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Kongzhuang coal mine of Shanghai Datun Energy Resources Co., Ltd. is a typical deep coal mine in eastern China. The mining disturbance of working face in deep coal mine leads to the fracture and movement of overlying strata and the damage of the aquifer in overlying strata, thereby causing water inrush disaster and posing a serious threat to the safety production in coal mine. Therefore, the temporal and spatial evolution mechanism of the water-conducting fractured zone of overlying strata in the Kongzhuang coal mine is researched systematically in this paper. Especially, the hydro-geological conditions and mining conditions in the Kongzhuang coal mine are analyzed; on this basis, the fracture and movement of overlying strata are simulated by physical similarity simulation test, and the temporal and spatial evolution rule of overlying strata in the Kongzhuang coal mine is obtained. Besides, the development height of “two zones” is measured by double-end water shutoff detection method, and the risk assessment for the water inrush disaster of the coal seam roof is carried out in the Kongzhuang coal mine. The research achievements in this paper indicate that the water-conducting channel formed in the mining process of #7 coal seam is the most important water-filling channel. Quaternary aquifer water recharges the mine indirectly through the bedrock aquifer, and the sandy mudstone with large thickness is the key layer to control the development of a water-conducting fracture zone. Meanwhile, the height of the caving zone is 26.7 m, about 8.3 times of mining height, and the height of the fracture zone is 68.3 m, approximately equal to 16.26 of the mining height. The results of #1 and #2 borehole leakages in the double-end water shutoff detection method show that the height of the water-conducting fractured zone is 63.70 m-65.27 m, and the split-to-mining ratio is 15.17-15.54. The water inrush risk of the coal seam roof shows that most of the 7436 working face is in the transition zone, and a small area around the cutting hole of the working face is in the relatively dangerous zone. Therefore, the innovation of this paper is that the temporal and spatial evolution mechanism of the water-conducting fractured zone of overlying strata in the Kongzhuang coal mine is revealed, which provides the theoretical guidance for the prediction and prevention of water inrush disaster in the coal mine with the similar mining conditions.

Five novel bisindole alkaloids, hunzeylanines A-E (1-5), with an unprecedented skeleton were isolated from the roots of Hunteria zeylanica. Compounds 1-5 represent the first examples of akuammine-pleioarpamine-type bisindole alkaloids fused with a dihydropyran unit. Their structures including absolute configurations were established through comprehensive spectroscopic data analyses and computational calculation methods. The plausible biogenetic pathway of 1 was also proposed. Alkaloids 1 and 2 displayed moderate cytotoxicity toward three human cancer cell lines (MDA-MB-231, AV3, and Huh7).

Breastfeeding is related to maternal health. However, the association of women’s breastfeeding duration with cognitive function in their later life is limited and inconsistent. The aim of this study was to accurately evaluate the association in Chinese postmenopausal women. We analyzed the data from Zhejiang Ageing and Health Cohort Study including 5487 postmenopausal women. Cognitive impairment was assessed via the Mini-Mental State Examination. Data on breastfeeding duration was collected in the reproductive history section within the questionnaire. Generalized additive models (GAMs) and logistic regression models, controlled for an extensive range of potential confounders, were generated to examine the associations. A U-shaped association was identified between breastfeeding duration and cognitive impairment based on GAM. The nadir with lowest odds of cognitive impairment was ascertained by quadratic model as 12 months. The logistic models showed that compared with women breastfeeding 12 months per child, the fully adjusted odds ratios (ORs) were 1.50 (95% Confidence Interval (CI): 1.20–1.88), 1.58 (95% CI: 1.29–1.93), 1.33 (95% CI: 1.06–1.68), 2.08 (95% CI: 1.64–2.65) for those averagely breastfeeding 12–18,>18 months, respectively. Furthermore, we did not observe significant effect modification of the association. Future longitudinal studies are needed to confirm the association.

This study explored the protective effect of atractylenolide Ⅰ(AO-Ⅰ) against acetaminophen(APAP)-induced acute liver injury(ALI) in mice and its underlying mechanism. C57 BL/6 J mice were randomly divided into a control group, an APAP group(500 mg·kg~(-1)), a low-dose combination group(500 mg·kg~(-1) APAP + 60 mg·kg~(-1) AO-Ⅰ), and a high-dose combination group(500 mg·kg~(-1) APAP + 120 mg·kg~(-1) AO-Ⅰ). ALI was induced by intraperitoneal injection of APAP(500 mg·kg~(-1)). AO-Ⅰ by intragastric administration was performed 2 hours before APAP treatment, and the control group received the same dose of solvent by intragastric administration or intraperitoneal injection. The protective effect of AO-Ⅰ against APAP-induced ALI was evaluated by detecting alanine aminotransferase(ALT) and aspartate aminotransferase(AST) levels in the plasma and Hamp;E staining in liver tissues of mice. The malondialdehyde(MDA) and glutathione(GSH) content and catalase(CAT) activity in mouse liver tissues were detected to evaluate the effect of AO-Ⅰ on APAP-induced oxidative stress in the liver. The proteins in the liver p38 mitogen-activated protein kinase(p38 MAPK), c-jun N-terminal kinase(JNK), and nuclear factor kappa-B p65(NF-κB p65) signaling pathways were measured by Western blot, and the liver inflammatory cytokines interleukin-1β(IL-1β) and interleukin-6(IL-6) were detected by real-time PCR. Compared with the APAP group, the combination groups showed reduced APAP-induced ALT level and liver MDA content, potentiated liver CAT activity, and elevated GSH content. Mechanistically, AO-Ⅰ treatment significantly inhibited APAP-up-regulated MAPK phosphorylation and NF-κB p65, and significantly reduced the transcriptional activities of IL-1β and IL-6, downstream targets of NF-κB p65. AO-Ⅰ can improve APAP-induced ALI and the underlying mechanism is related to the inhibition of the MAPK/NF-κB p65 signaling pathway in APAP-challenged mice.

Background Pulmonary arterial hypertension (PAH), characterized by pulmonary artery constriction and vascular remodeling, has a high mortality rate. New drugs for the treatment of PAH urgently need to be developed. Purpose This study was designed to investigate the vasorelaxant activity of OTNA in isolated pulmonary arteries, and explore its molecular mechanism. Methods Pulmonary arteries and thoracic aortas were isolated from mice, and vascular tone was tested with a Wire Myograph System. Nitric oxide levels were determined with DAF-FM DA and DAX-J2™ Red. Cellular thermal shift assays, microscale thermophoresis, and molecular docking were used to identify the interaction between OTNA and aryl hydrocarbon receptor (AhR). The levels of PI3K, p-PI3K, Akt, p-Akt, eNOS, p-eNOS, and AhR were analyzed by Western blotting. Results OTNA selectively relaxed the isolated pulmonary artery rings in an endothelium-dependent manner. Mechanistic study showed that OTNA induced NO production through activation of the PI3K/Akt/eNOS pathway in endothelial cells. Furthermore, we also found that OTNA directly bound to AhR and activated the PI3K/Akt/eNOS pathway to dilate pulmonary arteries by inhibiting AhR. Conclusions OTNA relaxes pulmonary arteries by antagonizing AhR. This study provides a new natural antagonist of AhR as a promising lead compound for PAH treatment.

Five novel bisindole alkaloids, hunzeylanines A-E (

Ervadivamines A (1) and B (2), two unprecedented trimeric monoterpenoid indole alkaloids, were isolated from Ervatamia divaricata. They are the first examples of vobasine-iboga-vobasine-type alkaloid with both C-C and C-N linkage patterns. Their structures including absolute configurations were fully accomplished by extensive spectroscopic analysis, single-crystal X-ray diffraction, and electric circular dichroism methods. The plausible biogenetic pathways of these trimeric alkaloids were also proposed. In addition, compound 1 exhibited significant cytotoxicity against four cancer cells.

Background/Aims: Renal ischemia-reperfusion injury (IRI) is a common consequence of acute kidney injury. Nicotinamide adenine dinucleotide phosphate (NADPH), which is derived from the pentose phosphate pathway, is essential for the proper functioning of essential redox and antioxidant defense systems. Previous studies have indicated that NADPH is responsible for protecting the brain from ischemic injury. The goal of this study was to analyze the protective function of NADPH in renal IRI. Methods: The IRI animal model was generated through a midline laparotomy surgery that clamped both sides of the renal pedicles for 40 min to induce renal ischemia. The in vitro model was generated by removing oxygen and glucose from human kidney epithelial cells (HK-2 cells), followed by reoxygenation to imitate IRI. Renal function and histopathological changes were observed and evaluated. Additionally, malondialdehyde and glutathione levels were determined in renal tissue homogenate as indicators of oxidative stress. ROS production in cells was determined by DHE staining. Protein biomarker expression was evaluated by western blot, apoptosis was analyzed by TUNEL staining, and p65 nuclear translocation was visualized by immunofluorescence. Results: Our data indicated that NADPH safeguarded the kidneys from histological and functional damage, and significantly reduce cell injury along with preventing potential increases in blood urea nitrogen and creatinine levels. Furthermore, we observed that NADPH increased glutathione levels, while reducing levels of malondialdehyde and reactive oxygen species. Additionally, our results suggested that NADPH treatment may alleviate IRI-induced apoptosis and inflammation. Conclusion: NADPH treatment may protect against renal IRI and should be further developed as a new treatment for acute kidney injury.

C–S–H-PCE nanocomposites (CPNs) serving as nucleation sites are a promising material to accelerate the cement hydration and gain high early strength for cementitious materials. This study aimed to investigate the effects of CPNs on the properties and hydration of cement mortar under different water-to-cement (w/c) ratios. CPNs were prepared via the co-precipitation method in MAPEG-PCE solution and characterized by means of XRD, FT-IR, DLS, TEM , TGA, and TOC . The mechanism and effect of CPNs on the early hydration of cement mortar with w/c ratios of 0.50, 0.40, and 0.35 were assessed in terms of mechanical properties, isothermal calorimetry, setting time XRD, TGA, SEM, and MIP. The results showed that CPNs significantly promoted the early strength development of mortar and a higher enhancement ratio was brought at a lower w/c ratio. Calorimetry and setting results also showed a greater hydration acceleration of samples dosed CPNs with lower w/c ratio. From the analysis of XRD and TGA, the content of CH and C–S–H in the samples dosed CPNs increased with the decrease of w/c ratio in 6 h, while exhibited an opposite trend in 12 h and 3 d. MIP and SEM results showed that CPNs led to a refinement of pore structure and dense morphology, especially at a low w/c ratio. Moreover, the underlying acceleration mechanism of cement hydration versus w/c ratio was that the seeding ability was enhanced for the low distance between cement and CPNs at a low w/c ratio. According to this research, the use of CPNs may be more practical in high-strength concrete.

Tanshinone Ⅱ_A( Tan Ⅱ_A),the liposoluble constituents of Salvia miltiorrhiza,can not only ameliorate the lipidic metabolism and decrease the concentration of lipid peroxidation,but also resist oxidation damage,scavenge free radicals and control inflammation,with a protective effect on prognosis after liver function impairment. Therefore,the studies on the exact mechanism of Tan Ⅱ_A in protecting the liver can provide important theoretical and experimental basis for the prevention and treatment effect of Tan Ⅱ_A for liver injury. In the present study,the protective effects and mechanism of Tan Ⅱ_A on 4-hydroxynonenal( 4-HNE)-induced liver injury were investigated in vitro. Normal liver tissues NCTC 1469 cells were used to induce hepatocytes oxidative damages by 4-HNE treatment. The protective effect of Tan Ⅱ_A on hepatocytes oxidative damages was detected by release amount of lactate dehydrogenase( LDH) analysis and hoechst staining. The protein expression changes of peroxisome proliferator-activated receptor α( PPARα) and peroxisome proliferator response element( PPRE) were analyzed by Western blot analysis in NCTC 1469 cells before and after Tan Ⅱ_A treatment. The gene expression changes of fatty aldehyde dehydrogenase( FALDH) were analyzed by Real-time polymerase chain reaction( PCR) analysis. The results showed that 4-HNE increased the release amount of LDH,lowered the cell viability of NCTC 1469 cells,and Tan Ⅱ_A reversed 4-HNE-induced hepatocyte damage. Western blot analysis and RT-PCR analysis results showed that 4-HNE decreased the expression of PPARα and FALDH and increased the expression of 4-HNE. However,the expression of PPARα and FALDH were increased significantly and the expression of 4-HNE was decreased obviously after Tan Ⅱ_A treatment. This study confirmed that the curative effect of Tan Ⅱ_A was obvious on hepatocytes damage,and the mechanism may be associated with activating PPARα and FALDH expression as well as scavenging 4-HNE.

The atom occupied sites, structures, tetragonal transformation and magnetic properties are studied by the first principles calculations. From least energy principle, the calculated equilibrium lattice parameter is 6.03 Å and 6.00 Å for Cu2MnAl type Ni2YIn (Y=Fe, Co) alloys, respectively. The Ni2YIn (Y=Fe, Co) alloys show steady martensitic phases at c/a=1.29 and c/a=1.36 based on the EBP’s method. Ni atoms and Y (Y=Fe, Co) contribute to the total magnetic moments, and keep parallel aligned in martensitic and austenitic phases. The Ni2YIn (Y=Fe, Co) alloys are the candidates for Ferromagnetic Shape Memory Alloys.

// Yun-fang Zhen 1, * , Song-tao Li 2, * , Yun-rong Zhu 3, * , Xiao-dong Wang 1 , Xiao-zhong Zhou 2 , Lun-qing Zhu 1 1 The Center of Diagnosis and Treatment for Children’s Bone Diseases, The Children’s Hospital Affiliated to Soochow University, Suzhou, China 2 The Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China 3 Department of Orthopedics, The Affiliated Jiangyin Hospital of Medical College of Southeast University, Jiangyin, China * These authors have contributed equally to this work Correspondence to: Lun-qing Zhu, email: zhulunqingszgk@163.com Xiao-dong Wang, email: xiaodongwangsz@163.com Xiao-zhong Zhou, email: zhouxiaozhongorth@163.com Keywords: osteosarcoma (OS), salinomycin, DNA-PKcs, microRNA-101, autophagy Received: September 09, 2016 Accepted: September 26, 2016 Published: October 17, 2016 ABSTRACT Malignant osteosarcoma (OS) is still a deadly disease for many affected patients. The search for the novel anti-OS agent is extremely urgent and important. Our previous study has proposed that salinomycin is a novel anti-OS agent. Here we characterized DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a primary salinomycin resistance factor in OS cells. DNA-PKcs inhibitors (NU7026, NU7441 and LY294002) or DNA-PKcs shRNA knockdown dramatically potentiated salinomycin-induced death and apoptosis of OS cells (U2OS and MG-63 lines). Further, forced-expression of microRNA-101 (“miR-101”) downregulated DNA-PKcs and augmented salinomycin’s cytotoxicity against OS cells. Reversely, over-expression of DNA-PKcs in OS cells inhibited salinomycin’s lethality. For the mechanism study, we show that DNA-PKcs is required for salinomycin-induced pro-survival autophagy activation. DNA-PKcs inhibition (by NU7441), shRNA knockdown or miR-101 expression inhibited salinomycin-induced Beclin-1 expression and autophagy induction. Meanwhile, knockdown of Beclin-1 by shRNA significantly sensitized salinomycin-induced OS cell lethality. In vivo , salinomycin administration suppressed U2OS xenograft tumor growth in severe combined immuno-deficient (SCID) mice, and its anti-tumor activity was dramatically potentiated with co-administration of the DNA-PKcs inhibitor NU7026. Together, these results suggest that DNA-PKcs could be a primary resistance factor of salinomycin in OS cells. DNA-PKcs inhibition or silence may thus significantly increase salinomycin’s sensitivity in OS cells.

With the output of an OPG/OPA pumped by the third harmonic output 355 nm of a pulsed Nd·YAG laser as radiation source, the emission spectrum of laser induced coal sample plasma is created. The emission spectral line shows the character of Lorenz profile. So Stark broadening is the main widening way of this plasma system. The spatial distribution of the plasma temperature and electron density is measured from the intensity and Stark broadening of the spectral lines. It is found that in the direction from vertical to plasma luminous flame, both plasma temperature and electron density are symmetrically relative to the center. While in the direction of parallel to plasma luminous flame, they are asymmetrically relative to the center. Plasma temperature and electron density is maximized in the centre of the flame, and the emission intensity of the plasma in the centre is also strong. So we ought to collect the emission spectrum in the plasma centre when using the technique of spectroscopy for the diagnosis of plasma characteristics. It is also found that there is a dip in the centre of some spectral lines. This indicates that there exists strong self-absorption in the plasma. The appearance of self-absorption varies with laser wavelength. It is most obvious when the wavelength is near to the center of the profile, because the transition probability is the largest at the center of the profile. Both emission intensity and self-absorption increase with laser energy. These experimental results can be interpreted as the increase of the particle density with laser energy. Thus we ought to select spectral lines with no self-absorption when measuring the parameters of the plasma with the technique of laser spectroscopy. This can ensure higher detection accuracy.

Dexamethasone (Dex) causes osteoblast cell injuries. In the present research, we tested the potential effect of SC79, a novel and specific Akt activator, against Dex in osteoblasts. In primary murine osteoblasts and osteoblastic MC3T3-E1 cells, pretreatment with SC79 significantly attenuated Dex-induced cell death. Further, Dex-induced mitochondrial permeability transition pore (mPTP) opening, cytochrome C release and apoptosis activation were dramatically alleviated with SC79 pretreatment in above cells. At the molecular level, SC79 activated Akt, which was indispensable for subsequent osteoblast protection against Dex. Akt inhibitors (LY294002, perifosine and MK-2206) blocked SC79-induced Akt activation and abolished its anti-Dex actions in osteoblasts. Further, SC79 activated Akt downstream Nrf2 (NF-E2-related factor 2) signaling and attenuated Dex-induced oxidative stress in osteoblasts. Nrf2 shRNA knockdown or S40T mutation almost reversed SC79-mediated anti-oxidant and cytoprotective activities in osteoblasts. Together, these results suggest that SC79 activates Akt-Nrf2 signaling to protect osteoblasts from Dex.