Fog Computing Model to Orchestrate the Consumption and Production of Energy in Microgrids.

Energy advancement and innovation have generated several challenges for large modernized cities, such as the increase in energy demand, causing the appearance of the small power grid with a local source of supply, called the Microgrid. A Microgrid operates either connected to the national centralized power grid or singly, as a power island mode. Microgrids address these challenges using sensing technologies and Fog-Cloudcomputing infrastructures for building smart electrical grids. A smart Microgrid can be used to minimize the power demand problem, but this solution needs to be implemented correctly so as not to increase the amount of data being generated. Thus, this paper proposes the use of Fog computing to help control power demand and manage power production by eliminating the high volume of data being passed to the Cloud and decreasing the requests' response time. The GridLab-d simulator was used to create a Microgrid, where it is possible to exchange information between consumers and generators. Thus, to understand the potential of the Fog in this scenario, a performance evaluation is performed to verify how factors such as residence number, optimization algorithms, appliance shifting, and energy sources may influence the response time and resource usage.

Taxonomic, phylogenetic, and trait Beta diversity in South American hummingbirds.

Comparison of the taxonomic, phylogenetic, and trait dimensions of beta diversity may uncover the mechanisms that generate and maintain biodiversity, such as geographic isolation, environmental filtering, and convergent adaptation. We developed an approach to predict the relationship between environmental and geographic distance and the dimensions of beta diversity. We tested these predictions using hummingbird assemblages in the northern Andes. We expected taxonomic beta diversity to result from recent geographic barriers limiting dispersal, and we found that cost distance, which includes barriers, was a better predictor than Euclidean distance. We expected phylogenetic beta diversity to result from historical connectivity and found that differences in elevation were the best predictors of phylogenetic beta diversity. We expected high trait beta diversity to result from local adaptation to differing environments and found that differences in elevation were correlated with trait beta diversity. When combining beta diversity dimensions, we observe that high beta diversity in all dimensions results from adaption to different environments between isolated assemblages. Comparisons with high taxonomic, low phylogenetic, and low trait beta diversity occurred among lowland assemblages separated by the Andes, suggesting that geographic barriers have recently isolated lineages in similar environments. We provide insight into mechanisms governing hummingbird biodiversity patterns and provide a framework that is broadly applicable to other taxonomic groups.

Role of proinflammatory cytokines on lipopolysaccharide-induced phase shifts in locomotor activity circadian rhythm.

We previously reported that early night peripheral bacterial lipopolysaccharide (LPS) injection produces phase delays in the circadian rhythm of locomotor activity in mice. We now assess the effects of proinflammatory cytokines on circadian physiology, including their role in LPS-induced phase shifts. First, we investigated whether differential systemic induction of classic proinflammatory cytokines could explain the time-specific behavioral effects of peripheral LPS. Induction levels for plasma interleukin (IL)-1α, IL-1ß, IL-6, or tumor necrosis factor (TNF)-α did not differ between animals receiving a LPS challenge in the early day or early night. We next tested the in vivo effects of central proinflammatory cytokines on circadian physiology. We found that intracerebroventricular (i.c.v.) delivery of TNF-α or interleukin IL-1ß induced phase delays on wheel-running activity rhythms. Furthermore, we analyzed if these cytokines mediate the LPS-induced phase shifts and found that i.c.v. administration of soluble TNF-α receptor (but not an IL-1ß antagonistic) prior to LPS stimulation inhibited the phase delays. Our work suggests that the suprachiasmatic nucleus (SCN) responds to central proinflammatory cytokines in vivo, producing phase shifts in locomotor activity rhythms. Moreover, we show that the LPS-induced phase delays are mediated through the action of TNF-α at the central level, and that systemic induction of proinflammatory cytokines might be necessary, but not sufficient, for this behavioral outcome.

Paying the circadian toll: the circadian response to LPS injection is dependent on the Toll-like receptor 4.

Systemic low doses of the endotoxin lipopolysaccharide (LPS) administered at CT15 (circadian time 12 corresponds to locomotor activity onset) induce phase delays of locomotor activity rhythms in mice. To evaluate if this effect was mediated by the Toll-like receptor 4 (TLR4), our present aim was to characterize the circadian behavior and LPS-induced circadian response of TLR4 (LPS receptor)-deficient mice (in C57bl/10 and C3H backgrounds). In mutants, we observed a free-running period and a light-induced phase delay similar to the one observed in their corresponding wild-type (WT) littermates. The LPS-induced phase delay, wheel running inhibition and c-Fos/Per-1 immunoreactivity in the paraventricular nuclei observed in WT mice was absent or significantly decreased in the TLR4-deficient mice. In conclusion, we show that LPS-induced circadian responses are mediated by TLR4.

[The effect of lipid emulsions on the mechanisms of organic defense in infectious injury]. / Efeito de emulsões lipídicas sobre mecanismos de defesa orgânica na agressão infecciosa.

For treatment of metabolic derangements in infective states intravenous lipidic emulsions have been used. Their use is however not harmless existing reports on fat inhibiting the function of blood polymorphonuclear leukocytes and macrophages. The purpose of the research reported herewith was to study in rats the effect of new intravenous lipidic emulsions containing medium chain triglycerides and long chain triglycerides and compare it with the effect of long chain triglycerides emulsion on function of polymorphonuclear leukocytes (chemotaxis, phagocytosis and bactericidal activity). The intraperitoneal implant of an E. coli capsule was used for the study. The transfusions of both lipidic emulsions in septic rats have not altered functions of polymorphonuclear leukocytes when compared with saline infusion. However there was found hepatic steatosis, hypertrophy and presence of fat globules in the Kupffer cells in rats infused with medium chain and long chain triglyceride emulsions. Sequential blood cultures obtained from rats infused with the emulsions showed increased bacterial growth with medium chain triglyceride emulsion. There was no significant difference between the rats that received both lipid infusions and those that received saline infusions as to the mortality. Our experimental study suggests that the use of fat emulsions in infective states be done with care and monitoring of seric triglycerides and steroids.

Monoclonal antibody OKT3 therapy in pediatric kidney transplant recipients.

Thirty-one pediatric patients with acute renal allograft rejection were treated with the monoclonal antibody OKT3. In 24 cases, increased doses of steroids followed by a polyclonal antithymocyte globulin were ineffective in reversing the rejection episode. Twenty-eight patients completed the prescribed minimum 10-day treatment course, with effective rejection reversal in 22. Three patients failed to complete the course of therapy: one because of leukopenia that developed after the first dose, one because of a clotted graft, and another because of symptomatic cytomegalovirus infection. The overall success rate of OKT3 for rejection reversal was 74%; however, 55% of recipients had rebound rejection, and 85% of patients had detectable anti-OKT3 antibodies after completion of the course of therapy. Ten patients were treated with a second course of OKT3, and in eight of these patients, rejection was at least temporarily reversed. The starting dose of OKT3 for second-course therapy was the same as that used during first-course therapy, but in five cases the dose was increased during the course because of inadequate therapeutic response. Seven of these patients lost their grafts a mean of 6.5 months after completion of second-course therapy. We looked for anti-OKT3 antibody in nine recipients after completion of a second treatment course and found it in all nine. Our observations regarding a second treatment course with this monoclonal antibody preparation suggest that although rejection reversal may be observed, ultimate graft survival is poor and anti-OKT3 antibody formation is enhanced.

OKT3 monoclonal antibody in pediatric kidney transplant recipients with recurrent and resistant allograft rejection.

Twelve pediatric patients, aged 28 months to 17 years, received OKT3 to reverse renal allograft rejection. In 11 patients, the rejection crisis was resistant to conventional antirejection therapy with high doses of prednisone or polyclonal antithymocyte globulin. Reversal of rejection was successful in 10 patients who completed a treatment course. Because of recurring resistant rejection, five patients received a second course of OKT3, which was successful in reversing the rejection crisis in two. Among these patients, the persistence or the appearance of high levels of circulating T3 lymphocytes after initiating the second treatment course correlated with treatment failure. The immediate side effects associated with OKT3 therapy were transient and medically manageable. We conclude that this monoclonal antibody preparation is a safe and effective treatment for pediatric renal allograft in recipients experiencing rejection crisis resistant to conventional therapy. However, the potential impact of this immunosuppressive medication on long-term renal allograft survival in this patient population remains to be determined.