MODELLING ELASTICITY OF INJECTION MOULDED SHORT FIBRE REINFORCED POLYMERS: COMPARISON BETWEEN EXPERIMENTAL AND ANALYTICAL APPROACHES

In this work we analysed a sample of short fibre reinforced polyamide extracted from an injection moulded plate. We derived local values of the elastic constants by two different numerical methods, one based on simulation and one based on the reconstruction of the sample's microstructure by micro - CT. Results were compared in terms of moduli of elasticity, assuming an orthotropic material model. Fibre orientation was first simulated by process simulation and results were checked against experimental data obtained by the optical section method. Then, fibre orientation data were used for micro-mechanical modelling of the elastic behaviour by means of mean field homogenisation tools. The experimentally based approach was based on micro computed tomography reconstructions of the inner structure of samples extracted from the injection moulded plate. Using numerical models based on the Cell Method, the elastic behaviour of the reconstructed volume was simulated and results were compared with analytical models based on process simulations and homogenization

Pressure Modulator Radiometer (PMR) tests

The pressure modulator technique was evaluated for monitoring pollutant gases in the Earth's atmosphere of altitude levels corresponding to the mid and lower troposphere. Using an experimental set up and a 110 cm sample cell, pressure modulator output signals resulting from a range of gas concentrations in the sample cell were examined. Then a 20 cm sample cell was modified so that trace gas properties in the atmosphere could be simulated in the laboratory. These gas properties were measured using an infrared sensor

A possible new approach in the prediction of late gestational hypertension: The role of the fetal aortic intima-media thickness

The aim was to determine the predictive role of combined screening for late-onset gestational hypertension by fetal ultrasound measurements, third trimester uterine arteries (UtAs) Doppler imaging, and maternal history. This prospective study on singleton pregnancies was conducted at the tertiary center of Maternal and Fetal Medicine of the University of Padua during the period between January 2012 and December 2014. Ultrasound examination (fetal biometry, fetal wellbeing, maternal Doppler study, fetal abdominal aorta intima-media thickness [aIMT], and fetal kidney volumes), clinical data (mother age, prepregnancy body mass index [BMI], and parity), and pregnancy outcomes were collected. The P value <0.05 was defined significant considering a 2-sided alternative hypothesis. The distribution normality of variables were assessed using Kolmogorov-Smirnoff test. Data were presented by mean (±standard deviation), median and interquartile range, or percentage and absolute values. We considered data from 1381 ultrasound examinations at 29 to 32 weeks’ gestation, and in 73 cases late gestational hypertension developed after 34 weeks’ gestation. The final multivariate model found that fetal aIMT as well as fetal umbilical artery pulsatility index (PI), maternal age, maternal prepregnacy BMI, parity, and mean PI of maternal UtAs, assessed at ultrasound examination of 29 to 32 weeks’ gestation, were significant and independent predictors for the development of gestational hypertension after 34 weeks’ gestation. The area under the curve of the model was 81.07% (95% confidence interval, 75.83%-86.32%). A nomogram was developed starting from multivariate logistic regression coefficients. Late-gestational hypertension could be independently predicted by fetal aIMT assessment at 29 to 32 weeks’ gestation, ultrasound Doppler waveforms, and maternal clinical parameters. Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc

Growth abnormalities of fetuses and infants

The objective of this special issue is to address recent research trends and developments about the advancements of image processing and vision in healthcare. A substantial number of papers were submitted, and after a thorough peer review process, some of these were selected to be included in this special issue. Growth abnormalities (either growth restriction or large for gestational age) during perinatal and postnatal life are a hot topic issue, since they are often linked to alteration of uterine environment caused by placental insufficiency, maternal metabolic syndrome, and in general under- or overnutrition of the fetus. These fetal abnormalities account for the leading causes of perinatal morbidity and mortality. Moreover, under the hypothesis of developmental origin of adult diseases, they bear consequences in later life, programming the infant physiology for a higher risk of noncommunicable diseases, cardiovascular adult diseases, and neurodevelopment delay. Low birth weight, caused either by preterm birth and/or by intrauterine growth restriction, is recently known to be associated with increased rates of cardiovascular disease and noninsulin dependent diabetes in adult life. The “developmental origins of adult disease” hypothesis, often called “the Barker hypothesis,” proposes that these diseases originate through adaptations of the fetus when it is undernourished. These adaptations may be cardiovascular, metabolic, or endocrine and they may permanently change the structure and function of the body, increasing coronary heart disease risk factors, such as hypertension, type 2 diabetes mellitus, insulin resistance, and hyperlipidaemia. This hypothesis originally involved from observation by Barker and colleagues that the regions in England with the highest rates of infant mortality in the early 20th century also had the highest rates of mortality from coronary heart disease decades later. As the most commonly registered cause of infant death at the start of 20th century was low birth weight, these observations led to the hypothesis that low birth weight babies who survived infancy and childhood might be at increased risk of coronary heart disease in later life. There is an increased evidence of the link between intrauterine and perinatal alterations and adult diseases. Although the main focus so far has been the timing of delivery and follow-up, the study of the pathophysiology and of possible recovery is of paramount importance and needs the contributions of physicians from several fields, biologists, bioinformaticians, and engineers

A microRNA profile of human CD8(+) regulatory T cells and characterization of the effects of microRNAs on Treg cell-associated genes.

Recently, regulatory T (Treg) cells have gained interest in the fields of immunopathology, transplantation and oncoimmunology. Here, we investigated the microRNA expression profile of human natural CD8(+)CD25(+) Treg cells and the impact of microRNAs on molecules associated with immune regulation. We purified human natural CD8(+) Treg cells and assessed the expression of FOXP3 and CTLA-4 by flow cytometry. We have also tested the ex vivo suppressive capacity of these cells in mixed leukocyte reactions. Using TaqMan low-density arrays and microRNA qPCR for validation, we could identify a microRNA 'signature' for CD8(+)CD25(+)FOXP3(+)CTLA-4(+) natural Treg cells. We used the 'TargetScan' and 'miRBase' bioinformatics programs to identify potential target sites for these microRNAs in the 3'-UTR of important Treg cell-associated genes. The human CD8(+)CD25(+) natural Treg cell microRNA signature includes 10 differentially expressed microRNAs. We demonstrated an impact of this signature on Treg cell biology by showing specific regulation of FOXP3, CTLA-4 and GARP gene expression by microRNA using site-directed mutagenesis and a dual-luciferase reporter assay. Furthermore, we used microRNA transduction experiments to demonstrate that these microRNAs impacted their target genes in human primary Treg cells ex vivo. We are examining the biological relevance of this 'signature' by studying its impact on other important Treg cell-associated genes. These efforts could result in a better understanding of the regulation of Treg cell function and might reveal new targets for immunotherapy in immune disorders and cancer

Factor structure and psychometric properties of the Italian version of the Homosexuality scale of the Trueblood Sexual Attitudes Questionnaire

The aim of the present study was to translate the Homosexuality scale of the Trueblood Sexual Attitudes Questionnaire into the Italian language and to assess its factor structure and psychometric properties in Italian psychology students. The questionnaire was originally developed and validated in U.S. college students, and later in Turkish social work students, showing high internal consistency. It measures attitudes toward several sexual practices and behaviors, regarding self and others. Particularly, the Homosexuality scale measures attitudes toward different sexual and romantic practices with people of the same sex. A total of 199 Italian psychology students participated to the study, and they were administered the Italian translation of the scale. We applied exploratory factor analysis and confirmatory factor analysis. Results showed that the scale has high internal consistency, and that the original two-factor model accounting for attitudes toward self and others fits the data well. Implications for education and assessment in student populations are discussed

Shannon Information Theory and Molecular Biology

The role and the contribution of Shannon Information Theory to the development of Molecular Biology has been the object of stimulating debates during the last thirty years. This seems to be connected with some semantic charms associated with the use of the word \u201cinformation\u201d in the biological context. Furthermore information itself, if viewed in a broader perspective, is far from being completely defined in a fashion that overcomes the technical level at which the classical Information Theory has been conceived. This review aims at building on the acknowledged contribution of Shannon Information Theory to Molecular Biology, so as to discover if it is only a technical tool to analyze DNA and proteinic sequences, or if it can rise, at least in perspective, to a higher role that exerts an influence on the construction of a suitable model for handling the genetic information in Molecular Biology

Chemoattractant Receptor Homologous to the T Helper 2 Cell (CRTH2) Is Not Expressed in Human Amniocytes and Myocytes

BACKGROUND: 15-deoxy-Δ 12,14- Prostaglandin J2 (15dPGJ2) inhibits Nuclear factor kappa B (NF-κB) in human myocytes and amniocytes and delays inflammation induced preterm labour in the mouse. 15dPGJ2 is a ligand for the Chemoattractant Receptor Homologous to the T helper 2 cell (CRTH2), a G protein-coupled receptor, present on a subset of T helper 2 (Th2) cells, eosinophils and basophils. It is the second receptor for Prostaglandin D2, whose activation leads to chemotaxis and the production of Th2-type interleukins. The cellular distribution of CRTH2 in non-immune cells has not been extensively researched, and its identification at the protein level has been limited by the lack of specific antibodies. In this study we explored the possibility that CRTH2 plays a role in 15dPGJ2-mediated inhibition of NF-κB and would therefore represent a novel small molecule therapeutic target for the prevention of inflammation induced preterm labour. METHODS: The effect of a small molecule CRTH2 agonist on NF-κB activity in human cultured amniocytes and myocytes was assessed by detection of p65 and phospho-p65 by immunoblot. Endogenous CRTH2 expression in amniocytes, myocytes and peripheral blood mononuclear cells (PBMCs) was examined by PCR, western analysis and flow cytometry, with amniocytes and myocytes transfected with CRTH2 acting as a positive control in flow cytometry studies. RESULTS: The CRTH2 agonist had no effect on NF-κB activity in amniocytes and myocytes. Although CRTH2 mRNA was detected in amniocytes and myocytes, CRTH2 was not detectable at the protein level, as demonstrated by western analysis and flow cytometry. 15dPGJ2 inhibited phospho-65 in PBMC'S, however the CRTH2 antagonist was not able to attenuate this effect. In conclusion, CRTH2 is not expressed on human amniocytes or myocytes and plays no role in the mechanism of 15dPGJ2-mediated inhibition of NF-κB