61 resultados para responsibility to protect (R2P)


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In this work, preliminary results of the use of hydrophobic thin films obtained by plasma deposition to protect grains and seeds are presented: grains coated by the films did not present biological degradation when stored in a saturated water vapor environment, but had their germination accelerated in the presence of water. A model that explains the difference of behavior of the films when exposed to water in vapor form or in liquid form, based on the formation of microchannels within the film that lead to water uptake in seeds, is presented. The model was successfully tested using quartz crystal measurements, which showed that the microchannels within the films can favor the adsorption and permeation of water when the films are immersed in water.

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The goal of this study was to evaluate the feasibility of preparing nanocapsules and nanoemulsions using tea tree oil as oily phase aiming to protect its volatilization. The nanostructures presented nanometric mean size (160-220 nm) with a polydispersity index below 0.25 and negative zeta potential. The pH values were 6.43 ± 0.37 and 5.98 ± 0.00 for nanoemulsions and nanocapsules, respectively. The oil content after preparation was 96%. The inclusion of tea tree oil in nanocapsules showed higher protection against volatilization. The analysis of mean size and polydispersity index of formulations presented no significant alteration during the storage time.

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The synthesis of magnetic materials such as nanostructured iron oxide has been intensively researched due to their broad applications in biomedicine. As these nanoparticles have high specific surface area, they are very reactive and can aggregate easily, and biodegrade when exposed to biological systems. Mesoporous silica is often employed as support matrix to protect the magnetic functional component, avoiding undesirable effects. In this context, this review describes various syntheses of silica-coated iron oxide nanoparticles, and their use in applications such as bioseparation, magnetic resonance imaging, hyperthermia and drug delivery systems showing the growing interest of these materials in biological area.

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Niacin (nicotinamide, nicotinic acid) interferes on homeostasis, DNA regulation, signaling and longevity. Nicotinic acid reduces synthesis of lipoproteins-apo-B and increases HDL. Its antilipemic action in liver produces: 1) inhibition of DGAT2, with decreased triacylglycerol synthesis, 2) downregulation of the b-chain of adenosine triphosphate synthase, leading to reduced HDL-apo-A-I catabolism. Nicotinic acid could increase redox potential in vascular endothelium. HM74A receptor activation in macrophages would be responsible for the release of prostaglandins, causing flushing in epidermis. HM74A agonists could assist in identifying antilipemic agents. Extended release niacin in combination with statin appears to protect cardiovascular system of patients with low HDL.

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Antimicrobials, among other veterinary drugs, are used worldwide in industry and agriculture to protect animal health and prevent economic loss. In recent years, they have been detected in various environmental compartments, including soil, surface and groundwater and have become a topic of research interest. Emphasizing this class of compounds, this review presents the different pathways which veterinary drugs enter in the environment, in particular contaminate soils. Also are presented regulatory aspects and guidelines, adsorption/desorption and degradation of these compounds in soils and the consequences of its dispersal in the environment.

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Brazilian universities and research institutions still fail to protect the knowledge and technology produced by their community of students, staff and professors while Intellectual Property (IP) issues along with the role of patents and their strategic management in educational and research institutions remain taboo or misunderstood. The focus of this work was to demystify these subjects, including IP, patents and their requirements, the decision to patent as well as tips for successful patenting. Any student, professor or researcher of an educational or research institution can invent and protect their technology. This paper shows how to make such a patent application.

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The main objective of the present study was to evaluate the effect of the sunhemp (Crotalaria juncea) host species on the protective ability of two mild strains of Passion fruit woodiness virus (PWV), named F-101 and F-144, which had failed to protect passion flowers (Passiflora edulis f. flavicarpa) in previous experiments. The nucleotide sequences of the capsid protein (CP) gene and the 3'-non-translated region (3'-NTR) of these mild strains and the severe strain of PWV-SP were compared to confirm their relationship. The results of two protective tests with sunhemp plants in the greenhouse and one test under field conditions showed that all plants infected with either mild strain were protected against infection and/or symptom expression of the severe strain of PWV-SP. Evaluation of the relative concentration of the mild strains in sun hemp leaves showed an apparent uniformity in virus distribution in the leaf tissues, different than that which was previously reported for these mild strains in passion flower leaves. These results agree with previous studies that showed the effect of the concentration of the protective strains and the host species in the protection process.

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In this note we describe the standard technical maneuver used in our department to protect the skin during thyroidectomy in order to get the best aesthetic result. We use surgical gloves to protect the skin during these operations to reduce the negative impact of thermal trauma and mechanical retractors and energy delivery devices at the edges of the skin incised. This practice is effective, inexpensive, rapid, reproducible and showed no complication in our experience of over 2,500 thyroidectomies.

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Duodenal trauma is an infrequent injury, but linked to high morbidity and mortality. Surgical management of duodenal injuries is dictated by: patient's hemodynamic status, injury severity, time of diagnosis, and presence of concomitant injuries. Even though most cases can be treated with primary repair, some experts advocate adjuvant procedures. Pyloric exclusion (PE) has emerged as an ancillary method to protect suture repair in more complex injuries. However, the effectiveness of this procedure is debatable. The "Evidence Based Telemedicine - Trauma & Acute Care Surgery" (EBT-TACS) Journal Club performed a critical appraisal of the literature and selected three relevant publications on the indications for PE in duodenal trauma. The first study retrospectively compared 14 cases of duodenal injuries greater than grade II treated by PE, with 15 cases repaired primarily, all of which penetrating. Results showed that PE did not improve outcome. The second study, also retrospective, compared primary repair (34 cases) with PE (16 cases) in blunt and penetrating grade > II duodenal injuries. The authors concluded that PE was not necessary in all cases. The third was a literature review on the management of challenging duodenal traumas. The author of that study concluded that PE is indicated for anastomotic leak management after gastrojejunostomies. In conclusion, the choice of the surgical procedure to treat duodenal injuries should be individualized. Moreover, there is insufficient high quality scientific evidence to support the abandonment of PE in severe duodenal injuries with extensive tissue loss.

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Chicks infected during the first two weeks of life with chicken anaemia virus (CAV) manifest clinical disease that can be avoided if the breeder hens transfer enough antibodies to their progeny. The objective of the present work was to establish the prevalence and titer of anti-CAV antibodies in some Brazilian broiler hen breeder flocks and verify in which phase of life the birds were infected. A total of 1,709 serum samples from 12 broiler hen flocks vaccinated against CAV and 64 unvaccinated flocks were analyzed for CAV antibodies with an enzyme-linked immunosorbent assay (ELISA). All non-vaccinated breeder flocks were found to be infected with CAV, with 89% of the hens tested presenting antibodies, 52% of these with titers considered high enough to protect their progeny against CAV infection. Likewise, all vaccinated hens had antibody titer to CAV capable of conferring protection to their progeny. Thus, vaccination of hens seems capable of conferring protection to chicks against clinically apparent CAV-associated disease.

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Thalidomide has been shown to selectively inhibit TNF-a production in vitro by lipopolysaccharide (LPS)-stimulated monocytes. TNF-a has been shown to play a pivotal role in the pathophysiology of endotoxic shock. Using a mouse model of LPS-induced shock, we investigated the effects of thalidomide on the production of TNF-a and other cytokines and on animal survival. After injection of 100-350 µg LPS into mice, cytokines including TNF-a, IL-6, IL-10, IL-1ß, GM-CSF and IFN-g were measured in the serum. Administration of 200 mg/kg thalidomide to mice before LPS challenge modified the profile of LPS-induced cytokine secretion. Serum TNF-a levels were reduced by 93%, in a dose-dependent manner, and TNF-a mRNA expression in the spleens of mice was reduced by 70%. Serum IL-6 levels were also inhibited by 50%. Thalidomide induced a two-fold increase in serum IL-10 levels. Thalidomide treatment did not interfere with the production of GM-CSF, IL-1ß or IFN-g. The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 µg to 300 µg in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death

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Toxoplasma gondii and Trypanosoma cruzi are intracellular parasites which, as part of their life cycle, induce a potent cell-mediated immunity (CMI) maintained by Th1 lymphocytes and IFN-g. In both cases, induction of a strong CMI is thought to protect the host against rapid parasite multiplication and consequent pathology and lethality during the acute phase of infection. However, the parasitic infection is not eliminated by the immune system and the vertebrate host serves as a parasite reservoir. In contrast, Leishmania sp, which is a slow growing parasite, appears to evade induction of CMI during early stages of infection as a strategy for surviving in a hostile environment (i.e., inside the macrophages which are their obligatory niche in the vertebrate host). Recent reports show that the initiation of IL-12 synthesis by macrophages during these parasitic infections is a key event in regulating CMI and disease outcome. The studies reviewed here indicate that activation/inhibition of distinct signaling pathways and certain macrophage functions by intracellular protozoa are important events in inducing/modulating the immune response of their vertebrate hosts, allowing parasite and host survival and therefore maintaining parasite life cycles.

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We have studied the effect of peroxynitrite (ONOO-) on the membrane cytoskeleton of red blood cells and its protection by melatonin. Analysis of the protein fraction of the preparation by SDS-PAGE revealed a dose-dependent (0-600 µM ONOO-) disappearance at pH 7.4 of the main proteins: spectrin, band 3, and actin, with the concomitant formation of high-molecular weight aggregates resistant to reduction by ß-mercaptoethanol (2%) at room temperature for 20 min. These aggregates were not solubilized by 8 M urea. Incubation of the membrane cytoskeleton with ONOO- was characterized by a marked depletion of free sulfhydryl groups (50% at 250 µM ONOO-). However, a lack of effect of ß-mercaptoethanol suggests that, under our conditions, aggregate formation is not mediated only by sulfhydryl oxidation. The lack of a protective effect of the metal chelator diethylenetriaminepentaacetic acid confirmed that ONOO--induced oxidative damage does not occur only by a transition metal-dependent mechanism. However, we demonstrated a strong protection against cytoskeletal alterations by desferrioxamine, which has been described as a direct scavenger of the protonated form of peroxynitrite. Desferrioxamine (0.5 mM) also inhibited the loss of tryptophan fluorescence observed when the ghosts were treated with ONOO-. Glutathione, cysteine, and Trolox® (1 mM), but not mannitol (100 mM), were able to protect the proteins against the effect of ONOO- in a dose-dependent manner. Melatonin (0-1 mM) was especially efficient in reducing the loss of spectrin proteins when treated with ONOO- (90% at 500 µM melatonin). Our findings show that the cytoskeleton, and in particular spectrin, is a sensitive target for ONOO-. Specific antioxidants can protect against such alterations, which could seriously impair cell dynamics and generate morphological changes.

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Clinical trials indicate that amifostine may confer protection on various normal tissues without attenuating anti-tumor response. When administered prior to chemotherapy or radiotherapy, it may provide a broad spectrum of cytoprotection including against alkylating drugs. The mechanism of protection resides in the metabolism at normal tissue site by membrane-bound alkaline phosphatase. Toxicity of this drug is moderate with hypotension, nausea and vomiting, and hypocalcemia being observed. We report a phase II study using amifostine as a protective drug against high-dose cyclophosphamide (HDCY) (7 g/m2), used to mobilize peripheral blood progenitor cells (PBPC) and to reduce tumor burden. We enrolled 29 patients, 22 (75.9%) affected by aggressive and 7 (24.1%) by indolent non-Hodgkin's lymphoma (NHL), who were submitted to 58 infusions of amifostine and compared them with a historical group (33 patients) affected by aggressive NHL and treated with VACOP-B followed by HDCY. The most important results in favor of amifostine were the reduction of intensity of cardiac, pulmonary and hepatic toxicity, and a significant reduction of frequency and severity of mucositis (P = 0.04). None of the 29 patients died in the protected group, while in the historical group 2/33 patients died because of cardiac or pulmonary toxicity and 2 patients stopped therapy due to toxicity. Amifostine did not prevent the aplastic phase following HDCY. PBPC collection and hematological recovery were adequate in both groups. The number of CFU-GM (colony-forming units-granulocyte/macrophage) colonies and mononuclear cells in the apheresis products was significantly higher in the amifostine group (P = 0.02 and 0.01, respectively). Side effects were mild and easily controlled. We conclude that amifostine protection should be useful in HDCY to protect normal tissues, with acceptable side effects.

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Lead has been shown to produce cognitive and motor deficits in young rats that could be mediated, at least in part, by inhibition of the zinc-containing heme biosynthetic enzyme delta-aminolevulinate dehydratase (ALA-D). In the present study we investigated the effects of lead and/or zinc treatment during the second stage of rapid postnatal brain development on brain, kidney and blood ALA-D specific activity, as well as the negative geotaxis behavior of rats. Eight-day-old Wistar rats were injected intraperitoneally with saline, lead acetate (8 mg/kg) and/or zinc chloride (2 mg/kg) daily for five consecutive days. Twenty-four hours after treatment, ALA-D activity was determined in the absence and presence of DL-dithiothreitol (DTT). The negative geotaxis behavior was assessed in 9- to 13-day-old rats. Treatment with lead and/or zinc did not affect body, brain or kidney weights or brain- or kidney-to-body weight ratios of the animals. In spite of the absence of effect of any treatment on ALA-D specific activity in brain, kidney and blood, the reactivation index with DTT was higher in the groups treated with lead or lead + zinc than in the control group, in brain, kidney and blood (mean ± SEM; brain: 33.33 ± 4.34, 38.90 ± 8.24, 13.67 ± 3.41; kidney: 33.50 ± 2.97, 37.60 ± 2.67, 15.80 ± 2.66; blood: 63.95 ± 3.73, 56.43 ± 5.93, 31.07 ± 4.61, respectively, N = 9-11). The negative geotaxis response behavior was not affected by lead and/or zinc treatment. The results indicate that lead and/or zinc treatment during the second stage of rapid postnatal brain growth affected ALA-D, but zinc was not sufficient to protect the enzyme from the effects of lead in brain, kidney and blood.