Geometric Distribution Weight Information Modeled Using Radial Basis Function with Fractional Order for Linear Discriminant Analysis Method

Fisher linear discriminant analysis (FLDA) is a classic linear feature extraction and dimensionality reduction approach for face recognition. It is known that geometric distribution weight information of image data plays an important role in machine learning approaches. However, FLDA does not employ the geometric distribution weight information of facial images in the training stage. Hence, its recognition accuracy will be affected. In order to enhance the classification power of FLDA method, this paper utilizes radial basis function (RBF) with fractional order to model the geometric distribution weight information of the training samples and proposes a novel geometric distribution weight information based Fisher discriminant criterion. Subsequently, a geometric distribution weight information based LDA (GLDA) algorithm is developed and successfully applied to face recognition. Two publicly available face databases, namely, ORL and FERET databases, are selected for evaluation. Compared with some LDA-based algorithms, experimental results exhibit that our GLDA approach gives superior performance

Giα proteins exhibit functional differences in the activation of ERK1/2, Akt and mTORC1 by growth factors in normal and breast cancer cells

Background In a classic model, Giα proteins including Gi1α, Gi2α and Gi3α are important for transducing signals from Giα protein-coupled receptors (GiαPCRs) to their downstream cascades in response to hormones and neurotransmitters. Our previous study has suggested that Gi1α, Gi2α and Gi3α are also important for the activation of the PI3K/Akt/mTORC1 pathway by epidermal growth factor (EGF) and its family members. However, a genetic role of these Giα proteins in the activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) by EGF is largely unknown. Further, it is not clear whether these Giα proteins are also engaged in the activation of both the Akt/mTORC1 and ERK1/2 pathways by other growth factor family members. Additionally, a role of these Giα proteins in breast cancer remains to be elucidated. Results We found that Gi1/3 deficient MEFs with the low expression level of Gi2α showed defective ERK1/2 activation by EGFs, IGF-1 and insulin, and Akt and mTORC1 activation by EGFs and FGFs. Gi1/2/3 knockdown breast cancer cells exhibited a similar defect in the activations and a defect in in vitro growth and invasion. The Giα proteins associated with RTKs, Gab1, FRS2 and Shp2 in breast cancer cells and their ablation impaired Gab1’s interactions with Shp2 in response to EGF and IGF-1, or with FRS2 and Grb2 in response to bFGF. Conclusions Giα proteins differentially regulate the activation of Akt, mTORC1 and ERK1/2 by different families of growth factors. Giα proteins are important for breast cancer cell growth and invasion.Fil: Wang, Zhanwei. University of Hawaii Cancer Center. Honolulu; Estados UnidosFil: Dela Cruz, Rica. University of Hawaii Cancer Center. Honolulu; Estados UnidosFil: Ji, Fang. Shanghai Jiao Tong University . Sahnghai; ChinaFil: Guo, Sheng. University of Hawaii Cancer Center. Honolulu; Estados Unidos. Shanghai Jiaotong University. Shangha; Estados UnidosFil: Zhang, Jianhua. Shanghai Jiaotong University. Shangha; Estados Unidos. University of Hawaii Cancer Center. Honolulu; Estados UnidosFil: Wang, Ying. David Geffen School of Medicine at UCLA. Los Angeles; Estados UnidosFil: Feng, Gen-Sheng. University of California at San Diego; Estados UnidosFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institutes of Health; Estados UnidosFil: Jiang, Meisheng. David Geffen School of Medicine at UCLA. Los Angeles; Estados UnidosFil: Chu, Wen Ming. University of Hawaii Cancer Center. Honolulu; Estados Unido

Wafer-Size and Single-Crystal MoSe_2 Atomically Thin Films Grown on GaN Substrate for Light Emission and Harvesting

Two-dimensional (2D) atomic-layered semiconductors are important for next-generation electronics and optoelectronics. Here, we designed the growth of an MoSe_2 atomic layer on a lattice-matched GaN semiconductor substrate. The results demonstrated that the MoSe_2 films were less than three atomic layers thick and were single crystalline of MoSe_2 over the entire GaN substrate. The ultrathin MoSe_2/GaN heterojunction diode demonstrated ∼850 nm light emission and could also be used in photovoltaic applications

Host-Guest Complexation of Amphiphilic Molecules at the Air-Water Interface Prevents Oxidation by Hydroxyl Radicals and Singlet Oxygen

The oxidation of antioxidants by oxidizers imposes great challenges to both living organisms and the food industry. Here we show that the host–guest complexation of the carefully designed, positively charged, amphiphilic guanidinocalix[5]arene pentadodecyl ether (GC5A‐12C) and negatively charged oleic acid (OA), a well‐known cell membrane antioxidant, prevents the oxidation of the complex monolayers at the air–water interface from two potent oxidizers hydroxyl radicals (OH) and singlet delta oxygen (SDO). OH is generated from the gas phase and attacks from the top of the monolayer, while SDO is generated inside the monolayer and attacks amphiphiles from a lateral direction. Field‐induced droplet ionization mass spectrometry results have demonstrated that the host–guest complexation achieves steric shielding and prevents both types of oxidation as a result of the tight and “sleeved in” physical arrangement, rather than the chemical reactivity, of the complexes

Host-Guest Complexation of Amphiphilic Molecules at the Air-Water Interface Prevents Oxidation by Hydroxyl Radicals and Singlet Oxygen

The oxidation of antioxidants by oxidizers imposes great challenges to both living organisms and the food industry. Here we show that the host–guest complexation of the carefully designed, positively charged, amphiphilic guanidinocalix[5]arene pentadodecyl ether (GC5A‐12C) and negatively charged oleic acid (OA), a well‐known cell membrane antioxidant, prevents the oxidation of the complex monolayers at the air–water interface from two potent oxidizers hydroxyl radicals (OH) and singlet delta oxygen (SDO). OH is generated from the gas phase and attacks from the top of the monolayer, while SDO is generated inside the monolayer and attacks amphiphiles from a lateral direction. Field‐induced droplet ionization mass spectrometry results have demonstrated that the host–guest complexation achieves steric shielding and prevents both types of oxidation as a result of the tight and “sleeved in” physical arrangement, rather than the chemical reactivity, of the complexes

Electroacupuncture of 2 Hz Has a Rewarding Effect: Evidence from a Conditioned Place Preference Study in Rats

Electroacupuncture (EA) has been used to suppress heroin craving in addicts and the conditioned place preference (CPP) for morphine in the rat. The question remained whether EA by itself will produce some rewarding effect. This was investigated using the CPP procedure in the present study. The results indicated that rats showed a significant preference to the 2 Hz EA-paired compartment. This rewarding effect of EA was prevented by pre-treatment with the opioid receptor antagonist naloxone [2 mg kg−1, intraperitoneally (i.p.)], CB1 cannabinoid antagonist AM251 (3 μg per rat, intracerebroventricularly) or D1 dopamine receptor antagonist SCH23390 (0.1 mg kg−1, i.p.), respectively. TempspacetempspaceIt is concluded that 2 Hz EA is capable of inducing CPP in the rat via the activation of the endogenous opioid-, cannabinoid- and dopamine-systems

Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma

<p>Abstract</p> <p>Background</p> <p>Downregulation of the putative tumor suppressor gene <it>SLC22A18 </it>has been reported in a number of human cancers. The aim of this study was to investigate the relationship between <it>SLC22A18 </it>downregulation, promoter methylation and the development and progression of human glioma.</p> <p>Method</p> <p><it>SLC22A18 </it>expression and promoter methylation was examined in human gliomas and the adjacent normal tissues. U251 glioma cells stably overexpressing <it>SLC22A18 </it>were generated to investigate the effect of <it>SLC22A18 </it>on cell growth and adherence <it>in vitro </it>using the methyl thiazole tetrazolium assay. Apoptosis was quantified using flow cytometry and the growth of <it>SLC22A18 </it>overexpressing U251 cells was measured in an <it>in viv</it>o xenograft model.</p> <p>Results</p> <p><it>SLC22A18 </it>protein expression is significantly decreased in human gliomas compared to the adjacent normal brain tissues. <it>SLC22A18 </it>protein expression is significantly lower in gliomas which recurred within six months after surgery than gliomas which did not recur within six months. <it>SLC22A18 </it>promoter methylation was detected in 50% of the gliomas, but not in the adjacent normal tissues of any patient. SLC22A18 expression was significantly decreased in gliomas with <it>SLC22A18 </it>promoter methylation, compared to gliomas without methylation. The <it>SLC22A18 </it>promoter is methylated in U251 cells and treatment with the demethylating agent 5-aza-2-deoxycytidine increased <it>SLC22A18 </it>expression and reduced cell proliferation. Stable overexpression of <it>SLC22A18 </it>inhibited growth and adherence, induced apoptosis <it>in vitro </it>and reduced <it>in vivo </it>tumor growth of U251 cells.</p> <p>Conclusion</p> <p><it>SLC22A18 </it>downregulation via promoter methylation is associated with the development and progression of glioma, suggesting that <it>SLC22A18 </it>is an important tumor suppressor in glioma.</p