Structural Insights into the Niemann-Pick C1 (NPC1)-Mediated Cholesterol Transfer and Ebola Infection.

Niemann-Pick disease type C (NPC) is associated with mutations in NPC1 and NPC2, whose gene products are key players in the endosomal/lysosomal egress of low-density lipoprotein-derived cholesterol. NPC1 is also the intracellular receptor for Ebola virus (EBOV). Here, we present a 4.4 Å structure of full-length human NPC1 and a low-resolution reconstruction of NPC1 in complex with the cleaved glycoprotein (GPcl) of EBOV, both determined by single-particle electron cryomicroscopy. NPC1 contains 13 transmembrane segments (TMs) and three distinct lumenal domains A (also designated NTD), C, and I. TMs 2-13 exhibit a typical resistance-nodulation-cell division fold, among which TMs 3-7 constitute the sterol-sensing domain conserved in several proteins involved in cholesterol metabolism and signaling. A trimeric EBOV-GPcl binds to one NPC1 monomer through the domain C. Our structural and biochemical characterizations provide an important framework for mechanistic understanding of NPC1-mediated intracellular cholesterol trafficking and Ebola virus infection.

A Coordination Polymer for the Fluorescence Turn-On Sensing of Saccharin, 2-Thiazolidinethione-4-carboxylic Acid, and Periodate.

A luminescent 1D coordination polymer (CP) [Zn2L2(H2O)4]·H2O (1, H2L = 1-(4-carboxyphenyl)-1H-pyrazole-3-carboxylic acid) was prepared by a solvothermal method. 1 shows excellent fluorescence properties and has an obvious fluorescence "turn-on" phenomenon for saccharin (SAC), 2-thiazolidinethione-4-carboxylic acid (TTCA), and periodate (IO4-). Between 0 and 60 µM concentration range of SAC, the fluorescence enhancement efficiency (KEC) of 1 reaches 1.00 × 105 M-1 with the limit of detection (LOD) of 90 nM. 1 is the first CP-based sensing material for SAC detection. For TTCA detection, the KEC is 2.73 × 105 M-1 at the 25-80 µM concentration range, and the LOD is 33 nM, the lowest LOD among the sensors that detect TTCA at present. For IO4- ion detection, when the IO4- ion concentration ranges from 0 to 10 µM, the KEC is 2.34 × 105 M-1 and the LOD is as low as 39 nM. In order to better understand the sensing phenomenon, we also discuss in detail the sensing mechanisms for SAC, TTCA, and IO4- ions.

Blocking Osa-miR1871 enhances rice resistance against Magnaporthe oryzae and yield.

MicroRNAs (miRNAs) play vital roles in plant development and defence responses against various stresses. Here, we show that blocking miR1871 improves rice resistance against Magnaporthe oryzae and enhances grain yield simultaneously. The transgenic lines overexpressing miR1871 (OX1871) exhibit compromised resistance, suppressed defence responses and reduced panicle number resulting in slightly decreased yield. In contrast, the transgenic lines blocking miR1871 (MIM1871) show improved resistance, enhanced defence responses and significantly increased panicle number leading to enhanced yield per plant. The RNA-seq assay and defence response assays reveal that blocking miR1871 resulted in the enhancement of PAMP-triggered immunity (PTI). Intriguingly, miR1871 suppresses the expression of LOC_Os06g22850, which encodes a microfibrillar-associated protein (MFAP1) locating nearby the cell wall and positively regulating PTI responses. The mutants of MFAP1 resemble the phenotype of OX1871. Conversely, the transgenic lines overexpressing MFAP1 (OXMFAP1) or overexpressing both MFAP1 and miR1871 (OXMFAP1/OX1871) resemble the resistance of MIM1871. The time-course experiment data reveal that the expression of miR1871 and MFAP1 in rice leaves, panicles and basal internode is dynamic during the whole growth period to manipulate the resistance and yield traits. Our results suggest that miR1871 regulates rice yield and immunity via MFAP1, and the miR8171-MFAP1 module could be used in rice breeding to improve both immunity and yield.

Osa-miR160a confers broad-spectrum resistance to fungal and bacterial pathogens in rice.

Rice production is threatened by multiple pathogens. Breeding cultivars with broad-spectrum disease resistance is necessary to maintain and improve crop production. Previously we found that overexpression of miR160a enhanced rice blast disease resistance. However, it is unclear whether miR160a also regulates resistance against other pathogens, and what the downstream signaling pathways are. Here, we demonstrate that miR160a positively regulates broad-spectrum resistance against the causative agents of blast, leaf blight and sheath blight in rice. Mutations of miR160a-targeted Auxin Response Factors result in different alteration of resistance conferred by miR160a. miR160a enhances disease resistance partially by suppressing ARF8, as mutation of ARF8 in MIM160 background partially restores the compromised resistance resulting from MIM160. ARF8 protein binds directly to the promoter and suppresses the expression of WRKY45, which acts as a positive regulator of rice immunity. Mutation of WRKY45 compromises the enhanced blast resistance and bacterial leaf blight resistance conferred by arf8 mutant. Overall, our results reveal that a microRNA coordinates rice broad-spectrum disease resistance by suppressing multiple target genes that play different roles in disease resistance, and uncover a new regulatory pathway mediated by the miR160a-ARF8 module. These findings provide new resources to potentially improve disease resistance for breeding in rice.

Suppression of high-fat-diet-induced obesity in mice by dietary folic acid supplementation is linked to changes in gut microbiota.

PURPOSE: To investigate whether the effects of dietary folic acid supplementation on body weight gain are mediated by gut microbiota in obesity. METHODS: Male C57 BL/6J conventional (CV) and germ-free (GF) mice both aged three to four weeks were fed a high-fat diet (HD), folic acid-deficient HD (FD-HD), folic acid-supplement HD (FS-HD) and a normal-fat diet (ND) for 25 weeks. Faecal microbiota were analyzed by 16S rRNA high-throughput sequencing, and the mRNA expression of genes was determined by the real-time RT-PCR. Short-chain fatty acids (SCFAs) in faeces and plasma were measured using gas chromatography-mass spectrometry. RESULTS: In CV mice, HD-induced body weight gain was inhibited by FS-HD, accompanied by declined energy intake, smaller white adipocyte size, and less whitening of brown adipose tissue. Meanwhile, the HD-induced disturbance in the expression of fat and energy metabolism-associated genes (Fas, Atgl, Hsl, Ppar-α, adiponectin, resistin, Ucp2, etc.) in epididymal fat was diminished, and the dysbiosis in faecal microbiota was lessened, by FS-HD. However, in GF mice with HD feeding, dietary folic acid supplementation had almost no effect on body weight gain and the expression of fat- and energy-associated genes. Faecal or plasma SCFA concentrations in CV and GF mice were not altered by either FD-HD or FS-HD feeding. CONCLUSION: Dietary folic acid supplementation differently affected body weight gain and associated genes' expression under HD feeding between CV and GF mice, suggesting that gut bacteria might partially share the responsibility for beneficial effects of dietary folate on obesity.

Synthesis of mesoporous-structured MIL-68(Al)/MCM-41-NH2 for methyl orange adsorption: Optimization and Selectivity.

Here, we report a novel amino-modified mesoporous-structured aluminum-based metal-organic framework adsorbent, MIL-68(Al)/MCM-41-NH2, for dye sewage treatment. The introduction of molecular sieves overcomes the inherent defects of microporous MOFs in contaminant transfer and provides more active sites to enhance adsorption efficiency. Compared with using organic amino ligands directly, this strategy is ten times cheaper. The composite was well characterized and analyzed in terms of morphology, structure and chemical composition. Batch experiments were carried out to study the influences of essential factors on the process, such as pH and temperature. In addition, their interactions and the optimum conditions were examined using response surface methodology (RSM). The adsorption kinetics, isotherms and thermodynamics were systematically elucidated. In detail, the adsorption process conforms to pseudo-second-order kinetics and follows the Sips and Freundlich isothermal models. Moreover, the maximum adsorption capacity Qs of methyl orange (MO) was 477 mg g-1. It could be concluded that the process was spontaneous, exothermic, and entropy-reducing. Several binary dye systems have been designed for selective adsorption research. Our material has an affinity for anionic pigments. The adsorption mechanisms were discussed in depth. The electrostatic interaction might be the dominant effect. Meanwhile, hydrogen bonding, π-π stacking, and pore filling might be important driving forces. The excellent thermal stability and recyclability of the adsorbent are readily noticed. After five reuse cycles, the composite still possesses a removal efficiency of 90% for MO. Overall, the efficient and low-cost composite can be regarded as a promising adsorbent for the selective adsorption of anionic dyes from wastewater.

Anthracene-Based Lanthanide Coordination Polymer: Structure, Luminescence, and Detections of UO22+, PO43-, and 2-Thiazolidinethione-4-carboxylic Acid in Water.

By the solvothermal assembly of Gd3+ and 5,5'-(anthracene-9,10-diyl)diisophthalic acid (H4adip), an anthracene-based lanthanide coordination polymer (CP), [Gd2(adip)(H2adip)(NMP)2]·DMF·3H2O (1; NMP = N-methylpyrrolidone; DMF = N,N-dimethylformamide), has been prepared. It possesses a 3D framework and a strong ligand-based blue emission. 1 could be applied as a multifunctional chemical sensor for UO22+, PO43-, and 2-thiazolidinethione-4-carboxylic acid (TTCA) with excellent selectivity, sensitivity, and anti-interference. In the 0-20 µM concentration range of UO22+, the quenching constant (KSV) is 4.05 × 104 M-1 with a detection limit of 1.42 µM. Fluorescence enhancement was observed when PO43- was added to the 1-H2O suspension. The slope of the linear relationship between the PO43- concentration in the 0-35 µM concentration range and I/I0 is 3.70 × 104 M-1 with a detection limit of 1.55 µM. When the TTCA concentration is lower than 20 µM, the fluorescence quenching constant KSV is 1.77 × 104 M-1 with a detection limit of 3.25 µM, which approaches the values reported of the best CP-based sensing materials for TTCA up to now. Moreover, the fluorescence quenching or enhancement mechanism was also investigated.

Effects of High Intensity Ultrasound on Physiochemical and Structural Properties of Goat Milk ß-Lactoglobulin.

This study aimed to compare the effects of high intensity ultrasound (HIU) applied at various amplitudes (20~40%) and for different durations (1~10 min) on the physiochemical and structural properties of goat milk ß-lactoglobulin. No significant change was observed in the protein electrophoretic patterns by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Deconvolution and second derivative of the Fourier transform infrared spectra (FTIR) showed that the percentage of ß-sheet of goat milk ß-lactoglobulin was significantly decreased while those of α-helix and random coils increased after HIU treatment The surface hydrophobicity index and intrinsic fluorescence intensity of samples was enhanced and increased with increasing HIU amplitude or time. Differential scanning calorimetry (DSC) results exhibited that HIU treatments improved the thermal stability of goat milk ß-lactoglobulin. Transmission electron microscopy (TEM) of samples showed that the goat milk ß-lactoglobulin microstructure had changed and it contained larger aggregates when compared with the untreated goat milk ß-lactoglobulin sample. Data suggested that HIU treatments resulted in secondary and tertiary structural changes of goat milk ß-lactoglobulin and improved its thermal stability.

The important role of connexin 43 in subarachnoid hemorrhage-induced cerebral vasospasm.

BACKGROUND: Gap junctions are involved in the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). However, the specific roles and regulatory functions of related connexin isoforms remain unknown. The aim of this study was to investigate the importance of connexin 43 (Cx43) in CVS and determine whether Cx43 alterations are modulated via the protein kinase C (PKC) signaling transduction pathway. METHODS: Oxyhemoglobin (OxyHb)-induced smooth muscle cells of basilar arterial and second-injection model in rat were used as CVS models in vitro and in vivo. In addition, dye transfer assays were used for gap junction-mediated intercellular communication (GJIC) observation in vitro and delayed cerebral ischemia (DCI) was observed in vivo by perfusion-weighted imaging (PWI) and intravital fluorescence microscopy. RESULTS: Increase in Cx43 mediated the development of SAH-induced CVS was found in both in vitro and in vivo CVS models. Enhanced GJIC was observed in vitro CVS model, this effect and increased Cx43 were reversed by preincubation with specific PKC inhibitors (chelerythrine or GF 109203X). DCI was observed in vivo on day 7 after SAH. However, DCI was attenuated by pretreatment with Cx43 siRNA or PKC inhibitors, and the increased Cx43 expression in vivo was also reversed by Cx43 siRNA or PKC inhibitors. CONCLUSIONS: These data provide strong evidence that Cx43 plays an important role in CVS and indicate that changes in Cx43 expression may be mediated by the PKC pathway. The current findings suggest that Cx43 and the PKC pathway are novel targets for developing treatments for SAH-induced CVS.

Interactions between ß-Lactoglobulin and 3,3'-Diindolylmethane in Model System.

The compound 3,3'-diindolylmethane (DIM) has a broad spectrum of anticancer activities. However, low stability and bioavailability limit its application. Elucidating interactions between DIM and ß-lactoglobulin (ß-LG) may be useful for fabricating whey protein-based protecting systems. Interaction with DIM increased the diameter and absolute zeta potential value of ß-LG. UV-absorption spectra suggested that there was a complex of DIM and ß-LG. ß-LG showed enhanced fluorescence intensity by complexing with DIM with a binding constant of 6.7 × 105 M-1. Upon interaction with DIM, ß-LG was decreased in secondary structure content of helix and turn while increased in ß-sheet and unordered. FT-IR spectra and molecular docking results indicated the roles of hydrophobic interaction and hydrogen bond for the formation of DIM and ß-LG nanocomplexes. Data suggested that ß-LG may be a good vehicle for making a protein-based DIM protection and delivery system due to the tight binding of DIM to ß-LG.

MIIP haploinsufficiency induces chromosomal instability and promotes tumour progression in colorectal cancer.

The gene encoding migration and invasion inhibitory protein (MIIP), located on 1p36.22, is a potential tumour suppressor gene in glioma. In this study, we aimed to explore the role and mechanism of action of MIIP in colorectal cancer (CRC). MIIP protein expression gradually decreased along the colorectal adenoma-carcinoma sequence and was negatively correlated with lymph node and distant metastasis in 526 colorectal tissue samples (p < 0.05 for all). Analysis of The Cancer Genome Atlas (TCGA) data showed that decreased MIIP expression was significantly associated with MIIP hemizygous deletion (p = 0.0005), which was detected in 27.7% (52/188) of CRC cases, and associated with lymph node and distant metastasis (p < 0.05 for both). We deleted one copy of the MIIP gene in HCT116 CRC cells using zinc finger nuclease technology and demonstrated that MIIP haploinsufficiency resulted in increased colony formation and cell migration and invasion, which was consistent with the results from siRNA-mediated MIIP knockdown in two CRC cell lines (p < 0.05 for all). Moreover, MIIP haploinsufficiency promoted CRC progression in vivo (p < 0.05). Genomic instability and spectral karyotyping assays demonstrated that MIIP haploinsufficiency induced chromosomal instability (CIN). Besides modulating the downstream proteins of APC/CCdc20 , securin and cyclin B1, MIIP haploinsufficiency inhibited topoisomerase II (Topo II) activity and induced chromosomal missegregation. Therefore, we report that MIIP is a novel potential tumour suppressor gene in CRC. Moreover, we characterized the MIIP gene as a novel CIN suppressor gene, through altering the stability of mitotic checkpoint proteins and disturbing Topo II activity. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

The Selection of Time Interval Between Surgery and Adjuvant Therapy in Early Stage Cervical Cancer.

OBJECTIVES: The optimal interval between surgery and adjuvant treatment has not yet been found in cervical cancer. And whether patients with different FIGO stage should choose different interval is unknown. The purpose of this study was to evaluate whether interval has a different effect on oncologic outcome for patients with different tumor stages. METHODS: We performed a retrospective study of 226 cervical cancer patients who were treated by surgery and adjuvant therapy from May 2005 to August 2015. All patients were divided into 2 groups according to the interval of 5 weeks. Overall survival (OS) and disease-free survival (DFS) were compared between patients with interval shorter and longer than 5 weeks in the whole group and subgroups. Recurrence patterns were also analyzed. Multivariate analysis was performed to explore clinical factors significantly associated with DFS, local recurrence-free survival and distant metastasis-free survival for patients with stage IB2-IIA. RESULTS: For patients with stage IA2-IB1, the 5-year OS and DFS were similar between groups of short and long interval with also the comparable results of local and distant failure. For patients with IB2-IIA, both the OS and DFS in the short-interval group were higher than that in the long-interval group. Besides, the rates of local recurrence were found higher in the group of long interval compared with short interval. Multivariable analysis indicated that time interval was an independent predictor of DFS and local recurrence-free survival for patients with stage IB2-IIA. CONCLUSIONS: In cervical cancer patients, time interval between surgery and adjuvant therapy may have different effects on the prognosis in different FIGO stages.

Genomically amplified Akt3 activates DNA repair pathway and promotes glioma progression.

Akt is a robust oncogene that plays key roles in the development and progression of many cancers, including glioma. We evaluated the differential propensities of the Akt isoforms toward progression in the well-characterized RCAS/Ntv-a mouse model of PDGFB-driven low grade glioma. A constitutively active myristoylated form of Akt1 did not induce high-grade glioma (HGG). In stark contrast, Akt2 and Akt3 showed strong progression potential with 78% and 97% of tumors diagnosed as HGG, respectively. We further revealed that significant variations in polarity and hydropathy values among the Akt isoforms in both the pleckstrin homology domain (P domain) and regulatory domain (R domain) were critical in mediating glioma progression. Gene expression profiles from representative Akt-derived tumors indicated dominant and distinct roles for Akt3, consisting primarily of DNA repair pathways. TCGA data from human GBM closely reflected the DNA repair function, as Akt3 was significantly correlated with a 76-gene signature DNA repair panel. Consistently, compared with Akt1 and Akt2 overexpression models, Akt3-expressing human GBM cells had enhanced activation of DNA repair proteins, leading to increased DNA repair and subsequent resistance to radiation and temozolomide. Given the wide range of Akt3-amplified cancers, Akt3 may represent a key resistance factor.

Compact broadband spectrometer based on upconversion and downconversion luminescence.

In this Letter, a compact spectrometer based on upconversion and downconversion luminescence for operation in the infrared, visible, and ultraviolet bands is presented. The proposed spectrometer has three components that are used for dispersion, frequency conversion, and detection. The conversion component converts the incident signal beam into a spectral window appropriate for the detection component. The detection component images the speckle pattern generated by scattering or diffraction in the random structure of the dispersion component. With the two-dimensional intensity data captured from both the speckle pattern and a calibration measurement process, one can reconstruct the spectra of the signal beam by solving a matrix equation. A smoothing simulated annealing algorithm has been implemented to improve the accuracy of the spectral reconstruction. We have analyzed possible sources of error in the algorithm and the corresponding limits of operation. The reported broadband, compact, high-resolution, luminescence-based spectrometer is well suited for portable spectroscopy applications.

Metallothionein 1H (MT1H) functions as a tumor suppressor in hepatocellular carcinoma through regulating Wnt/ß-catenin signaling pathway.

BACKGROUND: Metallothionein 1H (MT1H) expression level is downregulated in several kinds of tumors, including hepatocellular cancer (HCC). However, its biological functions and underlying mechanisms in HCC is largely unknown. The current study aimed to demonstrate the expression status, biological roles and potential mechanisms of MT1H in HCC. METHODS: We investigated the expression level of MT1H in the Cancer Genome Atlas (TCGA) dataset and a panel of 12 paired tumor/non-tumor tissues. In vitro, gain-of-function experiments were performed to examine the role of MT1H on HCC cell proliferation, invasion, and migration. Using bioinformatics assay, reporter assays, quantitative real-time PCR, and western blotting, we explored the possible mechanisms underlying the role of MT1H in HCC cells. In vivo nude mice experiments were performed to assess the anti-proliferative role of MT1H in HCC. RESULTS: Downregulation of MT1H was observed in TCGA dataset and a panel of 12 paired tumor/non-tumor tissues. Ectopic overexpression of MT1H in HepG2 and Hep3B cells inhibited cell proliferation, invasion, and migration. Gene Set Enrichment Analysis (GSEA) showed that MT1H might involve in regulation of Wnt/ß-catenin pathway. Top/Fop reporter assay confirmed that MT1H had an effect on Wnt/ß-catenin signaling. Real-time PCR showed MT1H expression decreased the expression of Wnt/ß-catenin target genes. Western blotting assay showed that overexpression of MT1H inhibited the nuclear translocation of ß-catenin and that the Akt/GSK-3ß axis mediated the modulatory role of MT1H on Wnt/ß-catenin signaling in HCC. In vivo nude mice experiments demonstrated that MT1H suppressed the proliferation of HCC cells. Taken together, MT1H suppressed the proliferation, invasion and migration of HCC cells via regulating Wnt/ß-catenin signaling pathway. CONCLUSIONS: This study demonstrated that through inhibiting Wnt/ß-catenin pathway, MT1H suppresses the proliferation and invasion of HCC cells. MT1H may be a potential target for HCC therapy.

Intrinsic Kinetics of Dimethyl Ether Synthesis from Plasma Activation of CO2 Hydrogenation over Cu-Fe-Ce/HZSM-5.

CO2 is activated in a plasma reactor followed by hydrogenation over a Cu-Fe-Ce/HZSM-5 catalyst, and the intrinsic kinetics of the plasma catalytic process are studied. Compared with CO2 hydrogenation using Cu-Fe-Ce/HZSM-5 alone, the CO2 conversion and the dimethyl ether selectivity for the plasma catalytic process are increased by 16.3 %, and 10.1 %, respectively, indicating that the CO2 was activated by the plasma to promote hydrogenation. A study of the intrinsic kinetics shows that the activation energies of methanol formation, the reverse water-gas shift reaction, and methanol dehydration to dimethyl ether are 149.34, 75.47, and 73.18 kJ mol-1 , respectively, which are lower than if Cu-Fe-Ce/HZSM-5 is used without plasma, indicating that the activation of CO2 in the plasma reduces the activation energy of the hydrogenation reaction and improves the yield of dimethyl ether.

Glioma progression is mediated by an addiction to aberrant IGFBP2 expression and can be blocked using anti-IGFBP2 strategies.

Insulin-like growth factor binding protein 2 (IGFBP2) overexpression is common in high-grade glioma and is both a strong biomarker of aggressive behaviour and a well-documented prognostic factor. IGFBP2 is a member of the secreted IGFBP family that functions by interacting with circulating IGFs to modulate IGF-mediated signalling. This traditional view of IGFBP2 activities has been challenged by the recognition of the diverse functions and cellular locations of members of the IGFBP family. IGFBP2 has been previously established as a driver of glioma progression to a higher grade. In this study, we sought to determine whether IGFBP2-overexpressing tumours are dependent on continued oncogene expression and whether IGFBP2 is a viable therapeutic target in glioma. We took advantage of the well-characterized RCAS/Ntv-a mouse model to create a doxycycline-inducible IGFBP2 model of glioma and demonstrated that the temporal expression of IGFBP2 has dramatic impacts on tumour progression and survival. Further, we demonstrated that IGFBP2-driven tumours are dependent on the continued expression of IGFBP2, as withdrawal of this oncogenic signal led to a significant decrease in tumour progression and prolonged survival. Inhibition of IGFBP2 also impaired tumour cell spread. To assess a therapeutically relevant inhibition strategy, we evaluated a neutralizing antibody against IGFBP2 and demonstrated that it impaired downstream IGFBP2-mediated oncogenic signalling pathways. The studies presented here indicate that IGFBP2 not only is a driver of glioma progression and a prognostic factor but is also required for tumour maintenance and thus represents a viable therapeutic target in the treatment of glioma. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Detection of defects on the surface of a semiconductor by terahertz surface plasmon polaritons.

We propose a new method for detecting small defects on the surface of a semiconductor by analyzing the transmission spectrum of terahertz surface plasmon polaritons. The field distributions caused by the detection of defects of different sizes are simulated. Experimentally, using a terahertz time domain spectrometer, we measure the transmission spectrum of terahertz surface plasmon polaritons passing through particles on the surface of an intrinsic InSb wafer. Our results show that the measured temporal waveform and frequency spectra are distinctly changed due to the presence of the particles, thereby confirming the effectiveness of this method for detecting defects. For increased detection efficiency, the frequency of the surface plasmon polaritons has to be slightly lower than the plasma frequency of the semiconductor. In comparison with traditional methods, our approach offers the merits of detecting both on-surface and subsurface defects, which is critical in monitoring the quality of semiconductor wafers.

Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer.

OBJECTIVES: Cervical cancer is one of the most common gynecologic malignant tumors. Propofol has been proposed to play a role of antitumor in various cancers. However, the functions and mechanisms of Propofol in cervical cancer is still not clear. METHODS: In vitro, the different concentrations of propofol were co-incubated with cervical cancer cell lines, including Hela, Caski and C-33A cells respectively. The pcDNA-HOTAIR plasmid was transfected into cells after the treatment of 10 µg/ml propofol. The cell viability and apoptosis were detected by MTT assay and TUNEL method. In vivo, propofol was injected into mice of transplantation tumor with Caski cells or with pcDNA-HOTAIR treated Caski cells. RESULTS: Propofol significantly decreased the cell viability and increased the cell apoptosis in Hela, Caski and C-33A cells, while HOTAIR overexpression promoted cell viability and inhibits cell apoptosis. mTOR/p70S6K protein expression levels were also markedly reduced by propofol but the effects were reversed with pcDNA-HOTAIR. In vivo, propofol inhibited the tumor size but had no inhibition effect in HOTAIR overexpression group. CONCLUSION: Propofol inhibited tumor size, cell viability and promoted cell apoptosis via inhibiting mTOR/p70S6K pathway mediated by HOTAIR in cervical cancer.

Miniature spectrometer based on diffraction in a dispersive hole array.

We present an ultra-compact spectrometer that uses a 10×10 hole array as the dispersive component. Our analysis shows that the two-dimensional intensity distribution can be modeled by a system of simultaneous linear equations when the size of each hole in the dispersive component has been pre-designed appropriately. One can readily recover the spectral contents of the input radiation by solving the linear equation system with regularized procedure. Experimental results show that the reconstruction range is at least within the entire visible band, which can be further extended if a near-infrared CCD is used. One therefore envisions strong potential for many wavelength analysis applications.