Design Broad Bandwidth Microwave Bandpass Filter Of 10 Ghz Operating Frequency Using HFSS

Microwave bandpass filter is the essential part in microwave circuits and wireless communication systems. This paper presents a new designing and simulation of broad bandwidth,low losses microwave bandpass filter operating at 10 GHz frequency using return loss method. The designing and simulation of the circuit has been carried out using Computer Aid Design (CAD) Ansoft HFSS software purchase from Ansys. The microwave filter circuit has designed with a parallel coupled line having a small dimension (10 × 10 mm2) of LaAlO3 substrate. The microwave circuit showed a high return loss -20 dB, broad bandwidth of 1.5 GHz, and operating frequency at 10 GHz. The results indicate the filter design and simulation using HFSS is reliable and have the opportunity to transfer from lab potential experiments to industry

Job Opportunities in Material(s) Technology

Materials are substances of universe which have properties that make them useful in structures, machines, devices, products, and systems. There are three closely connected areas of study related to materials, namely material(s) technology, materials engineering and materials science. Material(s) technology is a relatively comprehensive discipline that begins with the production of goods from raw materials to processing of materials into the shapes and forms needed for specific applications. Material(s) technologists work with materials such as metals, plastics, rubbers and ceramics. They study how the composition, structure, processing, and application of these materials, are inter-related

Impact of increasing dietary oil concentrations with a constant energy level on the tolerance of broiler chickens to a high ambient temperature

Broiler males (n= 140) were used in a straight-run experimental design and distributed randomly among four treatment groups with seven replicates per treatment and five broilers per replicate. During 21–42 d old, the chickens were fed iso-caloric and iso-nitrogenous diets containing four levels of dietary vegetable oils (DVO), of 2.7, 4, 6 and 8%. During d 25–27, 31–33, and 38–40 of age, broilers were exposed to heat stress for 4 h a day (1000–1400 h) at 34 ºC, 70–75 % relative humidity. Feeding an 8% DVO diet significantly increased body weight gain compared to the other DVO levels. The feed conversion ratio, protein conversion ratio, metabolizable energy conversion ratio and European production index were significantly enhanced due to feeding an 8% DVO diet compared to a diet containing 6% DVO. Feeding 8% DVO significantly increased the meat protein and lipid percentages, compared to the control group (2.7 % DVO), but decreased the plasma low-density lipoprotein, very-low-density lipoprotein and lymphocytes. Feeding 8% DVO significantly increased the mean cell volume and mean cell hemoglobin, and bursa weight and percentage compared to the control. In addition, 6 and 8% DVO significantly increased the plasma total antioxidant capacity compared to the control group, but decreased the malondialdehyde. Thus, broilers fed a diet containing 8% DVO have an increased tolerance to heat stress, as evidenced by increasing the productive performance, meat quality, blood hematological and biochemical traits, antioxidants and immunity

Improved prognostic classification of breast cancer defined by antagonistic activation patterns of immune response pathway modules.

BACKGROUND: Elucidating the activation pattern of molecular pathways across a given tumour type is a key challenge necessary for understanding the heterogeneity in clinical response and for developing novel more effective therapies. Gene expression signatures of molecular pathway activation derived from perturbation experiments in model systems as well as structural models of molecular interactions ("model signatures") constitute an important resource for estimating corresponding activation levels in tumours. However, relatively few strategies for estimating pathway activity from such model signatures exist and only few studies have used activation patterns of pathways to refine molecular classifications of cancer. METHODS: Here we propose a novel network-based method for estimating pathway activation in tumours from model signatures. We find that although the pathway networks inferred from cancer expression data are highly consistent with the prior information contained in the model signatures, that they also exhibit a highly modular structure and that estimation of pathway activity is dependent on this modular structure. We apply our methodology to a panel of 438 estrogen receptor negative (ER-) and 785 estrogen receptor positive (ER+) breast cancers to infer activation patterns of important cancer related molecular pathways. RESULTS: We show that in ER negative basal and HER2+ breast cancer, gene expression modules reflecting T-cell helper-1 (Th1) and T-cell helper-2 (Th2) mediated immune responses play antagonistic roles as major risk factors for distant metastasis. Using Boolean interaction Cox-regression models to identify non-linear pathway combinations associated with clinical outcome, we show that simultaneous high activation of Th1 and low activation of a TGF-beta pathway module defines a subtype of particularly good prognosis and that this classification provides a better prognostic model than those based on the individual pathways. In ER+ breast cancer, we find that simultaneous high MYC and RAS activity confers significantly worse prognosis than either high MYC or high RAS activity alone. We further validate these novel prognostic classifications in independent sets of 173 ER- and 567 ER+ breast cancers. CONCLUSION: We have proposed a novel method for pathway activity estimation in tumours and have shown that pathway modules antagonize or synergize to delineate novel prognostic subtypes. Specifically, our results suggest that simultaneous modulation of T-helper differentiation and TGF-beta pathways may improve clinical outcome of hormone insensitive breast cancers over treatments that target only one of these pathways.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Piezoelectric properties of Mg doped ZnO thin film using sol-gel method and spin coating

This reports about the synthesis of Mg doped ZnO thin film using spin-coating techniques through sol-gel method. For studying piezoelectric properties, optical properties and morphology, the prepared Mg doped ZnO thin film samples were characterized using Ultraviolet-Visible Spectroscopy (UV-Vis), Photoluminescence Spectroscopy (PL), X-ray Diffraction (XRD), Field Emission Scanning Electron Microscope (FESEM) and Ultrasonic Vibrator. The particle size was evaluated using Scherrer’s formula from XRD patterns. The results show the crystallite size decreased with increasing Mg concentrations. The optical properties showed that sample exhibit a blue shift in absorption in UV spectra indicating good optical properties. The morphology of grain size microstructure was observed from FESEM with results the grain size of the samples decreased with increasing Mg doping. The piezoelectric properties were evaluated using ultrasonic vibrator and multimeter to obtain potential difference for each sample. The results obtained that potential difference increase with increasing Mg contents and higher rotation of spin speed was used

A Novel Keratocan Mutation Causing Autosomal Recessive Cornea Plana

PURPOSE: Mutations in keratocan (KERA), a small leucine-rich proteoglycan, have recently been shown to be responsible for cases of autosomal recessive cornea plana (CNA2). A consanguineous pedigree in which cornea plana cosegregated with microphthalmia was investigated by linkage analysis and direct sequencing. METHODS: Linkage was sought to polymorphic microsatellite markers distributed around the CNA2 and microphthalmia loci (arCMIC, adCMIC, NNO1, and CHX10) using PCR and nondenaturing polyacrylamide gel electrophoresis before KERA was directly sequenced for mutations. RESULTS: Positive lod scores were obtained with markers encompassing the CNA2 locus, the maximum two-point lod scores of 2.18 at recombination fraction theta = 0 was obtained with markers D12S95 and D12S327. Mutation screening of KERA revealed a novel single-nucleotide substitution at codon 215, which results in the substitution of lysine for threonine at the start of a highly conserved leucine-rich repeat motif. Structural modeling predicts that the motifs are stacked into an arched beta-sheet array and that the effect of the mutation is to alter the length and position of one of these motifs. CONCLUSIONS: This report describes a novel mutation in KERA that alters a highly conserved motif and is predicted to affect the tertiary structure of the molecule. Normal corneal function is dependent on the regular spacing of collagen fibrils, and the predicted alteration of the tertiary structure of KERA is the probable mechanism of the cornea plana phenotype

The Relation between Surviving Gene Expression and Urinary Bladder Cancer Disease

Purpose: The aim of this study is to investigate the expression of survivin gene in patients suffering from urinary bladder cancer, thus contributing to further understanding of the molecular etiology of the disease by assessment of Survivin gene expression on both RNA and protein levels in urinary bladder tissue samples and Correlate between its expression and pathological prognostic parameters of patients with urinary bladder cancer risk. Methods: In the present study 26 cases of urinary bladder cancer and 26 cases of normal tissues far from tumor sites in the urinary bladder of the same patients (as control samples) were collected, also 10 paraffin-embedded tissue samples from consecutive of archival bladder specimens patients and 10 tissue samples that of healthy tissue from the same individual as control group were collected for immunohistochemical detection of survivin protein and real time PCR for survivin mRNA detection. Results: In normal tissues of control samples no expression for survivin gene has been noticed. However, in patients affected with bladder cancer the survivin expression was highly increased by increasing degree of tumor malignancy as indicated by real time PCR for survivin mRNA and immunohistochemistry for survivin protein. Conclusion: From this study, it is concluded that survivin protein was not expressed in normal bladder urothelium but was present in a high percentage in tissue samples of patients suffering from bladder cancer and its expression is associated with disease recurrence, tumor grade, progression and mortality

MSC-Regulated MicroRNAs Converge on the Transcription Factor FOXP2 and Promote Breast Cancer Metastasis

SummaryMesenchymal stem/stromal cells (MSCs) are progenitor cells shown to participate in breast tumor stroma formation and to promote metastasis. Despite expanding knowledge of their contributions to breast malignancy, the underlying molecular responses of breast cancer cells (BCCs) to MSC influences remain incompletely understood. Here, we show that MSCs cause aberrant expression of microRNAs, which, led by microRNA-199a, provide BCCs with enhanced cancer stem cell (CSC) properties. We demonstrate that such MSC-deregulated microRNAs constitute a network that converges on and represses the expression of FOXP2, a forkhead transcription factor tightly associated with speech and language development. FOXP2 knockdown in BCCs was sufficient in promoting CSC propagation, tumor initiation, and metastasis. Importantly, elevated microRNA-199a and depressed FOXP2 expression levels are prominent features of malignant clinical breast cancer and are associated significantly with poor survival. Our results identify molecular determinants of cancer progression of potential utility in the prognosis and therapy of breast cancer

The origins of estrogen receptor alpha-positive and estrogen receptor alpha-negative human breast cancer

Current hormonal therapies have benefited millions of patients with breast cancer. Their success, however, is often temporary and limited to a subset of patients whose tumors express estrogen receptor alpha (ER). The therapies are entirely ineffective in ER-negative disease. Recent studies suggest that there are many biological pathways and alterations involved in determining whether ER is expressed and how it is regulated during breast cancer evolution. Improving hormonal therapies, in addition to perfecting current strategies, will also target these newly discovered pathways and alterations, and others yet to be found. The present commentary will briefly highlight a few important observations and unanswered questions regarding ER status and growth regulation during breast cancer evolution, which hopefully will help to stimulate new thinking and progress in this important area of medial research