ENERGETIC ESTIMATION OF HEAT-RECOVERY COKE OVEN

Worldwide, steel production insistently seeks energy strength, pointing out the precision of application of all energy from the raw material with the objective of increasing production with quality and economically viable. In this sense, the energy assessment is the basis adopted to decide on the manufacture of coke in the industry. With this argument, this paper presents an energy analysis of Heat Recovery furnaces through calorific value, a method specified by the Energy Research Company of Brazil and the Brazilian Association of Metals and Materials for application in calculations in a productive environment. The data of the basic raw materials for the production of coke, the technological analysis and the energy estimation in the manufacture of coke in Coke Ovens Heat Recovery can be found in the proposed method. The present work presents result that demonstrate that the active and efficient use of the calorific value of metallurgical coal produces an energy quality coke for the manufacture of pig iron in the blast furnace.

STUDY OF PLASMA ION NITRIDING OF AISI H13 STEEL

This work studied the thermochemical treatment of AISI H13 steel used for extrusion of aluminum parts, by plasma ionic nitriding, with the objective of increasing the surface hardness of the mold, by forming an external layer of stable nitrides, increasing the resistance to wear, fatigue, corrosion and thermal resistance. Because it uses ions, plasma ion nitriding is more efficient than liquid and gas nitriding. This process is widely used for ferrous materials and aluminum. The main applications are for extrusion, material injection molds, cutting tools and automotive parts. In this work, samples of the AISI H13 steel were nitrided to be used as aluminum injection molds. The treatment was carried out at 300 oC in a sodium cyanide bath, for a period of 6 h at a pressure of 15 mTorr (2 Pa). The gaseous mixture inside the nitreter consisted of 80% N2 + 20% H2. After treatment, Vickers hardness measurements reached surface values of 963 HV. The results at the end of the treatment showed a 122 µm nitrided layer

Contribution to characterization of oxidative stress in HIV/AIDS patients

Infection by human immunodeficiency virus (HIV) causes persistent chronic inflammation. Viral Tat protein plays a role in the intracellular increase of reactive oxygen species (ROS) thus increasing apoptotic index, mostly the one mediated by FAS/CD95, and depleting CD4+ T lymphocytes. The aim of this study was to investigate whether there is a relationship between an extensive array of redox status indices (glutathione (GSH), malondialdehyde (MDA), peroxidation potential, total antioxidant status, glutathione peroxidase (GPx), superoxide dismutase (SOD), total hydroperoxide (TH), DNA fragmentation) and relative CD4, CD95, CD38/CD8 T lymphocyte counts in HIV/AIDS patients compared to healthy subjects. Blood samples from 85 HIV/AIDS patients and 40 healthy subjects were tested by spectrophotometric techniques in order to measure oxidative stress indices, and by flow cytometry to quantify T cell subsets. Patients were divided in two groups according to CDC 1993 guidelines. CD95 and CD38 increase paralleled the severity of HIV infection. Both a reduction of GSH levels and an increase in MDA and TH levels were detected in the plasma of HIV+ patients. These patients also showed an increase of DNA fragmentation in lymphocytes as well as a significant (P<0.05) reduction of GPx and an increase in SOD activity in erythrocytes. Relatively to the control group, HIV-infected patients had significantly differences in global indices of total antioxidant status. These results corroborate that substantial oxidative stress occurs during HIV infection. To our knowledge this study is the first relating oxidative stress indices with both CD38/CD8 and CD95 lymphocytes subsets

Effect of increase, of dietary micronutrient intake on oxidative stress indicators in HIV/AIDS patients

Several human studies in immunodeficiency virus (HIV) patients have identified macronutrient deficiencies as affecting progression to acquired immunodeficiency syndrome (AIDS) and death. Although the mechanisms are not known, micronutrient deficiencies may exacerbate the oxidative stress induced by HIV. In addition, infection and its evolution likely lead to an increased requirement for nutritional micronutrients, especially antioxidants. To evaluate this, 40 relatively healthy, institutionalized HIV-infected individuales were recruited for assessment before or three month after fresh fruit and vegetable supply were increased due to seasonal supply. Seven-day dietary records were recorded at the beginning (December) and end of the three-month study period (March). Oxidative stress indices and CD4+, CD38+/CD8+, and CD95+ T-lymphocyte subsets were also measured at these times. No significant differences were found in calorie or protein intake across the study period, but vitamin A, C, and E intakes all increased. A number of redox indicators were modified (increase total antioxidant status, glutathione peroxidase, and glutathione, and decrease: superoxide dismutase) during the study period. However, no change in malondialdehyde, hydroperoxides, or DNA damage was noted but a significant reduction in CD38+/CD8+ relative count was seen. Within the context and limitations of this study, the increase of dietary fruits and vegetable intake for three months had some beneficial effects on nutrition, systemic redox balance, and immune parameters in HIV-infected persons

ANALYSIS OF RESIDUAL STRESS BY X-RAY DIFFRACTION AND STUDY OF MICROSTRUCTURE IN WELDED JOINT OF ASTM A-36 MARINE STEEL

ASTM A-36 marine steel is one of the most used and classified as a medium strength carbon steel. Its characteristics and purpose are in common applications and in metallic structures in general, sawmills, walkways, agricultural machinery and implements, road, rail and oil implements. It is used in angles, round, flat and square bars and I, U and T profiles. In this work, 10 mm sheets, with a V chamfer, were welded using the MIG/MAG process and X-Ray Diffraction measurements were carried out to study of residual stresses caused by the welding process. Then samples were taken for metallography and microscopy in the Scanning Electron Microscope (SEM). They were also performed in the three regions of the weld: base metal (MB); thermally affected zone (ZTA) and in the molten zone (ZF) Brinell hardness tests, to determine the energy stored in the regions of the weld bead. Vickers Microhardness measurements were also made at the ZTA, as it is a very narrow range, to give more precision to the hardness measurements. The X-Ray Diffraction test showed that the air-cooled samples are compressive and the water-cooled samples are tensile. The micrographs of the samples, in the region of the weld, showed that the ferritic phase prevailed in the molten zone. It was also observed the precipitation of carbides and alloying elements, in addition to the presence of martensite. It is concluded, therefore, that the results for the MIG/MAG welding were satisfactory and recommended for the welding of ASTM A-36 Steel

A modifier locus on chromosome 5 contributes to L1 cell adhesion molecule X-linked hydrocephalus in mice

Humans with L1 cell adhesion molecule (L1CAM) mutations exhibit X-linked hydrocephalus, as well as other severe neurological disorders. L1-6D mutant mice, which are homozygous for a deletion that removes the sixth immunoglobulin-like domain of L1cam, seldom display hydrocephalus on the 129/Sv background. However, the same L1-6D mutation produces severe hydrocephalus on the C57BL/6J background. To begin to understand how L1cam deficiencies result in hydrocephalus and to identify modifier loci that contribute to X-linked hydrocephalus by genetically interacting with L1cam, we conducted a genome-wide scan on F2 L1-6D mice, bred from L1-6D 129S2/SvPasCrlf and C57BL/6J mice. Linkage studies, utilizing chi-square tests and quantitative trait loci mapping techniques, were performed. Candidate modifier loci were further investigated in an extension study. Linkage was confirmed for a locus on chromosome 5, which we named L1cam hydrocephalus modifier 1 (L1hydro1), p = 4.04 X 10(-11)

Inhibition of glial D-serine release rescues synaptic damage after brain injury

Synaptic damage is one of the most prevalent pathophysiological responses to traumatic CNS injury and underlies much of the associated cognitive dysfunction; however, it is poorly understood. The D-amino acid, D-serine, serves as the primary co-agonist at synaptic NMDA receptors (NDMARs) and is a critical mediator of NMDAR-dependent transmission and synaptic plasticity. In physiological conditions, D-serine is produced and released by neurons from the enzymatic conversion of L-serine by serine racemase (SRR). However, under inflammatory conditions, glial cells become a major source of D-serine. Here, we report that D-serine synthesized by reactive glia plays a critical role in synaptic damage after traumatic brain injury (TBI) and identify the therapeutic potential of inhibiting glial D-serine release though the transporter Slc1a4 (ASCT1). Furthermore, using cell-specific genetic strategies and pharmacology, we demonstrate that TBI-induced synaptic damage and memory impairment requires D-serine synthesis and release from both reactive astrocytes and microglia. Analysis of the murine cortex and acutely resected human TBI brain also show increased SRR and Slc1a4 levels. Together, these findings support a novel role for glial D-serine in acute pathological dysfunction following brain trauma, whereby these reactive cells provide the excess co-agonist levels necessary to initiate NMDAR-mediated synaptic damage