Cleaner fruit production has become important for producers worldwide because consumers and retail companies increasingly base their purchase decisions on environmental criteria. Green manure is a soil management practice that promotes soil nutrient enrichment and may improve crop yield. Nonetheless, the environmental impacts and economic analysis of combined green manure and tropical fruit production have not been performed. This work assesses the environmental impacts and profits resulting from the Brazilian melon, commercialized in Brazil. Melon production is analyzed under two cultivation systems: i) the conventional form practiced by farmers located in the São Francisco Valley region, Brazil, and ii) the conservationist system, based on a green manure experiment carried out in this same region. This study applies life cycle assessment to evaluate the environmental impacts of both systems, considering farm inputs production and transportation (energy power, fertilizers, pesticides, plastic, paper, and fuel) as well as melon production and transportation to the main national distribution market in São Paulo. The impact categories evaluated are climate change, soil acidification, freshwater and marine eutrophication, water depletion, human toxicity (cancer and non-cancer), and ecotoxicity. Scenario analysis is applied to assess impacts under different designed conditions for transportation, packing, and nitrogen fertilization. The profit analysis is performed by reducing the total production costs (inputs and services) from the revenue obtained from selling melons. Results indicate that the conservationist system causes lower impacts and lead to higher profit than the conventional system, for all assessed categories. The scenario analysis confirms that impacts can be further reduced in all categories when alternative melon transportation and fertilization practices are adopted. This work demonstrates that the environmental performance of Brazilian melon production can be improved with the addition of green manure and alternative transportation practices.
ObjectiveThe aim of this study was to evaluate the impact of iron overload on the profile of interleukin-10 levels, biochemical parameters and oxidative stress in sickle cell anemia patients. MethodsA cross-sectional study was performed of 30 patients with molecular diagnosis of sickle cell anemia. Patients were stratified into two groups, according to the presence of iron overload: Iron overload (n = 15) and Non-iron overload (n = 15). Biochemical analyses were performed utilizing the Wiener CM 200 automatic analyzer. The interleukin-10 level was measured by capture ELISA using the BD OptEIAT commercial kit. Oxidative stress parameters were determined by spectrophotometry. Statistical analysis was performed using GraphPad Prism software (version 5.0) and statistical significance was established for p-values < 0.05 in all analyses. ResultsBiochemical analysis revealed significant elevations in the levels of uric acid, triglycerides, very low-density lipoprotein (VLDL), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), urea and creatinine in the Iron overload Group compared to the Non-iron overload Group and significant decreases in the high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Ferritin levels correlated positively with uric acid concentrations (p-value < 0.05). The Iron overload Group showed lower interleukin-10 levels and catalase activity and higher nitrite and malondialdehyde levels compared with the Non-iron overload Group. ConclusionThe results of this study are important to develop further consistent studies that evaluate the effect of iron overload on the inflammatory profile and oxidative stress of patients with sickle cell anemia.
BackgroundAt the time of diagnosis, more than 50% of patients with myelodysplastic syndrome have a normal karyotype and are classified as having a favorable prognosis. However, these patients often show very variable clinical outcomes. Furthermore, current diagnostic tools lack the ability to look at genetic factors beyond karyotyping in order to determine the cause of this variability.ObjectiveTo evaluate the impact of p53 protein expression at diagnosis in patients with low-risk myelodysplastic syndrome.MethodsThis study enrolled 38 patients diagnosed with low-risk myelodysplastic syndrome. Clinical data were collected by reviewing medical records, and immunohistochemical p53 staining was performed on bone marrow biopsies.ResultsOf the 38 participants, 13 (34.21%) showed p53 expression in their bone marrow. At diagnosis, this group of patients also presented clinical features characteristic of a poor prognosis more often than patients who did not express p53. Furthermore, patients expressing p53 had a shorter median survival time compared to those without p53 expression.ConclusionThis study shows that the expression of p53 at diagnosis is a useful indicator of distinct clinical characteristics and laboratory profiles found in low-risk myelodysplastic syndrome patients. These data indicate that the immunohistochemical analysis of p53 may be a prognostic tool for myelodysplastic syndrome and should be used as an auxiliary test to help determine the best therapeutic choice.
The results demonstrated that IO is an important risk factor for enhanced oxidative stress in SCA.
The patients presented prevalence of TNF-alpha and IL-10 low-profile producer. The cytokine serum levels presented an association with the presence of polytransfusion and ACS in SCA patients.
The aim of the study was to investigate the possible anti-inflammatory and antioxidant effects of BAY 73-6691 on neutrophils from SCA patients. This study included 35 patients with a molecular diagnosis of SCA, whose neutrophils were isolated and treated with BAY 73-6691 at the concentrations 100, 10, 1.0 and 0.1 lg/mL. LDH release and MTT assays were performed to verify cell viability. To evaluate oxidative stress, the following parameters were determined by spectrophotometric assays: NO and malondialdehyde (MDA) levels and activity of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GPx). As inflammatory markers, myeloperoxidase (MPO) levels were evaluated by colorimetric assay and TNF-a by enzyme immunoassay. The results showed that neutrophils from SCA patients not treated with hydroxyurea (HU) had significantly lower NO levels and catalase and SOD activity, as well as significantly higher MDA, MPO and TNF-a levels when compared with neutrophils from SCA patients treated with HU and neutrophils from control group. Treatment of SCA neutrophils with BAY 73-6691 resulted in 94%, 200% and 168% increase in NOx levels, SOD and catalase activity, respectively. In addition, there was a reduction of approximately 46% and 45% in TNF-a and MPO levels, respectively. In SCAHU neutrophils, there was a 30% and 44% increase in NOx levels and SOD activity, respectively, and a 28% and 37% decrease in TNF-a and MPO levels, respectively. However, these effects were observed at cytotoxic doses only. The results of this study are original and demonstrate that inhibition of phosphodiesterase-9 in neutrophils from SCA patients with BAY 73-6691 was able to increase the NO bioavailability and attenuate oxidative stress and inflammation in neutrophils from patients not treated with HU.Sickle cell anaemia (SCA) is an inherited disease that results from a single mutation in the b-globin gene, leading to the production of unstable haemoglobin S (HbS) [1]. The haemoglobin polymerizes when deoxygenated and alters the normal biconcave-shaped erythrocyte to a sickle-shaped, unstable and rigid cell with a high expression of adhesion molecules [2]. Thus, SCA is characterized by intravascular haemolysis, chronic inflammation, vaso-occlusive events, endothelial damage and oxidative stress, which culminate in progressive microvascular damage in all organs [3][4][5].Leucocytes are now thought to play a fundamental role in the vaso-occlusive process, adhering to the endothelium and participating in reactive oxygen species (ROS) formation and inflammatory processes in the vasculature [6]. In addition, leucocytosis has been described as a risk factor for sickle crisis, stroke, silent cerebral infarction, acute chest syndrome and disease-related mortality [6][7][8]. Previous studies reported that in SCA individuals, leucocytes appear to exist in a chronic activated state in circulation, even in the basal state, and this activation causes the production of ROS in a NADPH oxidase-mediated respiratory burst [9,10].The reduced bi...
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