Two isomeric two-dimensional copper(I) coordination polymer materials based on an in situ generated 5-(3-pyridyl)tetrazole ligand show similar layer structures but distinct photoluminescent and ...photocatalytic properties, which present an interesting comparative study on the structure–property correlation between isomeric materials.
A multifunctional Cu(I) coordination polymer constructed from helical chains showed unusual mechanochromic, sensing of nitrobenzene and photocatalytic properties on degradation of organic dyes.
Low vitamin D status is associated with progression in patients with renal cell carcinoma (RCC). The present study found that vimentin, a mesenchymal marker, was accordingly upregulated, and ...E‐cadherin, an epithelial marker, was downregulated in RCC patients with low vitamin D status. Thus, we investigated the effects of calcitriol or vitamin D3, an active form of vitamin D, on epithelial‐mesenchymal transition (EMT) in RCC cells. RCC cells were treated by two models. In model 1, three RCC cell lines, ACHN, 786‐O and CAKI‐2, were incubated with either LPS (2.0 μg/mL) or transforming growth factor (TGF)‐β1 (10 ng/mL) in the presence or absence of calcitriol (200 nmol/L). In model 2, two RCC cell lines, ACHN and CAKI‐2, were incubated with calcitriol (200 nmol/L) only. Calcitriol inhibited migration and invasion not only in TGF‐β1‐stimulated but also in TGF‐β1‐unstimulated RCC cells. Moreover, calcitriol suppressed E‐cadherin downregulation and vimentin upregulation not only in TGF‐β1‐stimulated but also in TGF‐β1‐unstimulated ACHN and CAKI‐2 cells. Calcitriol attenuated LPS‐induced upregulation of MMP‐2, MMP‐7, MMP‐9, MMP‐26 and urokinase‐type plasminogen activator (u‐PA) in ACHN cells. In addition, calcitriol blocked TGF‐β1‐induced nuclear translocation of ZEB1, Snail and Twist1 in ACHN and CAKI‐2 cells. Mechanistically, calcitriol suppressed EMT through different signaling pathways: (i) calcitriol suppressed Smad2/3 phosphorylation by reinforcing physical interaction between vitamin D receptor (VDR) and Smad3 in TGF‐β1‐stimulated RCC cells; (ii) calcitriol inhibited signal transducer and activator of transcription (STAT)3 activation in LPS‐stimulated RCC cells; (iii) calcitriol inhibited β‐catenin/TCF‐4 activation by promoting integration of VDR with β‐catenin in TGF‐β1‐unstimulated RCC cells. Taken together, calcitriol inhibits migration and invasion of RCC cells partially by suppressing Smad2/3‐, STAT3‐ and β‐catenin‐mediated EMT.
Calcitriol suppressed EMT through two different signaling pathways: (i) calcitriol suppressed Smad2/3 phosphorylation by reinforcing physical interaction between vitamin D receptor (VDR) and Smad3 in TGF‐β1‐stimulated RCC cells; (ii) calcitriol inhibited β‐catenin/TCF‐4 activation by promoting integration of VDR with β‐catenin in TGF‐β1‐unstimulated RCC cells. Taken together, calcitriol inhibits migration and invasion of RCC cells by suppressing Smad2/3‐ and β‐catenin‐mediated EMT.
•Soil acidification naturally decreased by 0.071 per year in a tea plantation.•Long-term heavy urea-N fertilization can accelerate the soil acidification process.•Subsoil was more vulnerable to ...acidification by heavy nitrogen fertilization.•High N input caused Al3+ accumulation and base-cations’ depletion in the soil.
In tea (Camellia sinensis) plantation areas, soil acidification mainly results from excessive nitrogen fertilization. However, the proposed theoretical explanations for soil acidification due to nitrogen fertilization are still lacking empirical validation because most studies have used short-term incubation periods or pot experiments. Here, both soil and soil solution samples were taken from a tea plantation field (Ultisol in USDA taxonomy system, or Alisol in WRB taxonomy system) treated using different nitrogen application rates: 0 (N0), 119 (N119), 285 (N285), and 569 (N569)kgNha−1yr−1 for 8 years (2006–2013). Soil pH and the concentrations of the relevant cations and anions were also determined. With no nitrogen fertilization (N0), the surface soil pH decreased from 4.16 to 3.32 after 8 years in the tea plantation. Compared with no nitrogen fertilization (N0), high nitrogen fertilization (N569) significantly decreased the soil pH from 3.32 to 3.15 and 3.67 to 3.35 in the soil at depths of 0–40cm and 40–90cm, respectively. However, the low (N119) and moderate (N285) nitrogen treatments showed non-significant effects upon soil pH. Our results confirm the previous findings that a high nitrogen application rate can accelerate soil acidification in a tea plantation, and that the subsoil is particularly susceptible to acidification after heavy nitrogen fertilization. Soil acidification also significantly decreased the nutrient base cations Ca2+, Mg2+, and K+ in the soil. Our results suggest that heavy synthetic nitrogen fertilization should be partly replaced with compound or organic fertilizers to mitigate soil acidification and nutrient cation deficiency in tea plantation fields.
Porous silicon (pSi) nanomaterials are increasingly attractive for biomedical applications due to their promising properties such as simple and feasible fabrication procedures, tunable morphology, ...versatile surface modification routes, biocompatibility and biodegradability. This review focuses on recent advances in surface modification of pSi for controlled drug delivery applications. A range of functionalization strategies and fabrication methods for pSi-polymer hybrids are summarized. Surface engineering solutions such as stimuli-responsive polymer grafting, stealth coatings and active targeting modifications are highlighted as examples to demonstrate what can be achieved. Finally, the current status of engineered pSi nanomaterials for
applications is reviewed and future prospects and challenges in drug-delivery applications are discussed.
We present the formation of the largest titanium–oxo cluster, Ti42(μ3-O)60(OiPr)42(OH)12)6–, with the first fullerene-like Ti–O shell structure. The {Ti42O60} core of this compound exemplifies the ...same icosahedral (I h ) symmetry as C60, the highest possible symmetry for molecules. According to the coordination environments, the Ti centers in this cluster can be arranged into a Platonic {Ti12} icosahedron and an Archimedean {Ti30} icosidodecahedron. The solution stability of this cluster was confirmed by electrospray ionization mass spectrometry. The spherical body of the {Ti42O60} core has an inside diameter of 1.05 nm and an outside diameter of 1.53 nm, which could be directly visualized by high-resolution transmission electron microscopy. Our results demonstrate that titanium oxide can also form fullerene-like shell structures.
A new and facile approach to selectively functionalize the internal and external surfaces of porous silicon (pSi) for drug delivery applications is reported. To provide a surface that is suitable for ...sustained drug release of the hydrophobic cancer chemotherapy drug camptothecin (CPT), the internal surfaces of pSi films were first modified with 1-dodecene. To further modify the external surface of the pSi samples, an interlayer was applied by silanization with (3-aminopropyl)triethoxysilane (APTES) following air plasma treatment. In addition, copolymers of N-(2-hydroxypropyl) acrylamide (HPAm) and N-benzophenone acrylamide (BPAm) were grafted onto the external pSi surfaces by spin-coating and UV crosslinking. Each modification step was verified using attenuated total reflection-Fourier transform infrared (ATR-FTIR) spectroscopy, water contact angle (WCA) measurements, X-ray photoelectron spectroscopy (XPS) and scanning electron microscopy (SEM). In order to confirm that the air plasma treatment and silanization step only occurred on the top surface of pSi samples, confocal microscopy was employed after fluorescein isothiocyanate (FITC) conjugation. Drug release studies carried out over 17 h in PBS demonstrated that the modified pSi reservoirs released CPT continuously, while showing excellent stability. Furthermore, protein adsorption and cell attachment studies demonstrated the ability of the graft polymer layer to reduce both significantly. In combination with the biocompatible pSi substrate material, the facile modification strategy described in this study provides access to new multifunctional drug delivery systems (DDS) for applications in cancer therapy.
Several studies found that reduction of 5-hydroxymethylcytosine (5hmC), a marker of DNA hydroxymethylation highly enriched in developing brain, is associated with anxiety-like behaviors. This study ...aimed to investigate whether gestational arsenic (As) exposure induces anxiety-like behaviors in adult offspring by reducing DNA hydroxymethylation in the developing brain. The dams drank ultrapure water containing NaAsO2 (15 mg/L) throughout pregnancy. Anxiety-like behaviors were evaluated and developing brain 5hmC was detected. Results showed that anxiety-like behaviors were observed in As-exposed adult offspring. In addition, 5hmC content was reduced in As-exposed fetal brain. Despite no difference on Tet1, Tet2 and Tet3 expression, TET activity was suppressed in As-exposed fetal brain. Mechanistically, alpha-ketoglutarate (α-KG), a cofactor for TET dioxygenases, was reduced and Idh2, a key enzymatic gene for mitochondrial α-KG synthesis, was downregulated in As-exposed fetal brain. Of interest, ascorbic acid, a cofactor for TET dioxygenases, reversed As-induced suppression of TET activity. Moreover, ascorbic acid attenuated As-induced reduction of 5hmC in fetal brain. In addition, ascorbic acid alleviated As-induced anxiety-like behaviors in adult offspring. Taken together, these results suggest that gestational As exposure induces anxiety-like behaviors in adult offspring, possibly at part, by inhibiting DNA hydroxymethylation in developing brain.
Display omitted
•Gestational As exposure induces anxiety-like behaviors in adult offspring.•Gestational As exposure reduces 5hmC in fetal brain.•Gestational As exposure inhibits TET activity by reducing α-KG content in fetal brain.•AA attenuates As-induced reduction of 5hmC and TET activity in fetal brain.•AA alleviated As-induced anxiety-like behaviors in adult offspring.
Display omitted
•Environmental Cd exposure inhibits placental P4 synthesis and causes FGR.•Cd inhibits placental P4 synthesis by Parkin-dependent mitophagy.•PERK signaling mediates Cd-activated ...mitophagy in placental trophoblasts.•Placental mitophagy contributes to Cd-impaired fetal growth in mice.•FGR is associated with activated mitophagy and reduced P4 synthesis in human placenta.
Cadmium (Cd), an environmental toxicant, is positively associated with fetal growth restriction (FGR). However, the mechanism by which gestational exposure to Cd induces FGR remains unclear. This study designed in vitro and in vivo experiments to explore the role of placental mitophagy in Cd-impaired fetal growth. Based on our case-control study, we also investigated the association of placental mitophagy with reduced progesterone (P4) level and all-cause FGR. We firstly found environmental Cd exposure lowered the P4 content in maternal sera, placentae and amnioticfluids of mice. The level of three mitochondrial P4 synthases, including StAR, CYP11A1 and 3β-HSD, was also reduced in Cd-treated placentae. Furthermore, Cd triggered mitophagy, as determined by the degradation of two mitochondrial proteins HSP60 and COX IV, and the accumulation of co-localizations of TOM20 with LC3B or Parkin in placental trophoblasts. Correspondingly, Cd elevated mitochondrial Parkin level in placental trophoblasts. Mdivi-1, a mitophagy inhibitor, obviously attenuated Cd-induced reduction of placental P4 and FGR in mice. Moreover, mdivi-1 and Parkin siRNA (siR) markedly reversed Cd-caused P4 synthesis inhibition in human placental trophoblasts. Interestedly, the PERK/ATF4 signaling was activated in Cd-stimulated placental trophoblasts. PERK siR inhibited mitochondrial proteins degradation in Cd-stimulated placental trophoblasts. In particularly, mitophagy activation and P4 synthesis suppression occurred in small-for-gestational-age placentae based on our case-control study. Environmental Cd exposure induced FGR via activating PERK-regulated mitophagy and inhibiting P4 synthesis in placentaltrophoblasts. Furthermore, placental mitophagy was related to the reduced progesterone level and all-cause fetal growth restriction based on our case-control study. As above, placental mitophagy maybe the common mechanism of environmental toxicants-impaired fetal growth.
PDF
