Accurate Prediction of the Magnetic Ordering Temperature of Ultralow-Temperature Magnetic Refrigerants.

Adiabatic demagnetization refrigeration is known to be the only cryogenic refrigeration technology that can achieve ultralow temperatures (≪1 K) at gravity-free conditions. The key indexes to evaluate the performance of magnetic refrigerants are their magnetic entropy changes (-ΔSm) and magnetic ordering temperature (T0). Although, based on the factors affecting the -ΔSm of magnetic refrigerants, one has been able to judge if a magnetic refrigerant has a large -ΔSm, how to accurately predict their T0 remains a huge challenge due to the fact that the T0 of magnetic refrigerants is related to not only magnetic exchange but also single-ion anisotropy and magnetic dipole interaction. Here, we, taking GdCO3F (1), Gd(HCOO)F2, Gd2(SO4)3·8H2O, GdF3, Gd(HCOO)3 and Gd(OH)3 as examples, demonstrate that the T0 of magnetic refrigerants with very weak magnetic interactions and small anisotropy can be accurately predicted by integrating mean-field approximation with quantum Monte Carlo simulations, providing an effective method for predicting the T0 of ultralow-temperature magnetic refrigerants. Thus, the present work lays a solid foundation for the rational design and preparation of ultralow-temperature magnetic refrigerants in the future.

The Spectral Response of the Dual Microdisk Resonator Based on BaTiO3 Resistive Random Access Memory.

With the resistive random access memory (ReRAM) devices based on the Al/BaTiO3 (BTO)/ITO structure fabricated at hand, by cross-analyzing the resistive memory characteristics in terms of various barium titanate (BTO) film thicknesses, it is found that the device with 60 nm thick BTO can be switched more than 425 times, while the corresponding SET/RESET voltage, the on-off ratio, and the retention time are -0.69 V/0.475 V, 102, and more than 104 seconds, respectively. Furthermore, the aforementioned ReRAM with a low switching voltage and low power consumption is further integrated with a waveguide resonator in the form of a dual microdisk aligned in a parallel fashion. As the separation gap between the two microdisks is fixed at 15 µm, the ReRAM-mediated dual disk resonator would render a 180° phase reversal between the spectral outputs of the through-port and drop-port. If the gap is shortened to 10 and 5 µm, the expected phase reversal could also be retrieved due to the selective combinations of different memory states associated with each of the two ReRAM microdisks as witnessed by a series of characterization measurements.

A Gd-based borate-carbonate framework exhibiting a large magnetocaloric effect at a low magnetic field.

A 3D borate-carbonate framework, GdB(OH)4CO3 (1), was synthesized. Magnetic study reveals that its MCE is up to 33.5 J kg-1 K-1 at 2 K and 2 T, due to the introduction of a long magnetic exchange path of Gd-O-B-O-Gd leading to 1 exhibiting weak magnetic interaction.

Magnetocaloric Effect and Thermal Conductivity of a 3D Coordination Polymer of [Gd(HCOO)(C2O4)]n.

A 3D coordination polymer, [Gd(HCOO)(C2O4)]n was prepared. Its magnetocaloric effect (MCE) (32.7 J K-1 kg-1 at 2 K and 2 T) is significantly larger than that of commercial Gd3Ga5O12 (GGG) (14.6 J kg-1 K-1 at 2 K and 2 T), while its thermal conductivity (9.9 W m-1 K-1 at 3 K) is comparable to that of the commercial GGG (about 10 W m-1 K-1 at 3 K).

The emissions from co-firing of biomass and torrefied biomass with coal in a chain-grate steam boiler.

In this study, biomass of rice straw (RS) and wood (WD) and their torrefied biomass (RST and WDT) were used as solid biofuel (SBF) for co-firing individually with coal in a commercial continuous chain-grate steam boiler system, which was conducted at fixed input rate of heating value of mixture of SBF and coal and at fixed airflow rate. The effects of key system parameters on the gaseous and particulate pollutions and ash were examined. These include SBF type and blending ratio (RBL) of biomass (i.e., SBF) in the mixture of coal and biomass based on heating values for co-firing.The results indicated that wood, which possesses high heating value while less amount of ash, is more suitable for co-firing with coal than rice straw. Torrefaction can increase the heating value of biomass and homogenize its property, being beneficial to co-firing. Also, torrefaction can decompose the hydroxyl group of biomass, which makes biomass tending to possess hydrophobicity. This, in turn, helps the storage and transportation of biomass. Generally, adding the RS (with RBL = 5-10%), WD (2-15%), RST (2-10%) and WDT (2-20%), respectively, with coal decreases the emissions of NOx and SO2, but increases that of CO (except RST). The emission of HCl is little. The addition of biomass also increases the emission of fine particulate matters (PM) especially PM2.5 in the flue gases, raising PM2.5/PM100 from 34.87 to 78.35 wt.% (Case 50%WDT). These emissions for the Cases tested satisfy with Taiwanese emission standards of stationary sources which set limitations of NOx, SO2, CO and HCl < 350, 300, 2000 and 80 ppmv, while PM < 50 mg/m3, respectively. The results support the use of RS, WD, RST and WDT for co-firing with coal.Implications: This study examined the suitability of using solid bio-fuels to co-fire with coal in an industrial chain-grate steam boiler system with a capacity of 100 kW, in order to achieve carbon-free emissions. Both biomass and torrefied biomass of solid bio-fuel were tested. The findings would be useful for proper design and rational operation of solid bio-fuel/coal co-firing combustion matching the appeal of sustainable material management and circular economy of biomass, and of adaptation of global warming induced by greenhouse gases. It also provides information for policy-makers to promote the co-firing application of biomass and related bio-waste materials.

The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma.

Highly upregulated in liver cancer (HULC) is a long noncoding RNA (lncRNA), which has recently been identified as a key regulator in the progression of hepatocellular carcinoma, gliomas and gastric cancer. However, its role in epithelial ovarian carcinoma (EOC) remains unknown. In this study, HULC expression was examined in EOC, borderline and benign ovarian tumors, and normal ovarian tissues by RT-PCR. Ovarian cancer cell phenotypes, as well as autophagy-associated proteins were examined after HULC overexpression or downregulation by plasmid or small interfering RNA (siRNA) transfection, respectively. LncRNA-protein interactions were examined by ribonucleoprotein immunoprecipitation (RIP) assays. We found that HULC expression levels were higher in EOC tissues than normal samples. HULC overexpression induced cell proliferation, migration, invasion, whereas reduced cell apoptosis in vitro and induced tumor growth in vivo. In contrast, downregulation of HULC by siRNA transfection reduced cell proliferation, migration and invasion, and induced cell apoptosis and autophagy. Our results showed that HULC overexpression reduced ATG7, LC3-II and LAMP1 expression, while inducing SQSTM1 (P62) and ITGB1 expression. HULC downregulation had the opposite effects. Furthermore, RIP indicated that ATG7 interacted with HULC; ATG7 downregulation also induced cell proliferation, reduced apoptosis and inhibited autophagy in vitro by reducing LC3-II and LAMP1 expression, while inducing SQSTM1 expression. Furthermore, ATG7 co-transfection with HULC reversed the oncogenic effects of HULC both in vitro and in vivo; however, downregulating ATG7 did not affect cell migration and invasive ability. We found that ITGB1 siRNA co-transfection with HULC reversed the function of HULC in inducing ovarian cancer cell migration and invasive ability. Taken together, our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1.

The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression.

FOXA1 (forkhead box A1), a member of the FOXA transcription factor superfamily, plays an important role in tumor occurrence and development. However, the relationship between FOXA1 and ovarian cancer has not been reported. We examined normal ovarian tissue and ovarian cancer tissue and found increased FOXA1 expression in the cancer tissue. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays demonstrated that transfection with small interfering RNA to silence FOXA1 (si-FOXA1) in ovarian cancer cell lines decreased cell proliferation and induced apoptosis and S-phase arrest. In addition, si-FOXA1 transfection inhibited cell migration and invasion. Western blotting showed that si-FOXA1 transfection decreased the levels of YY1-associated protein 1, cyclin-dependent kinase 1, cyclin D1, phosphatidylinositol-3 kinase, E2F transcription factor 1, B-cell lymphoma 2, and vascular endothelial growth factor A protein. Based on these results, we suggest that FOXA1 plays a catalytic role in ovarian cancer pathogenesis and development by affecting the expression of the above-mentioned proteins.

E2F-1 targets miR-519d to regulate the expression of the ras homolog gene family member C.

E2F1 (E2F transcription factor 1) can act as a tumor suppressor or oncogene. We report the molecular mechanism of E2F1 in ovarian carcinoma tumorigenesis and progression. E2F1 expression levels in ovarian carcinoma tissue were examined by immunohistochemistry. After E2F1 plasmid transfection and E2F1-microRNA-519d (miR-519d)/si-RhoC (Ras homolog gene family member C) co-transfection, ovarian cancer cell phenotypes and the related molecules were examined in vitro and in vivo. E2F1 was overexpressed in type I and type II ovarian carcinoma as compared to normal ovary tissues and normal fallopian tube tissues, respectively. E2F1 overexpression promoted cell proliferation, G1-S progression, survival, migration, and invasion in vitro; miR-519d or siRhoC co-transfection reversed E2F1 oncogenic effects. E2F1 overexpression promoted tumor growth in vivo; miR-519d overexpression inhibited it. E2F1 overexpression increased RhoC, Bcl-2, cyclin D1, survivin, MMP2 (matrix metalloproteinase 2), MMP9, STAT3 (signal transducer and activator of transcription 3), and HuR (ELAV-like RNA-binding protein 1) expression; miR-519d overexpression decreased their expression. E2F1 downregulated miR-519d directly and miR-519d downregulated RhoC directly. Conversely, miR-519d directly downregulated E2F1, There is a direct repressive regulatory loop between E2F1 and miR-519d. We provide evidence that E2F1/miR-519d/RhoC is a promising signaling pathway for diagnosing and treating ovarian carcinoma.

The role of metastasis-associated in colon cancer 1 (MACC1) in endometrial carcinoma tumorigenesis and progression.

Metastasis-associated in colon cancer-1 (MACC1), has recently been identified as a key regulator in the progression of many cancers. However, its role in endometrial carcinoma (EC) remains unknown. MACC1 expression was determined in EC and normal endometrial tissues by immunohistochemistry. EC cell phenotypes and related molecules were examined after MACC1 downregulation by Small interfering RNA (siRNA) or microRNA (miRNA) transfection. We found that MACC1 was highly expressed in EC tissues than normal samples, and was significantly different in FIGO staging (I and II vs. III and IV), the depth of myometrial infiltration (<1/2 vs. ≥1/2), lymph nodes metastasis (negative vs. positive), besides, MACC1 overexpression was correlated with lower cumulative and relapse-free survival rate. MACC1 downregulation by siRNA transfection significantly induced G1 phrase arrest, suppressed EC cell proliferation, migration, and invasion. In addition, MACC1 downregulation also reduced expression of Cyclin D1 and Cyclin-dependent Kinase 2 (CDK2), N-cadherin (N-Ca), α-SMA, matrix metalloproteinase 2 (MMP2), and MMP9, but increased expression of E-cadherin (E-Ca). Bioinformatic predictions and dual-luciferase reporter assays indicate that MACC1 is a possible target of miR-23b. MiR-23b overexpression reduced MACC1 expression in vitro and induced G1 phrase arrest, suppressed cell proliferation, migration, and invasion. MiR-23b transfection also reduced Cyclin D1 and CDK2, N-Ca, α-SMA, MMP2, MMP9 expression, but increased E-Ca expression. Furthermore, the nude mouse xenograft assay showed that miR-23b overexpression suppressed tumour growth through downregulating MACC1 expression. Taken together, our results demonstrate for the first time that MACC1 may be a new and important diagnosis and therapeutic target of endometrial carcinoma.

MicroRNA-93 Promotes Epithelial-Mesenchymal Transition of Endometrial Carcinoma Cells.

MicroRNA-93, derived from a paralog (miR-106b-25) of the miR-17-92 cluster, is involved in the tumorigenesis and progression of many cancers such as breast, colorectal, hepatocellular, lung, ovarian, and pancreatic cancer. However, the role of miR-93 in endometrial carcinoma and the potential molecular mechanisms involved remain unknown. Our results showed that miR-93 was overexpressed in endometrial carcinoma tissues than normal endometrial tissues. The endometrial carcinoma cell lines HEC-1B and Ishikawa were transfected with miR-93-5P, after which cell migration and invasion ability and the expression of relevant molecules were detected. MiR-93 overexpression promoted cell migration and invasion, and downregulated E-cadherin expression while increasing N-cadherin expression. Dual-luciferase reporter assay showed that miR-93 may directly bind to the 3' untranslated region of forkhead box A1 (FOXA1); furthermore, miR-93 overexpression downregulated FOXA1 expression while miR-93 inhibitor transfection upregulated FOXA1 expression at both mRNA and protein level. In addition, transfection with the most effective FOXA1 small interfering RNA promoted both endometrial cancer cell migration and invasion, and downregulated E-cadherin expression while upregulating N-cadherin expression. Therefore, we suggest that miR-93 may promote the process of epithelial-mesenchymal transition in endometrial carcinoma cells by targeting FOXA1.

Role of glycogen synthase kinase-3ß inhibitor AZD1080 in ovarian cancer.

BACKGROUND: Glycogen synthase kinase-3ß (GSK-3ß) is a multifunctional serine/threonine kinase that plays an important role in cancer tumorigenesis and progression. We investigated the role of the GSK-3ß inhibitor AZD1080 in ovarian cancer cell lines. METHODS: A2780 and OVCAR3 ovarian cancer cell lines were exposed to AZD1080, after which cell proliferation, cell cycle, invasion, and migration assays were performed. Phalloidin staining was used to observe lamellipodia formation. Reverse transcription polymerase chain reaction and Western blot were used to assess the respective mRNA and protein expression levels of GSK-3ß, CDK2, CDK1, cyclin D1, matrix metalloproteinase-9 (MMP9), and Bcl-xL. RESULTS: AZD1080 exposure suppressed ovarian cancer cell proliferation, invasion, migration, and lamellipodia formation, and induced G1 arrest, which was concentration dependent. AZD1080 also significantly downregulated GSK-3ß, CDK2, CDK1, cyclin D1, MMP9, and Bcl-xL expression at both mRNA and protein levels. CONCLUSION: Taken together, our results demonstrate that the GSK-3ß inhibitor AZD1080 suppresses ovarian cancer development and therefore may indicate a new direction for ovarian cancer treatment.

The role of glycogen synthase kinase-3ß (GSK-3ß) in endometrial carcinoma: A carcinogenesis, progression, prognosis, and target therapy marker.

PURPOSE: Glycogen synthase kinase-3ß (GSK-3ß) is a serine/threonine kinase involved in cancer development. Herein, we demonstrated the role of GSK-3ß in endometrial cancer (EC) and identified new therapeutic targets. RESULTS: GSK-3ß was overexpressed in EC tissues, and was positively correlated with International Federation of Gynecology and Obstetrics (FIGO) staging, dedifferentiation, and myometrial infiltration depth. Besides, GSK-3ß overexpression predicted lower cumulative and relapse-free survival rate. si-GSK-3ß transfection suppressed cell proliferation, migration, invasion, and promoted cell apoptosis through downregulating NF-kB, Cyclin D1 and MMP9 expression whereas upregulating P21 expression. Bioinformatic predictions and dual-luciferase reporter assays showed that GSK-3ß was a possible target of miR-129. MiR-129 transfection reduced GSK-3ß expression, and exhibited the same trend as si-GSK-3ß transfection in cell function experiments. The nude mouse xenograft assay showed that miR-129 overexpression may suppress tumor growth through downregulating GSK-3ß expression. Further studies showed that AZD1080, a GSK-3ß inhibitor, could also inhibit EC cell proliferation, migration and invasion, while induced cell apoptosis through modulating relevant genes downstream of GSK-3ß signaling. EXPERIMENTAL DESIGN: GSK-3ß expression was determined in EC tissue and normal endometrial tissues by immunohistochemistry. After GSK-3ß down-regulation by si-GSK-3ß, microRNA-129 mimic transfection or GSK-3ß inhibitor exposure, EC cell phenotypes and related molecules were examined. CONCLUSIONS: Our results demonstrate for the first time that GSK-3ß may be a novel and important therapeutic target for the treatment of endometrial carcinoma. GSK-3ß inhibitor AZD1080 may be an effective drug for treating endometrial carcinoma.

MicroRNA-505 functions as a tumor suppressor in endometrial cancer by targeting TGF-α.

BACKGROUND: Endometrial carcinoma (EC) is one of the most lethal gynecologic cancers. Patients frequently have regional or distant metastasis at diagnosis. MicroRNAs are small non-coding RNAs that participate in numerous biological processes. Recent studies have demonstrated that miR-505 is associated with several types of cancer; however, the expression and function of miR-505 have not been investigated in EC. METHODS: miR-505 expression in normal endometrial tissue, endometrial carcinomas were quantified by Quantitative reverse transcription PCR. The endometrial carcinoma cell lines HEC-1B and Ishikawa were each transfected with miR-505 or scrambled mimics, after which cell phenotype and expression of relevant molecules were assayed. Dual-luciferase reporter assay and a xenograft mouse model were used to examine miR-505 and its target gene TGF-α. RESULTS: RT-PCR results demonstrated that miR-505 was significantly downregulated in human EC tissues compared to normal endometrial tissues. Besides, miR-505 expression was negatively associated with FIGO stage (stage I-II vs. III-IV), and lymph node metastasis (negative vs. positive). In vitro, overexpression of miR-505 significantly suppressed EC cell proliferation, increased apoptosis and reduced migratory and invasive activity. A miR-505 binding site was identified in the 3' untranslated region of TGF-α mRNA (TGFA) using miRNA target-detecting software; a dual luciferase reporter assay confirmed that miR-505 directly targets and regulates TGFA. RT-PCR and Western-blotting results indicated that overexpressing miR-505 reduced the expression of TGF-α and the TGF-α-regulated proteins MMP2, MMP9, CDK2, while induced Bax and cleaved-PARP expression in EC cells. In vivo, overexpression of miR-505 reduced the tumorigenicity and inhibited the growth of xenograft tumors in a mouse model of EC. CONCLUSIONS: Taken together, this study demonstrates that miR-505 acts as tumor suppressor in EC by regulating TGF-α.

The correlation between microRNA490-3p and TGFα in endometrial carcinoma tumorigenesis and progression.

MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate the translation of messenger RNAs by binding their 3'-untranslated region (3' UTR). MiR-490-3p has been reported to be a suppressor in various human cancers; however, little is known about the biological functions of miR-490-3p in endometrial cancer (EC). In our study, we found that MiR-490-3p mRNA expression was significantly lower in ECs than in normal endometrial tissues. MiR-490-3p mRNA expression was also negatively associated with depth of invasion (mucosa vs. muscular and serosa) and lymph node metastasis (negative vs. positive) in EC. MiR-490-3p overexpression reduced proliferation; promoted G1 arrest and apoptosis; suppressed migration and invasion; and reduced TGFα, NF-kB, cyclin D1, survivin, matrix metalloproteinase 2 (MMP2) mRNA and protein expression, and improved Bax mRNA and protein expression. The dual-luciferase reporter assay indicated that miR-490-3p directly targeted TGFα by binding its 3' untranslated region. MiR-490-3P transfection also suppressed tumor development and TGFα expression (as determined by immunohistochemistry and western blotting) in vivo in the xenograft mouse model. This is the first demonstration that miR-490-3P might act as a suppressor in EC tumorigenesis and progression by targeting TGFα. Our results provide a theoretical basis for the further study on the molecular target for endometrial cancer.

MicroRNA-372 inhibits endometrial carcinoma development by targeting the expression of the Ras homolog gene family member C (RhoC).

Here we explore the role of microRNA-372 (miR-372) in tumorigenesis and development of endometrial adenocarcinoma (EC) and analyze the underlying mechanism. We found that miR-372 expression is much lower in EC than normal endometrial specimens. Cell function experiments demonstrated that miR-372 overexpression suppressed cell proliferation, migration, and invasion, and led to a G1 phase arrest and promoted the apoptosis of endometrial carcinoma cells in vitro. The nude mouse xenograft assay demonstrated that miR-372 overexpression suppressed tumor growth. RT-PCR and Western blot assays detected the expression of known targets of miR-372 in other malignant tumors and found Cyclin A1 and Cyclin-dependent Kinase 2 (CDK2) was downregulated by miR-372. Bioinformatic predictions and dual-luciferase reporter assays found that RhoC was a possible target of miR-372. RT-PCR and Western blot assays demonstrated that miR-372 transfection reduced the expression of RhoC, matrix metalloproteinase 2 (MMP2) and MMP9, while it increased the expression of cleaved poly (ADP ribose) polymerase (PARP) and bcl-2-associated X protein (Bax). The cell function experiments that transfected siRNA with RhoC showed the same trend as those which were transfected with miR-372. Taken together, our results demonstrated for the first time that miR-372 suppresses tumorigenesis and the development of EC; RhoC is a new and potentially important therapeutic target.

MicroRNA-186 induces sensitivity of ovarian cancer cells to paclitaxel and cisplatin by targeting ABCB1.

BACKGROUND: Recent studies have shown that microRNAs may regulate the ABCB1 gene (ATP-binding cassette, sub-family B [MDR/TAP], member 1). Computational programs have predicted that the 3'-untranslated region (3'-UTR) of ABCB1 contains a potential miRNA-binding site for miR-186. Here, we investigated the role of miR-186 in sensitizing ovarian cancer cells to paclitaxel and cisplatin. RESULTS: Human ovarian carcinoma cell lines OVCAR3, A2780, A2780/DDP, and A2780/Taxol were exposed to paclitaxel or cisplatin with or without miR-186 transfection, and cell viability was determined by MTT assay. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis were used to assess the MDR1, GST-π, and MRP1 expression levels. Dual-luciferase reporter assay was used to reveal the correlation between miR-186 and ABCB1. Lower miR-186 while higher MDR1 and GST-π mRNA expression levels were found in the A2780/Taxol and A2780/DDP cells than in the A2780 cells. After miR-186 transfection, all the cell lines showed increased sensitivity to paclitaxel and cisplatin. MiR-186 transfection induced apoptosis while anti-miR-186 transfection reduced apoptosis. The dual-luciferase reporter assay verified that that miR-186 combined with the 3'-untranslated region (UTR) of ABCB1. MDR1 and GST-π mRNA and protein expression levels were downregulated after transfection with miR-186 but upregulated following anti-miR-186 transfection compared to the mock and negative control cancer cells; however, the MRP1 expression levels did not significantly differ among the groups. CONCLUSION: Our results are the first to demonstrate that miR-186 may sensitize ovarian cancer cell to paclitaxel and cisplatin by targeting ABCB1 and modulating the expression of GST-π.