Behaviour of Surface Defects in Wire Rod Rolling

Defects are often present in rolled products, such as wire rod. The markets demand for wire rod without any defects has increased. In the final wire rod products, defects originating from the steel making, casting, pre-rolling of billets and during the wire rod rolling can appear. In this work, artificial V-shaped longitudinal surface cracks has been analysed experimentally and by means of FEM. The results indicate that the experiments and FEM calculations show the same tendency except in two cases, where instability due to a fairly “round” false round bars disturbed the experiment. FE studies in combination with practical experiments are necessary in order to understand the behaviour of the material flows in the groove and to explain whether the crack will open up as a V-shape or if it will be closed as an I-shape.

Evolution of artificial defects during shape rolling

Very often defects are present in rolled products. For wire rods, defects are very deleterious since the wire rods are generally used directly in various applications. For this reason, the market nowadays requires wire rods to be completely defect-free. Any wire with defects must be rejected as scrap which is very costly for the production mill. Thus, it is very important to study the formation and evolution of defects during wire rod rolling in order to better understand and minimize the problem, at the same time improving quality of the wire rods and reducing production costs. The present work is focused on the evolution of artificial defects during rolling. Longitudinal surface defects are studied during shape rolling of an AISI M2 high speed steel and a longitudinal central inner defect is studied in an AISI 304L austenitic stainless steel during ultra-high-speed wire rod rolling. Experimental studies are carried out by rolling short rods prepared with arteficial defects. The evolution of the defects is characterised and compared to numerical analyses. The comparison shows that surface defects generally reduce quicker in the experiments than predicted by the simulations whereas a good agreement is generally obtained for the central defect.

Studies of Design and Assembly Defects on Integrated and Modular Architectures

It is known that despite companies’ efforts to improve the quality of their products, design and assembly defects results in large repair costs both in terms of repair and providing feedback to the origin of the defect. The purpose of this paper is to study these types of defects and the defect rates in design and assembly. The paper presents a web based questionnaire answered by 29 companies. The result shows that the defect rate (defects per product) spanned from 0.01 to 10. Also, design and assembly defects covered 46%, 23% respectively, of all occurred defects. A case study is also presented, performed at a company who recently implemented a modular architecture. In this company, defects from 5 700 integrated product architectures are compared with defects from 431 modular architectures. The average defect rate increased by 21.5% – from 0.65 to 0.79 – when a more modular architecture has been implemented. Furthermore, the study showed that the assembly defects have decreased while the design defects increased. The results presented in this paper will also support the development of the MPV (Module Property Verification) method which is briefly described.

Proliferative Defects and Formation of a Double Cortex in Mice Lacking Mltt4 and Cdh2 in the Dorsal Telencephalon

Radial glial cells (RGCs) in the ventricular neuroepithelium of the dorsal telencephalon are the progenitor cells for neocortical projection neurons and astrocytes. Here we showthatthe adherens junction proteins afadin and CDH2 are criticalforthe control of cell proliferation in the dorsal telencephalon and for the formation of its normal laminar structure. Inactivation of afadin or CDH2 in the dorsal telenceph-alon leads to a phenotype resembling subcortical band heterotopia, also known as “double cortex,” a brain malformation in which heterotopic gray matter is interposed between zones of white matter. Adherens junctions between RGCs are disrupted in the mutants, progenitor cells are widely dispersed throughout the developing neocortex, and their proliferation is dramatically increased. Major subtypes of neocortical projection neurons are generated, but their integration into cell layers is disrupted. Our findings suggest that defects in adherens junctions components in mice massively affects progenitor cell proliferation and leads to a double cortex-like phenotype.

Comparison between two methods for cardiac output measurement in propofol-anesthetized dogs: thermodilution and Doppler

ObjectiveTo compare cardiac output (CO) measured by Doppler echocardiography and thermodilution techniques in spontaneously breathing dogs during continuous infusion of propofol. To do so, CO was obtained using the thermodilution method (CO(TD)) and Doppler evaluation of pulmonary flow (CO(DP)) and aortic flow (CO(DA)).Study designProspective cohort study.AnimalsEight adult dogs weighing 8.3 +/- 2.0 kg.MethodsPropofol was used for induction (7.5 +/- 1.9 mg kg-1 IV) followed by a continuous rate infusion at 0.7 mg kg-1 minute-1. The animals were positioned in left lateral recumbency on an echocardiography table that allowed for positioning of the transducer at the 3rd and 5th intercostal spaces of the left hemithorax for Doppler evaluation of pulmonary and aortic valves, respectively. CO(DP) and CO(DA) were calculated from pulmonary and aortic velocity spectra, respectively. A pulmonary artery catheter was inserted via the jugular vein and positioned inside the lumen of the pulmonary artery in order to evaluate CO(TD). The first measurement of CO(TD), CO(DP) and CO(DA) was performed 30 minutes after beginning continuous infusion (T0) and then at 15-minute intervals (T15, T30, T45 and T60). Numeric data were submitted to two-way anova for repeated measurements, Pearson's correlation coefficient and Bland & Altman analysis. Data are presented as mean +/- SD.ResultsAt T0, CO(TD) was lower than CO(DA). CO(DA) was higher than CO(TD) and CO(DP) at T30, T45 and T60. The difference between the CO(TD) and CO(DP), when all data were included, was -0.04 +/- 0.22 L minute-1 and Pearson's correlation coefficient (r) was 0.86. The difference between the CO(TD) and CO(DA) was -0.87 +/- 0.54 L minute-1 and r = 0.69. For CO(TD) and CO(DP), the difference was -0.82 +/- 0.59 L minute-1 and r = 0.61.ConclusionDoppler evaluation of pulmonary flow was a clinically acceptable method for assessing the CO in propofol-anesthetized dogs.

Cardiac function in dogs with chronic Chagas cardiomyopathy undergoing autologous stem cell transplantation into the coronary arteries

This study assessed the effects of a single intracoronary injection of autologous stem cells on the cardiac function of dogs with Chagas cardiomyopathy. Bone-marrow-derived stem cells were delivered into the right and left coronary arteries of 5 mature dogs with mildly compromised cardiac function due to chronic Chagas cardiomyopathy. Blood pressure and electrocardiographic and echocardiographic parameters were recorded at monthly intervals for 6 mo in the 3 dogs that survived. Although no changes were observed in the electrocardiogram and blood pressure, there was a significant increase in peak velocity of aortic flow 3 mo after stem cell transplantation. Pre-ejection period, isovolumic relaxation time, and the Tei index of myocardial performance were reduced significantly 4 mo after the procedure. All significant changes persisted to the end of the study. The results suggest that the transplantation of autologous bone-marrow-derived stem cells into the coronary arteries of dogs with Chagas cardiomyopathy may have a beneficial effect but the small number of dogs studied was a limitation.

Effects of weight loss on the cardiac parameters of obese dogs

A obesidade é uma das doenças nutricionais mais frequentemente observada em cães e pode provocar sérios problemas de saúde, como os distúrbios cardiovasculares. Realizou-se este estudo visando avaliar algumas das possíveis alterações estruturais e funcionais cardíacas decorrentes da correção da obesidade canina. Para isso foram utilizados 18 cães obesos divididos pelo peso corporal em Grupo I (até 15kg), Grupo II (entre 15,1 e 30 kg) e Grupo III (acima de 30 kg). Os animais foram submetidos à restrição calórica de forma a perderem 15% do peso vivo. Foram realizados os exames ecocardiográfico em modo-M, eletrocardiográfico e mensuração da pressão arterial dos animais antes do início do tratamento da obesidade e após atingirem o peso meta. Os resultados revelaram que após a redução de peso ocorreram diminuições significativas da espessura da parede livre do ventrículo esquerdo durante a sístole e diástole no Grupo III, diminuição da pressão arterial sistólica no Grupo III e também da pressão arterial média no Grupo II. Assim, concluiu-se que a perda de peso pode reverter as alterações estruturais cardíacas, como a hipertrofia excêntrica do ventrículo esquerdo em cães obesos acima de 30 kg, como também reduzir a pressão arterial sistêmica em cães obesos submetidos à restrição calórica mediante administração de dieta hipocalórica.

Venous tone and cardiac function in the South American rattlesnake Crotalus durissus: mean circulatory filling pressure during adrenergic stimulation in anaesthetised and fully recovered animals

The effects of adrenergic stimulation on mean circulatory filling pressure (MCFP), central venous pressure (P-CV) and stroke volume (Vs), as well as the effects of altered MCFP through changes of blood volume were investigated in rattlesnakes (Crotalus durissus). MCFP is an estimate of the upstream pressure driving blood towards the heart and is determined by blood volume and the activity of the smooth muscle cells in the veins (venous tone). MCFP can be determined as the plateau in P-CV during a total occlusion of blood flow from the heart.Vs decreased significantly when MCFP was lowered by reducing blood volume in anaesthetised snakes, whereas increased MCFP through infusion of blood (up to 3 ml kg(-1)) only led to a small rise in Vs. Thus, it seems that end-diastolic volume is not affected by an elevated MCFP in rattlesnakes. To investigate adrenergic regulation on venous tone, adrenaline as well as phenylephrine and isoproterenol (alpha- and beta-adrenergic agonists, respectively) were infused as bolus injections (2 and 10 mu g kg(-1)). Adrenaline and phenylephrine caused large increases in MCFP and P-CV, whereas isoproterenol decreased both parameters. This was also the case in fully recovered snakes. Therefore, adrenaline affects venous tone through both alpha- and beta-adrenergic receptors, but the alpha-adrenergic receptor dominates at the dosages used in the present study. Injection of the nitric oxide donor SNP caused a significant decrease in P-CV and MCFP. Thus, nitric oxide seems to affect venous tone.

Analysis of cardiac autonomic modulation in obese and eutrophic children

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Energy Expenditure, Lipid Profile, Oxidative Stress, and Cardiac Energy Metabolism After Growth Hormone Treatment in Obese Young Rats

Obesity is rampant in modern society and growth hormone (GH) could be useful as adjunct therapy to reduce the obesity-induced cardiovascular damage. To investigate GH effects on obesity, initially 32 male Wistar rats were divided into two groups (n = 16): control (C) was fed standard-chow and water and hyper-caloric (H) was fed hypercaloric chow and 30% sucrose in its drinking water. After 45 days, both C and H groups were divided into two subgroups (n = 8): C + PL was fed standard-chow, water and received saline subcutaneously; C + GH was fed standard-chow, water, and received 2 mg/kg/day GH subcutaneously; H + PL was fed hypercaloric diet, 30% sucrose in its drinking water, and received saline subcutaneously; and H + GH was fed hypercaloric diet, 30% sucrose in its drinking water, and received GH subcutaneously. After 75 days of total experimental period, H + PL rats were considered obese, having higher body weight, body mass index, Lee-index, and atherogenic index (AI) compared to C + PL. Obesity was accompanied by enhanced myocardial lipid hydroperoxide (LH) and lactate dehydrogenase (LDH), as well of depressed energy expenditure (RMR) and oxygen consumption(VO(2))/body weight. H + GH rats had higher fasting RMR, as well as lower AI and myocardial LH than H + PL. Comparing C + GH with C + PL, despite no effects on morphometric parameters, lipid profile, myocardial LH, and LDH activity, GH enhanced fed RMR and myocardial pyruvate dehydrogenase. In conclusion, the present study brought new insights into the GH effects on obesity related cardiovascular damage demonstrating, for the first time, that GH regulated cardiac metabolic pathways, enhanced energy expenditure and improved the lipid profile in obesity condition. Growth hormone in standard fed condition also offered promising therapeutic value enhancing pyruvate-dehydrogenase activity and glucose oxidation in cardiac tissue, thus optimizing myocardial energy metabolism.

Loss of nuclear poly(A)-binding protein 1 causes defects in myogenesis and mRNA biogenesis

The nuclear poly(A)-binding protein 1 (PABPN1) is a ubiquitously expressed protein that plays a critical role in polyadenylation. Short expansions of the polyalanine tract in the N-terminus of PABPN1 lead to oculopharyngeal muscular dystrophy (OPMD), which is an adult onset disease characterized by eyelid drooping, difficulty in swallowing and weakness in the proximal limb muscles. Although significant data from in vitro biochemical assays define the function of PABPN1 in control of poly(A) tail length, little is known about the role of PABPN1 in mammalian cells. To assess the function of PABPN1 in mammalian cells and specifically in cells affected in OPMD, we examined the effects of PABPN1 depletion using siRNA in primary mouse myoblasts from extraocular, pharyngeal and limb muscles. PABPN1 knockdown significantly decreased cell proliferation and myoblast differentiation during myogenesis in vitro. At the molecular level, PABPN1 depletion in myoblasts led to a shortening of mRNA poly(A) tails, demonstrating the cellular function of PABPN1 in polyadenylation control in a mammalian cell. In addition, PABPN1 depletion caused nuclear accumulation of poly(A) RNA, revealing that PABPN1 is required for proper poly(A) RNA export from the nucleus. Together, these experiments demonstrate that PABPN1 plays an essential role in myoblast proliferation and differentiation, suggesting that it is required for muscle regeneration and maintenance in vivo.

Pkc1 acts through Zds1 and Gic1 to suppress growth and cell polarity defects of a yeast eIF5A mutant

eIF5A is a highly conserved putative eukaryotic translation initiation factor that has been implicated in translation initiation, nucleocytoplasmic transport, mRNA decay, and cell proliferation, but with no precise function assigned so far. We have previously shown that high-copy PKCI suppresses the phenotype of tif51A-1, a temperature-sensitive mutant of eIF5A in S. cerevisiae. Here, in an attempt to further understand how Pkc1 functionally interacts with eIF-5A, it was determined that PKCI suppression of tif51A-1 is independent of the cell integrity MAP kinase cascade. Furthermore, two new suppressor genes, ZDS1 and GIC1, were identified. We demonstrated that ZDS1 and ZDS2 are necessary for PKC1, but not for GIC1 suppression. Moreover, high-copy GIC1 also suppresses the growth defect of a PKCI mutant (stt1), suggesting the existence of a Pkc1-Zds1-Gic1 pathway. Consistent with the function of Gic1 in actin organization, the tif51A-1 strain shows an actin polarity defect that is partially recovered by overexpression of Pkc1 and Zds1 as well as Gic1. Additionally, PCL1 and BNI1, important regulators of yeast cell polarity, also suppress tif51A-1 temperature sensitiviiy Taken together, these data strongly Support the correlated involvement of Pkc1 and eIF5A in establishing actin polarity, which is essential for bud formation and G1/S transition in S. cerevisiae.

Presence of autoantibodies against HeLa small nuclear ribonucleoproteins in chagasic and non-chagasic cardiac patients

We detected anti-human small nuclear ribonucleoprotein (snRNP) autoantibodies in chagasic patients by different immunological methods using HeLa snRNPs. ELISA with Trypanosoma cruzi total lysate antigen or HeLa human U small nuclear ribonucleoproteins (UsnRNPs) followed by incubation with sera from chronic chagasic and non-chagasic cardiac patients was used to screen and compare serum reactivity. Western blot analysis using a T. cruzi total cell extract was also performed in order to select some sera for Western blot and immunoprecipitation assays with HeLa nuclear extract. ELISA showed that 73 and 95% of chronic chagasic sera reacted with HeLa UsnRNPs and T. cruzi antigens, respectively. The Western blot assay demonstrated that non-chagasic cardiac sera reacted with high molecular weight proteins present in T. cruzi total extract, probably explaining the 31% reactivity found by ELISA. However, these sera reacted weakly with HeLa UsnRNPs, in contrast to the chagasic sera, which showed autoantibodies with human Sm (from Stefanie Smith, the first patient in whom this activity was identified) proteins (B/B', D1, D2, D3, E, F, and G UsnRNP). Immunoprecipitation reactions using HeLa nuclear extracts confirmed the reactivity of chagasic sera and human UsnRNA/RNPs, while the other sera reacted weakly only with U1snRNP. These findings agree with previously reported data, thus supporting the idea of the presence of autoimmune antibodies in chagasic patients. Interestingly, non-chagasic cardiac sera also showed reactivity with T. cruzi antigen and HeLa UsnRNPs, which suggests that individuals with heart disease of unknown etiology may develop autoimmune antibodies at any time. The detection of UsnRNP autoantibodies in chagasic patients might contribute to our understanding of how they develop upon initial T. cruzi infection.