71 research outputs found
Neutral Radius Value Determination by Numerical Simulation Method at Ring Upsetting Test
Ring upsetting represents a basic operation for bulk forming process and has particular significance since it is used for contact friction determination. At ring upsetting by flat dies, metal flow depends upon tribological conditions present at contact surface. Thereby, two variants of metal flow are possible: a) two-way flow from neutral radius that is present at lower friction coefficient values, followed by ring’s inner radius reduction and ring’s outer radius increase. In such circumstances, neutral radius is found between inner and outer radius. b) one-way flow that occurs at higher friction coefficient values, where neutral radius is lower than ring’s inner radius. This paper is presenting the results of determination of relation between neutral radius value and friction coefficient. Such relation is determined by numerical simulation, by using Simufact.Forming software. Experimental verification of neutral radius position is conducted by metallographic analysis, for two friction coefficient values. Friction coefficient values are determined by ring upsetting by using dies, where in one case of ring upsetting, contact surfaces were ion implanted with nitroge
Financial evaluation of kidney transplant with hepatitis C viremic donors to uninfected recipients
Identification of quantitative trait loci for survival in the mutant dynactin p150Glued mouse model of motor neuron disease.
Amyotrophic lateral sclerosis (ALS) is the most common degenerative motor neuron disorder. Although most cases of ALS are sporadic, 5-10% of cases are familial, with mutations associated with over 40 genes. There is variation of ALS symptoms within families carrying the same mutation; the disease may develop in one sibling and not in another despite the presence of the mutation in both. Although the cause of this phenotypic variation is unknown, it is likely related to genetic modifiers of disease expression. The identification of ALS causing genes has led to the development of transgenic mouse models of motor neuron disease. Similar to families with familial ALS, there are background-dependent differences in disease phenotype in transgenic mouse models of ALS suggesting that, as in human ALS, differences in phenotype may be ascribed to genetic modifiers. These genetic modifiers may not cause ALS rather their expression either exacerbates or ameliorates the effect of the mutant ALS causing genes. We have reported that in both the G93A-hSOD1 and G59S-hDCTN1 mouse models, SJL mice demonstrated a more severe phenotype than C57BL6 mice. From reciprocal intercrosses between G93A-hSOD1 transgenic mice on SJL and C57BL6 strains, we identified a major quantitative trait locus (QTL) on mouse chromosome 17 that results in a significant shift in lifespan. In this study we generated reciprocal intercrosses between transgenic G59S-hDCTN1 mice on SJL and C57BL6 strains and identified survival QTLs on mouse chromosomes 17 and 18. The chromosome 17 survival QTL on G93A-hSOD1 and G59S-hDCTN1 mice partly overlap, suggesting that the genetic modifiers located in this region may be shared by these two ALS models despite the fact that motor neuron degeneration is caused by mutations in different proteins. The overlapping region contains eighty-seven genes with non-synonymous variations predicted to be deleterious and/or damaging. Two genes in this segment, NOTCH3 and Safb/SAFB1, have been associated with motor neuron disease. The identification of genetic modifiers of motor neuron disease, especially those modifiers that are shared by SOD1 and dynactin-1 transgenic mice, may result in the identification of novel targets for therapies that can alter the course of this devastating illness
The role of sex in the pathophysiology of pulmonary hypertension
Pulmonary arterial hypertension (PAH) is a progressive disease characterised by increased pulmonary vascular resistance and pulmonary artery remodelling as result of increased vascular tone and vascular cell proliferation, respectively. Eventually, this leads to right heart failure. Heritable PAH is caused by a mutation in the bone morphogenetic protein receptor-II (BMPR-II). Female susceptibility to PAH has been known for some time, and most recent figures show a female-to-male ratio of 4:1. Variations in the female sex hormone estrogen and estrogen metabolism modify FPAH risk, and penetrance of the disease in BMPR-II mutation carriers is increased in females. Several lines of evidence point towards estrogen being pathogenic in the pulmonary circulation, and thus increasing the risk of females developing PAH. Recent studies have also suggested that estrogen metabolism may be crucial in the development and progression of PAH with studies indicating that downstream metabolites such as 16α-hydroxyestrone are upregulated in several forms of experimental pulmonary hypertension (PH) and can cause pulmonary artery smooth muscle cell proliferation and subsequent vascular remodelling. Conversely, other estrogen metabolites such as 2-methoxyestradiol have been shown to be protective in the context of PAH. Estrogen may also upregulate the signalling pathways of other key mediators of PAH such as serotonin
The Zwicky Transient Facility: System Overview, Performance, and First Results
The Zwicky Transient Facility (ZTF) is a new optical time-domain survey that uses the Palomar 48 inch Schmidt telescope. A custom-built wide-field camera provides a 47 deg^2 field of view and 8 s readout time, yielding more than an order of magnitude improvement in survey speed relative to its predecessor survey, the Palomar Transient Factory. We describe the design and implementation of the camera and observing system. The ZTF data system at the Infrared Processing and Analysis Center provides near-real-time reduction to identify moving and varying objects. We outline the analysis pipelines, data products, and associated archive. Finally, we present on-sky performance analysis and first scientific results from commissioning and the early survey. ZTF's public alert stream will serve as a useful precursor for that of the Large Synoptic Survey Telescope
Meconium stained amniotic fluid: Antenatal, intrapartum, postnatal management:review [Mekonyum Boyal Amniyotik Sv: Antenatal, ntrapartum, Postnatal Yönetim]
Approximately 13o of all live births are complicated by meconium stained amniotic fluid and only 5o of neonates born through of them develop meconium aspiration syndrome (MAS). In case of meconium stained amniotic fluid and respiratory distress MAS should be ruled out. Meconium aspiration may occur in utero or in first a few inspirations. Chronic fetal hypoxia and acidosis may cause fetal gasping and meconium aspiration in utero. Respiratory distress may ta ke place by the aspiration of meconium stained amniotic fluid in the nasopharynx of normal new born. Severity criteria for MAS are also defined. Mild MAS is a disease that requires less than 40o oxygen for less than 48 hours, moderate MAS is disease that requires more than 40o oxygen for mo re than 48 hours with no air leak, and severe MAS is a disease that requires assisted ventilation for more than 48 hours and is often associated with persistent pulmonary hypertension. The principal of prenatal management is to consider mecoium stained amniotic fluid as a sign of fetal distress and to follow closely the other signs of fetal distress. Intrapartum suctioning is not very effective and if the infant is vigorous defined as strong respiratory efforts, good muscle tone and a heart rate grea ter than 100 bpm, intubation and tracheal aspiration is not necessary. Pharmacotherapy of MAS in dude sedation and analgesia, pulmonary care, antibiotics, anti inflammatory agents and pulmonary vasodilators, surfactant and surfactant lavage. Copyright © 2012 by Türki ye Klinikleri
Primjena SEM i EDS analiza u istraživanju poroznosti Al-Si-Cu lijevanog stapa
Porosity formation was detected in the casting thinnest section in the proximity of the as cast surface and near the wall centerline. In order to investigate the cause of the porosity formation light microscopy was used to define as cast structure. After initial findings SEM and EDS analyses were performed. Based on the results it is possible to define cause of the observed porosity. A number of pores originates from the mould filling stage and entrainment of the oxide films, while others appear due to insufficient feeding during solidification.Kod najtanjeg presjeka stijenke odljevka otkrivena je pojava poroznosti neposredno ispod površine stijenke, kao i u zoni sredine stijenke. Kako bi se utvrdio uzrok pojave poroznosti primijenjena je svjetlosna mikroskopija za određivanje lijevane strukture. Nakon prvobitnih opažanja provedene su SEM i EDS analize. Na temelju dobivenih rezultata moguće je odrediti uzroke nastanka otkrivene poroznosti. Određeni broj pora nastaje zbog zarobljavanja oksidnog filma tijekom faze popunjavanja kalupa, dok je ostatak poroznosti posljedica neadekvatnog napajanja tijekom skrućivanja
Use of SEM and EDS analysis in the investigation of Al-Si-Cu piston alloy cast porosity
Porosity formation was detected in the casting thinnest section in the proximity of the as cast surface and near the wall centerline. In order to investigate the cause of the porosity formation light microscopy was used to define as cast structure. After initial findings SEM and EDS analyses were performed. Based on the results it is possible to define cause of the observed porosity. A number of pores originates from the mould filling stage and entrainment of the oxide films, while others appear due to insufficient feeding during solidification
The serial changes of Perfusion Index in preterm infants with patent ductus arteriosus: Is perfusion index clinically significant?
PubMed ID: 27277201Background: Perfusion Index (PI) which reflects the peripheral blood flow may help early detection and treatment decision of hemodynamically significant patent ductus arteriosus (hsPDA) in preterm infants. The present study is designed to analyze the usefulness of PI level in early detection of hsPDA in preterm infants. METHODS: Preterm infants born before 36 gestational weeks were assessed for PI and simultaneous echocardiography. Based on echocardiography, each infant is categorized into no-PDA (group 1), non-hsPDA (group 2) and hsPDA (group 3). Heart rate (HR), mean arterial pressure (MAP), body temperature and oxygen saturation (SpO2) and concomitant PI were measured on days 1, 2, 3 and 4. RESULTS: In all preterm infants (N.=42) PI significantly increased from 0.7 on day 1 to 1.4 on day 4. The HR did not change by the days; however, the MAP increased on days 3 and 4 compared to day 1. In hsPDA group, the median PI was 0.7 (IQR, 0.4) on day 1 compared to 0.9 (IQR, 0.2) on day 2. PI is significantly lower in hsPDA group compared to no-PDA group on day 1 and 2; however, this difference disappeared at 48 hour on the intravenous ibuprofen treatment (on day 3 and 4). CONCLUSIONS: PI may predict the perfusion disorder and help to decide for treatment of hsPDA and was also helpful to monitor the response to treatment in hsPDA patients. © 2014 Edizioni Minerva Medica
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