propoxy)‑2‑phenyl‑1H‑benzo[de]isoquinoline‑1,3(2H)‑dione and 3b = 2‑benzyl‑5‑(3‑(bis(pyridin‑2‑ylmethyl)amino)propoxy)‑1H‑benzo[de]isoquinoline‑1,3(2H)‑dione, were synthesized and structurally characterized. 3b-Pt showed higher anti-tumor properties in vitro against human non-small cell lung cancer NCI-H460 cells (0.89 ± 0.25 μM) than 3a-Pt (11.32 ± 0.47 μM) and cisplatin (11.09 ± 1.01 μM). In addition, 3b-Pt induced NCI-H460 cell apoptosis through inhibition of the telomerase activity and dysfunction of mitochondria.

Two new Pt(II) complexes with sorafenib (SRFN) and regorafenib (RGFN), having the general formulae [Pt(SRFN)(DMSO)Cl2] (SRFN-Pt) and [Pt(RGFN)(DMSO)Cl2] (RGFN-Pt), were prepared and characterized by ESI-MS, IR, UV–Vis spectroscopy, elemental analyses, and 1H and 13C NMR, respectively. The anticancer activities of SRFN-Pt and RGFN-Pt were evaluated by MTT assay with NCI-H460 (human non-small cell lung cancer NCI-H460 cell line), SK-OV-3 (ovarian cancer cell line), SK-OV-3/DDP (cisplatin-resistant SK-OV-3 cell line), T-24 (human bladder cancer cell line), HeLa (cervical cancer cell line), A549/DDP (cisplatin-resistant A549/DDP non-small cell lung cancer cell line) cancer cells and in the normal HL-7702 cells. The results suggested that SRFN-Pt and RGFN-Pt were more effective against the A549/DDP tumor cells (IC50 = 1.18 ± 0.15 μM and 0.13 ± 0.03 μM) than SRFN (45.03 ± 0.79 μM), RGFN (40.11 ± 2.15 μM), and cisplatin (97.63 ± 1.06 μM), respectively, and RGFN-Pt was more effective than SRFN-Pt. In addition, SRFN-Pt and RGFN-Pt induced G2/M and S phase arrest. Cytotoxic mechanism studies revealed that SRFN-Pt and RGFN-Pt triggered mitochondria-mediated apoptotic cell death at low concentration. RGFN-Pt exhibited obvious priority on the in vitro antitumor activity than SRFN-Pt, which should be undoubtedly correlated with the key roles of the fluoro substituted groups in the RGFN ligand of RGFN-Pt. The in vitro anti-tumor activity studies suggested that RGFN-Pt pointed to a new direction in developing Pt(II) drugs as anti-cancer agent.

[Image: see text] Three novel Ru(II) complexes, namely, (RuCl(2)[L(a)][DMSO](2))·H(2)O (Ru1), (RuCl(2)[L(b)][DMSO](2)) (Ru2), and (RuCl(2)[L(c)][DMSO](2)) (Ru3), which respectively contain 3-(2′-benzimidazolyl)coumarin (L(a)), 3-(2′-benzimidazolyl)-7-fluoro-coumarin (L(b)), and 3-(2′-benzimidazolyl)-7-methoxyl-coumarin (L(c)), were first designed and characterized. Ru2 showed potent antitumor activity against NCI-H460 cells (IC(50) = 0.30 ± 0.02 μM) and high selectivity between NCI-H460 cancer cells and normal HL-7702 cells. Ru2 induced NCI-H460 apoptosis via telomerase inhibition, which involved DNA damage, cell-cycle distribution, and S phase-protein down-regulation. However, Ru1 did not demonstrate such effects in NCI-H460 cells, which is undoubtedly associated with the key regulatory role of the 7-fluoro substituted group in the L(b) ligand of Ru2. Ru2 exhibited considerably higher anticancer efficacy (inhibition rate [IR] = 61.3%) compared with cisplatin (IR= 25.5%) in a NCI-H460 xenograft mouse model. Thus, this coumarin Ru(II) compound is a promising Ru2-targeting telomerase anticancer agent.

Herein, we report the design and synthesis of three novel binuclear platinum(II) complexes, [Pt(tpbtpy)Cl][Pt(DMSO)Cl3] (tpbtpy-Pt), [Pt(dthbtpy)Cl][Pt(DMSO)Cl3]⋅CH3OH (dthbtpy-Pt), and [Pt(qlbtpy)Cl][Pt(DMSO)Cl3]⋅CH3OH (qlbtpy-Pt) with 4′-(3-thiophenecarboxaldehyde)-2,2′:6′,2″-terpyridine (tpbtpy), 4′-(3,5-bis (1,1-dimethylethyl)-2-hydroxy-benzaldehyde)-2,2′:6′,2″-terpyridine (dthbtpy) and 4′-(2-quinolinecarboxaldehyde)-2,2′:6′,2″-terpyridine (qlbtpy) as ligands, respectively. All three novel binuclear platinum(II) complexes tpbtpy-Pt, dthbtpy-Pt, and qlbtpy-Pt were characterized by single-crystal X-ray diffraction analysis, spectroscopic analysis (ESI-MS, IR, 1H NMR), and elemental analysis. Additionally, the cytotoxicity of tpbtpy-Pt, dthbtpy-Pt and qlbtpy-Pt was assessed with human non-small cell lung cancer cell line (NCI H460 cells), yielding IC50 values in the range of 0.35–12.09 μM with tpbtpy-Pt as the most potent and qlbtpy-Pt as the least potent complexes. Mechanistic studies indicated that tpbtpy-Pt and dthbtpy-Pt induced apoptosis through mitochondrial dysfunction and telomerase inhibition. In a NCI H460 xenograft model, when administered at 10.0 mg kg−1 every 2 days, tpbtpy-Pt was shown to significantly reduce tumor growth (tumor growth inhibition rate (IR) = 70.1%, p

Five novel lanthanides(iii) complexes, [Lu(Me)(MBrQ)2NO3] (MeMBrQ-Lu), [Ho(MeO)(MBrQ)2NO3] (MeOMBrQ-Ho), [Ho(Me)(MBrQ)2NO3] (MeMBrQ-Ho), [La(Me)2(BrQ)2NO3] (MeBrQ-La) and [Sm(Me)(BrQ)2(CH3OH)NO3] (MeBrQ-Sm), have been synthesized, in which 2,2′-bipyridyl (4,4′-dimethyl-2,2′-bipyridyl (Me) and 4,4′-dimethoxy-2,2′-bipyridine (MeO)) and 5,7-dibromo-8-quinolinoline derivatives (5,7-dibromo-2-methyl-8-quinolinol (MBrQ-H) and 5,7-dibromo-8-quinolinol (BrQ-H)) act as the chelating ligands. The in vitro cytotoxic activities of the five Ln(iii) complexes have been studied with the SK-OV-3/DDP, NCI-H460 and HeLa cancer cells. MeMBrQ-Lu, MeOMBrQ-Ho, MeMBrQ-Ho, MeBrQ-La and MeBrQ-Sm show higher cytotoxicity against the HeLa cells (IC50 values of 1.00 nM–3.45 μM) than cisplatin (13.11 ± 0.53 μM). In particular, the MeOMBrQ-Ho and MeMBrQ-Ho complexes exhibit superior cytotoxic activity, with IC50 values at 1.00 ± 0.34 nM and 125.00 ± 1.08 nM. We further demonstrate that MeOMBrQ-Ho and MeMBrQ-Ho inhibit the proliferation of HeLa cells by inhibiting telomerase and targeting mitochondria to induce DNA damage-mediated apoptosis. In addition, MeOMBrQ-Ho significantly inhibits tumor growth with a tumor growth inhibition rate (IR) of 50.8% in a HeLa mouse xenograft model. Taken together, MeOMBrQ-Ho is a novel lanthanide(iii) complex with promising antitumor activity.

Two rhodium(III) and iron(III) complexes of 4′-(3-thiophenecarboxaldehyde)-2,2′:6′,2″-terpyridine (tpatpy): [Rh(tpatpy)Cl3]·CH3OH (tpatpy-Rh) and [Fe(tpatpy)Cl3] (tpatpy-Fe) have been prepared and characterized. Tpatpy-Rh (5.03 ± 1.15 μM) and tpatpy-Fe (18.02 ± 0.45 μM) exhibited greater cytotoxicity than the tpatpy ligand (70.11 ± 0.28 μM) and cisplatin (61.21 ± 1.39 μM) against SK-OV-3/DDP cells. In addition, tpatpy-Rh inhibited telomerase by down-regulation of c-myc and hTERT, as well as induced SK-OV-3/DDP cell arrest in the S phase.

In the present study, one novel Pt(II) complex, [Pt(CTD)(DMSO)Cl2] (1) with 9‑chloro‑5,6,7,8‑tetrahydroacridine (CTD) as ligand, was synthesized and fully characterized. The CTD Pt(II) complex 1 was an anti-cancer drug candidate, and it possessed potent therapeutic efficacy for hepatocellular carcinoma (HCC). To explore its mechanism against HCC, Hep‑G2 cells were treated with the CTD Pt(II) complex 1 in vitro. MTT assay showed that the CTD Pt(II) complex 1 had inhibitory activity against five human cancer cells, such as SK‑OV‑3, Hep‑G2, NCI‑H460, MGC80‑3 and HL‑7702, and it displayed the strongest inhibitory activity against Hep‑G2 cells with an IC50 value of 10.48 ± 0.83 μM. Moreover, the CTD Pt(II) complex 1 also exhibited selective cytotoxicity toward the cancer cells. In addition, the CTD Pt(II) complex 1 had low toxicity against non-cancerous HL‑7702 cells. The CTD Pt(II) complex 1 caused mitochondrial dysfunction, leading to the down-regulation of bcl‑2 protein and up-regulation of some mitochondria-initiated apoptotic proteins (including apaf‑1, cytochrome c and bax) in Hep‑G2 cells. Taken together, the CTD Pt(II) complex 1-triggered Hep‑G2 cell apoptosis was mainly mediated via interaction with c‑myc promoter and disruption of mitochondrial pathway. Collectively, our findings supported that the CTD Pt(II) complex 1 could be used as a potential drug candidate for chemoprevention or chemotherapy of HCC.

Two new Pt(II) and Ru(II) complexes, [Pt(BFCY)Cl2] (1) and [RuCl2(BMCY)(DMSO)] (2) with 3-(1H-benzoimidazol-2-yl)-8-fluoro-chromen-2-ylideneamine (BFCY) and 3-(1H-benzoimidazol-2-yl)-8-methyl-chromen-2-ylideneamine (BMCY), were synthesized. The BFCY Pt(II) complex 1 adopted an approximately four-coordinated square planar geometry, while BMCY complex 2 formed a distorted octahedral geometry. Among the seven selected human cancer cell lines, the two new Pt(II) and Ru(II) complexes 1 and 2 exhibited more potent activities against cisplatin-resistant SK-OV-3/DDP tumor cells (IC50 = 2.08 ± 1.04 μM and 18.06 ± 0.36 μM, respectively), compared with the free BFCY and BMCY ligands as well as cisplatin. In addition, the BFCY Pt(II) complex 1 could induce cell cycle arrest in S phase and regulate the S-phase cell cycle-related proteins. Remarkably, the BFCY Pt(II) complex 1 also induced mitochondrial dysfunction.

Four new Pt(II) complexes, [Pt(La)]Cl (1), [Pt(Lb)]Cl (2), [Pt(Lc)]Cl (3) and [Pt(Ld)]Cl (4) with the naphthalene imide derivatives La–Ld as ligands were designed and prepared. MTT assay indicated that 1–4 exhibited proliferation inhibiting activity against human non-small cell lung cancer (NCI-H460) cells, especially 1–3 showed superior activity (IC50 = 0.10–8.56 μM) compared with cisplatin (IC50 = 12.01 ± 1.03 μM). Various experiments showed that 3 as a telomerase inhibitor induced NCI-H460 cell apoptosis via inhibition of the telomerase and dysfunction of mitochondria. In vivo evaluation results suggested that 3 could significantly inhibit the growth of tumor cells in NCI-H460 tumor-bearing mice and the tumor growth inhibition rate (TGI) reached 40.7%. These results demonstrated that 3 is a telomerase inhibitor and a promising anti-cancer agent.

Four novel bifluorescent Zn(II)-cryptolepine-cyclen complexes, namely [Zn(BQTC)]Cl

In this work, we designed and synthesized tacrine platinum(II) complexes [PtClL(DMSO)]⋅CH3OH (Pt1), [PtClL(DMP)] (Pt2), [PtClL(DPPTH)] (Pt3), [PtClL(PTH)] (Pt4), [PtClL(PIPTH)] (Pt5), [PtClL(PM)] (Pt6) and [PtClL(en)] (Pt7) with 4,4′-dimethyl-2,2′-bipyridine (DMP), 4,7-diphenyl-1,10-phenanthroline (DPPTH), 1,10-phenanthroline (PTH), 2-(1-pyrenecarboxaldehyde) imidazo [4,5-f]-[1,10] phenanthroline (PIPTH), 2-picolylamine (PM) and 1,2-ethylenediamine (en) as telomerase inhibitors and p53 activators. Biological evaluations demonstrated that Pt1 Pt7 exhibited cytotoxic activity against the tested NCI H460, Hep-G2, SK-OV-3, SK-OV-3/DDP and MGC80-3 cancer cell lines, with Pt5 displaying the highest cytotoxicity. Pt5 exhibited an IC50 value of 0.13 ± 0.16 μM against SK-OV-3/DDP cancer cells and significantly reduced tumor growth in a Hep-G2 xenograft mouse model (tumor growth inhibition (TGI) = 40.8%, p Pt7 displayed low cytotoxicity against normal HL-7702 cells. Mechanistic studies revealed that these compounds caused cell cycle arrest at the G2/M and S phases, and regulated the expression of CDK2, cyclin A, p21, p53 and p27. Further mechanistic studies showed that Pt5 induced SK-OV3/DDP cell apoptosis via dysfunction of mitochondria, inhibition of the telomerase activity by directly targeting the c-myc promoter, and activation of the p53 signaling pathway. Taken together, Pt5 has the potential to be further developed as a new antitumor drug.

A dinuclear palladium(II) complex, [Pd2(μ‑OAc‑κO,O)2(phpy‑κN,C)2] (1), with 2‑phenylpyridine (H‑phpy) as a ligand was synthesized and characterized by IR, ESI-MS, single-crystal X-ray diffraction, and elemental analysis. By the MTT assay, the dinuclear palladium(II) complex 1 showed lower cytotoxic activity toward normal HL-7702 cells (IC50 = 85.89 ± 0.89 μM). However, it displayed high cytotoxicity against SK-OV-3, NCI-H460, T-24, and HeLa cells, with IC50 values of 5.50 ± 1.08, 0.46 ± 0.28, 7.93 ± 1.16 and 0.35 ± 0.29 μM, respectively. Importantly, we found that this Pd(II) complex exhibited lower toxicity and better anticancer activity than that of cisplatin. Further cellular assays, including Western blotting and flow cytometry, gave evidence that apoptosis after treatment with the dinuclear palladium(II) complex 1 may be induced by the intrinsic mitochondrial dysfunction pathway.

Two novel platinum(ii) complexes, [PtCl2(H-MeOBC)(DMSO)] (Pt1) and [Pt2Cl3(MeOBC)(DMSO)2] (Pt2), with 3-(2'-benzimidazolyl)-8-methoxycoumarin (H-MeOBC) as the ligand were synthesized and evaluated for their antiproliferative activity. Among all the tumor cells, dual-Pt(ii) complex Pt2 exhibited the most potent activity, with an IC50 value of 0.5 ± 0.2 μM against cisplatin-resistant SK-OV-3/DDP cancer cells. In the case of SK-OV-3/DDP cells, Pt2 displayed a 20.1-196.0-fold increased activity when compared with cisplatin, H-MeOBC and Pt1. Importantly, Pt1 and Pt2 displayed low inhibitory rates against normal HL-7702 cells. Further investigation revealed that Pt2 is a novel telomerase inhibitor binding to c-myc promoter elements. Mechanistic studies demonstrated that dual-Pt(ii) complex Pt2 arrests the cell cycle at the G2/M phase and induces apoptosis and causes mitochondrial dysfunction.

In the development of modern logistics, ports which are the hub of land and water transportation of goods, have been playing a more and more significant role in international trade and logistics. In order to form logistics service supply chain alliance of port enterprises, enhance service efficiency of port logistics, it finds out that there are shortage in some aspects by investigating and comparing, including development layout of port service, basic establishment, standard of logistics and technology training and supply chain alliance construction progress. On the basis, in the era of supply chain management or Port Logistics, it provides some suggests for building the alliance in ports service supply chain. These suggestions can provide some advantage for port logistics development.

The motivation of this paper was to study the characteristics of start-up and the feature of shockwave under low Mach number in hypersonic inlet. The characteristics of flow field and shockwave at the critical starting Mach number (Ma3.8) without back pressure were numerically studied in the hypersonic inlet in which the design condition was Ma6. The results showed that the flow field and shockwave were unstable, and they were under some certain periodic oscillation state at the critical starting Mach number (Ma3.8). The total mass flow rate between inflow and outlet, the mass flow of throat, and the mass average Mach number of outlet all also showed periodic oscillation. Unmatched mass flow that passed through the throat that could not all pass through the exit of isolator was the induced reason of periodic oscillation. The block of the max mass flux flow through the area of throat was the main factor that caused the periodic oscillation of flow field and shockwave. The unmatched mass flux in internal channel leads to periodic “split out” and “swallow in” of “separation bubble” from the internal channel, which formed the periodic oscillation of flow field and shockwave.

Three new non-cisplatin analogs [Rh(BID1)(CH3OH)]⋅CH3OH (Rh-1), [Rh(BID2)(CH3OH)]⋅CH3OH (Rh-2) and [Rh(BID3)(CH3OH)]⋅2CH3OH (Rh-3) bearing benzimidazole derivatives (BID1−BID-3) were first prepared as potential anti-tumor compounds. The Rh-3 complex with 8-fluoro group in BID-3 ligand exhibited potential antiproliferative activity against multidrug-resistant human lung adenocarcinoma A549/DDP and cisplatin-resistant human ovarian cancer SK-OV-3/DDP cells, at most 5.0 fold more potent than Rh-1, Rh-2 and cisplatin under the same conditions. Importantly, Rh-1−Rh-3 are more selective for A549/DDP cells versus human normal liver HL-7702 cells. The Rh-2 and Rh-3 caused mitochondrial dysfunction was in the following order: Rh-3 > Rh-2. The different biological behavior of Rh-1−Rh-3 may correlate with different 8-substituted groups in benzimidazole derivatives.

Herein, a series of transition metal complexes, [Zn(DQ)2(CH3OH)2] (1), [Zn(DMQ)2(CH3OH)2] (2), [Co(DQ)2(CH3OH)2] (3), [Co(DMQ)2(CH3OH)2] (4), [Ni(DQ)2(CH3OH)2] (5), [Cu(DMQ)2(CH3OH)2] (6), [Mn(DQ)2(H2O)2] (7) and [Mn(DMQ)2(H2O)2] (8), containing 6,7-dichloro-5,8-quinolinedione (DQ) and 6,7-dichloro-2-methyl-5,8-quinolinedione (DMQ) ligands have been synthesized and characterized as potential antitumor agents. These complexes 1–8 exhibited evident anti-tumor activity in HeLa (cervical), MCF-7 (breast), Hep-G2 (hepatoma), T-24 (bladder), and SK-OV-3 (ovarian) human cancer cells. Interestingly, complexes 1–8 showed higher cytotoxicity than cisplatin against human cervical HeLa cells, and less cytotoxicity on the HL-7702 nontumorigenic cells. Mechanism studies suggested that complexes 1 and 2 arrested the cell cycle in the G1 phase and induced cancer cell death through mitochondrial dysfunction pathways. The cytotoxicity of 2 was higher than that of 1. The different biological behavior of 1 and 2 may correlate with the presence of a 2-methyl group in 6,7-dichloro-2-methyl-5,8-quinolinedione (DMQ) ligand. In general, our study demonstrated that Zn(II) complex 2 with 6,7-dichloro- 2-methyl-5,8-quinolinedione showed high potential to be developed as a mitochondria-targeted metal antitumor agent.

Here, two new cyclometallated iridium(III) complexes, [Ir(BrQ)(L1)2] (Ir-1) and [Ir(BrQ)(L2)2] (Ir-2) containing 5-bromo-8-quinolinol (H-BrQ), 2-phenylpyridine (H-L1) and 1-phenylpyrazole (H-L2) ligands have been explored as an anticancer agents targeting mitochondria. The cyclometallated iridium(III) complexes Ir-1 and Ir-2 exhibits excellent antineoplastic activity and promising selectivity towards cervical carcinoma HeLa, with IC50 values were 3.53 ± 0.44 μM and 0.50 ± 0.39 μM, as compared to the human HL-7702 healthy cells and cisplatin-resistant SK-OV-3/DDP cancer cells. Flow cytometry confirmed that cervical carcinoma HeLa cells were caused apoptosis after being treatment with Ir-1 and Ir-2. Along with the decrease of mitochondrial membrane potential (MMP) level, massive release of cytochrome c (cyto C), clear changes in apoptosis-associated proteins, and triggers caspase-mediated mitochondrial dysfunction apoptosis pathways.

To determine the H9C2 cell damage and NLRP3 inflammasome activation trigged by soluble uric acid (UA).H9C2 cells were treated with UA. The cellular damage was examined after 12 h, 24 h and 48 h of treatment using MTS and lactic dehydrogenase (LDH). The apoptosis of H9C2 cells was analyzed by flow cytometry (FCM). NLRP3 inflammasome activation was reflected by the protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and Caspase-1 detected by Western blot. The mitochondria and cytoplasm were separated and the release of cytochrome C was detected by Western blot to analyze the damage of mitochondria. The impacts of NAC, a ROS inhibitor, on the cell viability and NLRP3 inflammasome activation were analyzed. The expression of UCP2 was detected by Western blot and immunofluorescence (IF).Dose response and time dependent effects of UA on cellular damage and cell apoptosis was observed. UA up-regulated the expression of NLRP3 inflammasome-related molecules. UA damaged the mitochondria. NAC improved the cell viability and inhibited NLRP3 inflammasome activation. UA down-regulated the expression of UCP2.Soluble UA can down-regulate the expression of UCP2, damage the mitochondria and activate NLRP3 inflammasome, resulting in cellular damage of H9C2 cells.

BACKGROUND This study aims to investigate the clinical value of contrast-enhanced ultrasound (CEU) before temporary inferior vena cava filter (IVCF) recovery in patients with deep venous thrombosis, in order to provide ultrasound signs for the recovery of IVCF in clinical practice. METHODS The CEU manifestations of patients with deep vein thrombosis before temporary IVCF recovery were retrospectively analyzed. With the manifestations of digital subtraction angiography (DSA) or results of the surgical recovery of IVCF as the standard, the detection rate of a thrombus in IVCF was compared between conventional ultrasound and CEU, and the role of CEU in detecting complications of IVCF was analyzed. RESULTS In the 103 patients with IVCF, conventional ultrasound and CEU did not reveal any filter displacement and deformation, as well as infection. In 86 patients, filters were successfully recovered under DSA. In one patient, the filter was removed surgically. In 16 patients, recovery failed or was given up, and inferior vena cava (IVC) angiography was performed. The recovery rate of IVCF was 84.5%. Among all cases, thrombi were found within the filters or around the filter in 23 patients. The detection rate of thrombi was 47.8% (11/23) by conventional ultrasound and 82.6% (19/23) by CEU, and the difference between these two methods was statistically significant (P

With lanthanum chloride solution as raw material, and use the hydrogen peroxide of clean and pollution-freeobtained from oxidation reaction as auxiliary reagent, and with the carrier gas together form spray pyrolysis to obtain lanthanum oxide. On the one hand, in the hydrogen peroxide system, the temperature of direct pyrolysis reaction of lanthanum chloride solution decreased obviously, The reaction temperature is decreased from 1280°C to 1000°C or less. That reduce the energy consumption and simplify the requirements of pyrolysis equipment technology. The production process does not use NH3.H2O and NaOH to precipitate. It does not produce the traditional process of NH4+, Na+ to pollute water. It can greatly reduce the damage to the environment, and can product with high yield, high purity of the rare earth oxide. This method not only applies to the pyrolysis of the rare earth chloride solution, also applies to metal chloride solution, such as FeCl3, AlCl3, NiCl2. It was shown that the reaction temperature has been effectively reduced, VLaCl3: VH2O2 with 1: 1.5 can get high purity of La2O3.

Based on ABAQUS finite element analysis software simulation, the finite element model for dynamic analysis of rigid pile composite foundation and superstructure interaction system is established, which selects the two kinds of models, by simulating the soil dynamic constitutive model, selecting appropriate artificial boundary.The influence of rigid pile composite foundation on balance and imbalance of varying rigidity is analyzed under seismic loads. The result shows that the maximum bending moment and the horizontal displacement of the long pile is much greater than that of the short pile under seismic loads, the long pile of bending moment is larger in the position of stiffness change. By constrast, under the same economic condition, the aseismic performance of of rigid pile composite foundation on balance of varying rigidity is better than that of rigid pile composite foundation on imbalance of varying rigidity.

It is found that cuprous sulfite, zinc sulfate and zinc sulfide were the main phases of copper and zinc in zinc leach residue, through analyzing its composition and phase characteristics by XRF and XRD. The method that cooperate sulfuric acid leaching with oxidant was chosen. 60 g/L H2SO4 at 60 °C for 2 h with 4% KMnO4 and liquid/solid ratio of 5..1, 84.29 % of Cu and 92.02 % of Zn are extracted. The ion concentration of copper and zinc are tested by UV-VIS spectrophotometer and EDTA titration respectively. The results show that the amount of acid is sufficient for leaching at the condition of 60 g/L H2SO4 and liquid/solid ratio of 5..1. At the same time, copper change from low valence into high valence after adding KMnO4 which strengthen the leaching, and the chemical reaction can reach balance at 60 °C for 2 h. This method has good extraction effect on copper and zinc.

A new composite electrolyte for lithium-ion batteries (LIBS) was prepared by combining N-methyl-N-propylpyrrolidinium bis (trifluoromethanesulfonyl) imide (PYR13TFSI), N-methyl-N-pr-opylpiperidinium bis (trifluoromethanesulfonyl) imide (PP13TFSI) and lithium difluoro (oxalate) bor-ate (LiDFOB). Graphite electrode was tested in the LiDFOB-containing electrolyte, exhibiting higher reversible charge/discharge capacity and better cyclic stability. An initial charge capacity of 351.5 mAh⋅g-1 is obtained and a stable capacity of above 332.8 mAh⋅g-1 is retained after 30 cycles. The coulombic efficiency remains high above 99.3%. The outstanding cell performance was associ-ated with the formation of stable solid electrolyte interface (SEI) film on the surface of electrodes derived from LiDFOB.

N-methyl-N-allylpyrrolidinium bis (trifluoromethanesulfonyl) imide (PYR1ATFSI) with substantial supercooling behavior is synthesized to develop low temperature electrolyte for lithium-ion batteries. Additive fluoroethylene carbonate (FEC) in LiTFSI/PYR1ATFSI/EC/PC/EMC is found that it can reduce the freezing point. LiFePO4/Li coin cells with the FEC-PYR1ATFSI electrolyte exhibit good capacity retention, reversible cycling behavior at low temperatures. The good performance can be attributed to the decrease in the freezing point and the polarization of the composite electrolyte.