Curcumin is a phytochemical which exhibits significant inhibitory effect in multiple cancers including prostate cancer. MicroRNA-34a (miR-34a) was found to be a master tumor suppressor miRNA and regulated the growth of cancer cells. To date, however, the role of miR-34a in the anticancer action of curcumin against prostate cancer has been rarely reported. In the present study, we showed that curcumin altered the expression of cell cycle-related genes (cyclin D1, PCNA, and p21) and inhibited the proliferation of prostate cancer cells. Furthermore, we found that curcumin significantly upregulated the expression of miR-34a, along with the downregulated expression of β-catenin and c-myc in three prostate cancer cell lines. Inhibition of miR-34a activated β-catenin/c-myc axis, altered cell cycle-related genes expression and significantly suppressed the antiproliferation effect of curcumin in prostate cancer cells. Findings from this study revealed that miR-34a plays an important role in the antiproliferation effect of curcumin in prostate cancer.

Prostate cancer is the most common malignancy in men. Phthalate esters are a class of environmental endocrine disruptors and were reported to be cancer promoting agents, however the potential role of phthalate esters in prostate cancer has been rarely reported. Mounting evidence has shown that miR-34a is a master tumor suppressor miRNA in cancer. The aim of this study was to investigate the role of butyl benzyl phthalate (BBP), one of the typical phthalate esters, in cell proliferation of prostate cancer cells. Human prostate cancer LNCaP and PC-3 cells were exposed to low dose of BBP for 6 days. The results showed that 10(-6) and 10(-7) mol/L BBP increased the expression of cyclinD1 and PCNA, decreased p21 expression, and induced cell growth in both LNCaP and PC-3 cells. Furthermore, we found that BBP significantly downregulated the expression of miR-34a, along with upregulation of miR-34a target gene c-myc. Using cell tranfection of miR-34a mimic and inhibitor, we demonstrated that BBP promoted cell proliferation through miR-34a/c-myc axis in prostate cancer cells. Findings from this study could provide new insight into the involvement and the molecular mechanism of phthalate esters on prostate cancer.

Prostate cancer is one of the most commonly diagnosed cancers in man. Studies have shown that phthalates may act as promoters in various types of cancer; however, the role of phthalates in prostate cancer has been rarely reported. The MAPK/AP-1 pathway is a vital regulator of cell proliferation in cancer. In this report we found that three typical phthalates, diethylhexyl phthalate (DEHP), Butyl benzyl phthalate (BBP) and Dibutyl phthalate (DBP), up-regulated cyclinD1 and PCNA, down-regulated P21, inducing proliferation of prostate cancer cells. Furthermore, we found that phthalates increased the expression of p-ERK5 and p-p38, along with upregulation of AP-1 (p-c-fos and p-c-jun). In studies with ERK5 and a p38 inhibitor, our data showed that downregulation of p-ERK5 or p38 inhibited phthalate-triggered cell proliferation. Taken together, findings from this study suggest that phthalates activate MAPK/AP-1 pathway and may potentially promote cell proliferation in prostate cancer, thus providing new insight into the effects and the underlying mechanism of phthalates on prostate cancer.

Neuronal cell death is an important feature of neurodegeneration. Aluminum is associated with neurodegenerative disorders, particularly Alzheimer's disease. However, the underlying mechanisms by which aluminum induces neuronal apoptosis remain to be elucidated. miR-19 is a key miRNA implicated in regulating cell survival process, while the role of miR-19 in Alzheimer's disease has not been investigated. In the present study, we showed that Aluminum maltolate (Al-malt), a lipophilic Al complex which is a common component of human diet with the ability to facilitate the entry of Al into the brain, induced apoptosis in human neuroblastoma SH-SY5Y cells, along with downregulation of miR-19a/miR-19b, upregulation of miR-19-targeted PTEN, and alterations of its downstream apoptosis related proteins including AKT, p53, Bax, and Bcl-2. miR-19 overexpression attenuated Al-malt-induced apoptosis as well as changes in the expression of apoptosis related proteins in SH-SY5Y cells. We further revealed that exposure of rats to Al-malt for 12 weeks at doses relevant to human exposure significantly elevated Al concentrations in serum and brain tissues. Al-malt dose-dependently induced apoptosis in rat brain, as evidenced by increased caspase activation and increased TUNEL staining. Consistent with in vitro results, Al-malt reduced miR-19 expression and altered the expression of apoptotic related proteins in rat brain. Taken together, our data suggest for the first time that miR-19 modulation is critically involved in Al-induced neural cell apoptosis. Findings from this study could provide new insight into the molecular mechanisms of Al-associated neurodegenerative pathogenesis.

Aluminum (Al)-induced apoptosis is considered as the major cause of its neurotoxicity. Folic acid possesses neuroprotective function by preventing neural cell apoptosis. microRNAs (miRNAs) are important regulators of gene expression participating in cellular processes. As a key component of the miR-17-92 cluster, miR-19 is implicated in regulating apoptotic process, while its role in the neuroprotective effect of folic acid has not been investigated. The present study aimed to investigate the potential involvement and function of miR-19 in the protective action of folic acid against Al-induced neural cell apoptosis. Human SH-SY5Y cells were treated with Al-maltolate (Al-malt) in the presence or absence of folic acid. Results showed that Al-malt-induced apoptosis of SH-SY5Y cells was effectively prevented by folic acid. Al-malt suppressed the expression of miR-19a/19b, along with alterations of miR-19 related apoptotic proteins including PTEN, p-AKT, p53, Bax, Bcl-2, caspase 9 and caspase 3; and these effects were ameliorated by folic acid. miR-19 inhibitor alone induced apoptosis of SH-SY5Y cells. Combination treatment of folic acid and miR-19 inhibitor diminished the neuroprotective effect of folic acid. These findings demonstrated that folic acid protected neuronal cells against Al-malt-induced apoptosis by preventing the downregulation of miR-19 and modulation of miR-19 related downstream PTEN/AKT/p53 pathway.

Glycyrrhiza glabra (licorice) has been known to possess various pharmacological properties including anti-inflammatory, antioxidants, antiviral, and hepatoprotective activities. Magnesium isoglycyrrhizinate (MgIG), a magnesium salt of 18-α glycyrrhizic acid stereoisomer, is clinically used for the treatment of inflammatory liver diseases. However, the mechanism by which MgIG exerts its anti-inflammatory effects remains unknown. In the present study, we investigated the inhibitory potential of MgIG in phospholipase A 2 (PLA 2 )/arachidonic acid (AA) pathway and release of the pathway-generated inflammatory lipid mediators in RAW264.7 macrophages. Results revealed that MgIG suppressed LPS-induced activation of PLA 2 and production of AA metabolites such as prostaglandin E 2 (PGE 2 ), prostacyclin (PGI 2 ), thromboxane 2 (TXB 2 ), and leukotrienes (LTB 4 ) in macrophages. Furthermore, LPS-induced AA-metabolizing enzymes including COX-2, COX-1, 5-LOX, TXB synthase, and PGI 2 synthase were significantly inhibited by MgIG. Taken together, our data suggest that modulation of cyclooxygenase (COXs) and 5-lipoxygenase (LOX) pathways in AA metabolism could be a novel mechanism for the anti-inflammatory effects of MgIG.

Breast cancer is the most common cancer in women. Bisphenol A (BPA), as a known endocrine disrupter, is closely related to the development of breast cancer. Curcumin has been clinically used in chemopreventation and treatment of cancer; however, it remains unknown whether microRNAs are involved in curcumin‐mediated protection from BPA‐associated promotive effects on breast cancer. In the present study, we showed that BPA exhibited estrogenic activity by increasing the proliferation of estrogen‐receptor‐positive MCF‐7 human breast cancer cells and triggering transition of the cells from G1 to S phase. Curcumin inhibited the proliferative effects of BPA on MCF‐7 cells. Meanwhile, BPA‐induced upregulation of oncogenic miR‐19a and miR‐19b, and the dysregulated expression of miR‐19‐related downstream proteins, including PTEN, p‐AKT, p‐MDM2, p53, and proliferating cell nuclear antigen, were reversed by curcumin. Furthermore, the important role of miR‐19 in BPA‐mediated MCF‐7 cell proliferation was also illustrated. These results suggest for the first time that curcumin modulates miR‐19/PTEN/AKT/p53 axis to exhibit its protective effects against BPA‐associated breast cancer promotion. Findings from this study could provide new insights into the molecular mechanisms by which BPA exerts its breast‐cancer‐promoting effect as well as its target intervention. Copyright © 2014 John Wiley & Sons, Ltd.

Abstract Tobacco smoke is the leading cause of lung cancer. High-grade malignant pulmonary neuroendocrine tumors, including small cell lung cancers (SCLCs) and large cell neuroendocrine carcinomas (LCNECs), are almost exclusively associated with tobacco smoking. Unanalogous to most of other lung tumors such as squamous cell carcinomas, adenocarcinoma, adenosquamous carcinoma or carcinoid, no precursor lesions for high-grade lung neuroendocrine tumors have so far been identified. The purpose of the present study was to investigate the effects of tobacco smoke on pulmonary neuroendocrine alterations in phenotypically normal cells in vivo. Male BALB/c mice were exposed to tobacco smoke for 6h/day, 7days/week for 12 weeks. Pulmonary histology, neuroendocrine differentiation as well as MAPK/AP-1 activation were examined in lung tissues. Exposure to tobacco smoke significantly induced expression of neuroendocrine differentiation markers such as chromogranin A, neural cell adhesion molecule/(CD56), synaptophysin, and neuron specific enolase, as demonstrated by immunohistochemistry, Western blotting and real-time PCR. The expression levels of epithelial markers, including E-cadherin, zona ocludens-1, cytokeratin 5 and involucrin, were downregulated by tobacco smoke. Moreover, tobacco smoke significantly increased levels of p-ERK1/2, p-JNK and p-p38, while it suppressed p-ERK5 level. Expression of Jun and Fos proteins were differentially regulated by tobacco smoke. Taken together, the present study provides experimental evidence for the first time that tobacco smoke induces pulmonary neuroendocrine differentiation, shedding new light on the carcinogenic process of pulmonary neuroendocrine tumors. Citation Format: Wei Xie, Zhaofeng Liang, Ying Yin, Chunfeng Xie, Hao Geng, Li Zhao, Rui Wu, Xiaoting Li, Feifei Deng, Jieshu Wu, Shanshan Geng, Mingming Zhu, Jianyun Zhu, Weiwei Zhu, Cong Huang, Caiyun Zhong. Tobacco smoke induces pulmonary neuroendocrine alterations in vivo. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3182. doi:10.1158/1538-7445.AM2014-3182

Energy saving has become the survival of the enterprise,pharmaceutical companies(large turbine blower) is one of the largest power consumption equipment.In the production process to meet the requirements,energy transformation system of EI290-3.5/0.96 type centrifuge compared to EI420 saving more than 30%,which can save electricity about 3 000 000 Yuan/a for company,energy-saving effect is remarkable.

The continuous development of the world economy, resulting in contradiction between the increasing demand for energy and traditional energy shortage is more and more outstanding. Compared with the international, China's energy shortage phenomenon is more serious, how to promote the energy saving of industrial enterprises and the new energy, renewable energy, rational development and utilization of, is an arduous task facing now. Before and after the arch reconstruction, increasing the preheating tank, a draught fan and a blower to adjust the proportion of transformation through the measures such as boiler of coal-fired boiler combustion energy-saving reformation, modified chaff boiler, create economic and social benefits of double effect, in industrial energy efficiency demonstration of far-reaching significance.

目的：探讨丙烯酰胺（AA）对人SH-SY5Y神经细胞凋亡和miR-21表达的影响。方法：不同浓度丙烯酰胺作用于人神经母细胞瘤SH-SY5Y细胞24 h后,采用四甲基偶氮唑盐（MTT）法测定丙烯酰胺对SH-SY5Y细胞活力的影响,Hoechst 33258荧光染色法检测细胞凋亡,real-time PCR检测miR-21表达水平,Western blot检测PTEN、p-AKT、AKT、Bcl-2、Bax、caspase 9和caspase 3蛋白表达。结果：丙烯酰胺剂量依赖性地降低SH-SY5Y细胞活性,Hoechst 33258染色显示明显细胞凋亡形态变化;丙烯酰胺显著降低SH-SY5Y细胞miR-21的表达,同时升高PTEN、Bax、caspase 9、caspase 3水平并降低p-AKT和Bcl-2表达。结论：丙烯酰胺可通过线粒体途径诱导SH-SY5Y神经细胞凋亡,其机制可能与丙烯酰胺引起miR-21表达下调有关。

In the production of power and energy management based on the long-term practice,this paper summed up the "safe,reliable,economic,reasonable" eight-character policy.In this paper,pharmaceutical enterprises in compressed air system supply side problems in the process of layout design,combined with my years on the compressed air system supply side practice and improvement of.