激光诱导羟基磷灰石夹层纸表面碳化实现无墨打印

传统的油墨打印具有方便快捷的优势,但打印过程中墨水或碳粉的大量使用对人体和环境造成了不可忽视的危害。基于激光的高能粒子特性和光热辐射热效应,利用激光欠焦和聚焦两种工作模式,可实现激光无墨打印和微区加工。本文报道了一种基于羟基磷灰石的“有机-无机-有机”三明治结构多功能纸,并利用激光的光热辐射效应使功能纸表层有机材料——纤维素纤维表面温度升高,实现表层均匀碳化,夹层无机材料——羟基磷灰石阻挡能量继续传导防止纸张烧穿,以此来达到无墨打印的效果。基于激光烧蚀的无墨打印,能够显著降低打印成本,有利于激光烧蚀打印技术的推广。此外,采用激光烧蚀打印技术作用于功能纸上的打印效果具有稳定、绿色环保等特点,在档案存储用纸、食品包装用纸和后天致盲患者阅读等方面具有广泛的应用。

Dietary preferences and potential ecological impact on the zooplankton community of Nemopilema nomurai based on stable isotope and fatty acid analyses

Information on the dietary composition and food preferences of the giant jellyfish Nemopilema nomurai is important for understanding the trophic drivers of jellyfish outbreaks and their ecological consequences.We used fatty acid(FA)and stable isotope(SI)biomarkers to analyze the diet of N.nomurai from the Yellow Sea in August 2016.N.nomurai was found at all sampling stations,with abundances ranging from 59 inds./km^(2) to 1651 inds./km^(2).There were no significant differences between large(>80 cm in diameter)and small(20–30 cm in diameter)medusae,either in FA compositions or in SI values,which suggests that large and small jellyfi sh have the same food composition and similar trophic levels.Compared to other zooplanktons,the relatively high levels of C20꞉4n-6 in total FAs(~12%)indicates that organic detritus contributes considerably to the food composition of the jellyfish.The mixed model Stable Isotope Analysis in R(SIAR)revealed that N.nomurai tended to prey on smaller organisms(<1000μm in diameter)which comprised about 70%of its diet.This means the N.nomurai blooms will put high feeding pressure on the small plankton.The similar SI values and FA composition indicates that krill may share the same food resources with N.nomurai,which suggests that the jellyfi sh blooms may affect krill populations as a result of food competition.

Arbuscular mycorrhizal fungi regulate plant mineral nutrient uptake and partitioning in iron ore tailings undergoing eco-engineered pedogenesis

Excess available K and Fe in Fe ore tailings with organic matter amendment and water-deficiencies may restrain plant colonization and growth,which hinders the formation of eco-engineered soil from these tailings for sustainable and cost-effective mine site rehabilitation.Arbuscular mycorrhizal(AM)fungi are widely demonstrated to assist plant growth under various unfavorable environments.However,it is still unclear whether AM symbiosis in tailings amended with different types of plant biomass and under different water conditions could overcome the surplus K and Fe stress for plants in Fe ore tailings,and if so,by what mechanisms.Here,host plants(Sorghum sp.Hybrid cv.Silk),either colonized or noncolonized by the AM fungi(Glomus spp.),were cultivated in lucerne hay(LH,C:N ratio of 18)-or sugarcane mulch(SM,C:N ratio of 78)-amended Fe ore tailings under well-watered(55%water-holding capacity(WHC)of tailings)or water-deficient(30%WHC of tailings)conditions.Root mycorrhizal colonization,plant growth,and mineral elemental uptake and partitioning were examined.Results indicated that AM fungal colonization improved plant growth in tailings amended with plant biomass under water-deficient conditions.Arbuscular mycorrhizal fungal colonization enhanced plant mineral element uptake,especially P,both in the LH-and SM-amended tailings regardless of water condition.Additionally,AM symbiosis development restrained the translocation of excess elements(i.e.,K and Fe)from plant roots to shoots,thereby relieving their phytotoxicity.The AM fungal roles in P uptake and excess elemental partitioning were greater in LH-amended tailings than in SM-amended tailings.Water deficiency weakened AM fungal colonization and functions in terms of mineral element uptake and partitioning.These findings highlighted the vital role AM fungi played in regulating plant growth and nutrition status in Fe ore tailings technosol,providing an important basis for involvement of AM fungi in the eco-engineered pedogenesis of Fe ore tailings.

Discovery of a highly potent and orally available importin-β1 inhibitor that overcomes enzalutamide-resistance in advanced prostate cancer

Nuclear transporter importin-β1 is emerging as an attractive target by virtue of its prevalence in many cancers.However,the lack of druggable inhibitors restricts its therapeutic proof of concept.In the present work,we optimized a natural importin-β1 inhibitor DD1 to afford an improved analog DD1-Br with better tolerability(>25 folds)and oral bioavailability.DD1-Br inhibited the survival of castration-resistant prostate cancer(CRPC)cells with sub-nanomolar potency and completely prevented tumor growth in resistant CRPC models both in monotherapy(0.5 mg/kg)and in enzalutamidecombination therapy.Mechanistic study revealed that by targeting importin-β1,DD1-Br markedly inhibited the nuclear accumulation of multiple CRPC drivers,particularly AR-V7,a main contributor to enzalutamide resistance,leading to the integral suppression of downstream oncogenic signaling.This study provides a promising lead for CRPC and demonstrates the potential of overcoming drug resistance in advanced CRPC via targeting importin-β1.

Sequence stratigraphic analysis of superimposed coal measure gas-bearing system in Daning-Jixian block,eastern margin of Ordos Basin,China

The identification of superimposed gas-bearing systems in coal measures is the basis for expediting the optimization of coal measure gas co-production.Through the analysis of drill cores and log data of Upper Carboniferous Benxi Formation to the member 8 of Middle Permian Lower Shihezi Formation in Daning-Jixian block,eastern margin of Ordos Basin,four distinct superimposed coal measure gas-bearing systems were identified,and their formation mechanism was discussed from the sequence stratigraphic perspective.Type Ⅰ system mainly contains multiple coal seams,shales and sandstone layers.Type Ⅱ system is dominated by multiple coal seams and shales.Type Ⅲ is characterized by multiple sandstone layers,and type Ⅳ system is dominated by limestones and mudstones.In general,the gas-bearing systems deposited in barrier-lagoon are type Ⅱ,those deposited in carbonate tidal flats are type IV,and those deposited in the delta front are types Ⅰ and Ⅲ.The marine mudstone,acting as a key layer near the maximum flooding surface,exhibits very low permeability,which is the main factor contributing to the formation of superimposed gas-bearing systems.The sedimentary environment plays a significant role in controlling the distribution of gas-bearing systems.Notably,the vertical gas-bearing systems in the south-western region,where delta front and lagoon facies overlap,are more complex than those in the north-eastern delta front facies.

Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation

The clinical application of doxorubicin(DOX) in cancer chemotherapy is limited by its lifethreatening cardiotoxic effects. Chrysophanol(CHR), an anthraquinone compound isolated from the rhizome of Rheum palmatum L., is considered to play a broad role in a variety of biological processes.However, the effects of CHR’s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9 C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide(3 AB)and ABT888. Ectopic expression of PARP1 effectively blocked this CHR’s cardioprotection against DOX-induced cardiomyocyte injury in H9 C2 cells. Furthermore, pre-administration with both CHR and 3 AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague–Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy.

Targeting castration-resistant prostate cancer with a novel RORγ antagonist elaiophylin

Prostate cancer(PCa)patients who progress to metastatic castration-resistant PCa(mCRPC)mostly have poor outcomes due to the lack of effective therapies.Our recent study established the orphan nuclear receptor RORγas a novel therapeutic target for CRPC.Here,we reveal that elaiophylin(Elai),an antibiotic from Actinomycete streptomyces,is a novel RORy antagonist and showed potent antitumor activity against CRPC in vitro and in vivo.We demonstrated that Elai selectively binded to RORy protein and potently blocked RORγtranscriptional regulation activities.Structure-activity relationship studies showed that Elai occupied the binding pocket with several key interactions.Furthermore,Elai markedly reduced the recruitment of RORγto its genomic DNA response element(RORE),suppressed the expression of RORγtarget genes AR and AR variants,and significantly inhibited PCa cell growth.Importantly,Elai strongly suppressed tumor growth in both cell line based and patient-derived PCa xenograft models.Taken together,these results suggest that Elai is novel therapeutic RORγinhibitor that can be used as a drug candidate for the treatment of human CRPC.

Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loop via NRF2 in cancer therapeutic resistance

Metabolic and epigenetic reprogramming play important roles in cancer therapeutic resistance.However,their interplays are poorly understood.We report here that elevated TIGAR(TP53-induced glycolysis and apoptosis regulator),an antioxidant and glucose metabolic regulator and a target of oncogenic histone methyltransferase NSD2(nuclear receptor binding SET domain protein 2),is mainly localized in the nucleus of therapeutic resistant tumor cells where it stimulates NSD2 expression and elevates global H3K36me2 mark.Mechanistically,TIGAR directly interacts with the antioxidant master regulator NRF2 and facilitates chromatin recruitment of NRF2,H3K4me3 methylase MLL1 and elongating Pol-II to stimulate the expression of both new(NSD2)and established(NQO1/2,PRDX1 and GSTM4)targets of NRF2,independent of its enzymatic activity.Nuclear TIGAR confers cancer cell resistance to chemotherapy and hormonal therapy in vitro and in tumors through effective maintenance of redox homeostasis.In addition,nuclear accumulation of TIGAR is positively associated with NSD2 expression in clinical tumors and strongly correlated with poor survival.These findings define a nuclear TIGAR-mediated epigenetic autoregulatory loop in redox rebalance for tumor therapeutic resistance.

The poly(ADP-ribosyl)ation of BRD4 mediated by PARP1 promoted pathological cardiac hypertrophy

The bromodomain and extraterminal(BET)family member BRD4 is pivotal in the pathogenesis of cardiac hypertrophy.BRD4 induces hypertrophic gene expression by binding to the acetylated chromatin,facilitating the phosphorylation of RNA polymerases II(Pol II)and leading to transcription elongation.The present study identified a novel post-translational modification of BRD4:poly(ADPribosyl)ation(PARylation),that was mediated by poly(ADP-ribose)polymerase-1(PARP1)in cardiac hypertrophy.BRD4 silencing or BET inhibitors JQ1 and MS417 prevented cardiac hypertrophic responses induced by isoproterenol(ISO),whereas overexpression of BRD4 promoted cardiac hypertrophy,confirming the critical role of BRD4 in pathological cardiac hypertrophy.PARP1 was activated in ISOinduced cardiac hypertrophy and facilitated the development of cardiac hypertrophy.BRD4 was involved in the prohypertrophic effect of PARP1,as implied by the observations that BRD4 inhibition or silencing reversed PARP1-induced hypertrophic responses,and that BRD4 overexpression suppressed the antihypertrophic effect of PARP1 inhibitors.Interactions of BRD4 and PARP1 were observed by coimmunoprecipitation and immunofluorescence.PARylation of BRD4 induced by PARP1 was investigated by PARylation assays.In response to hypertrophic stimuli like ISO,PARylation level of BRD4 was elevated,along with enhanced interactions between BRD4 and PARP1.By investigating the PARylation of truncation mutants of BRD4,the C-terminal domain(CTD)was identified as the PARylation modification sites of BRD4.PARylation of BRD4 facilitated its binding to the transcription start sites(TSS)of hypertrophic genes,resulting in enhanced phosphorylation of RNA Pol II and transcription activation of hypertrophic genes.The present findings suggest that strategies targeting inhibition of PARP1-BRD4 might have therapeutic potential for pathological cardiac hypertrophy.