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AbstractBrazil is the major global soybean producer with ca. 40 million hectares grown annually. In recent years, there has been a growing interest by beekeepers to migrate their hives close to soybean fields, to allow honey bees, Apis melliferaL. 1758 (Hymenoptera – Apidae) to forage in. To understand the effect of honey bee pollination on the soybean yield, one experiment was set up in Londrina, Brazil, to assess the yield of soybeans and its components, whose flowers were visited by honey bees, compared to those not visited. The experiment was repeated for three consecutive years, during the 2017 to 2020 soybean growing seasons. Treatments consisted of (1) open plots, with free access by honey bees; (2) caged plots with a honey bee hive inside; and (3) caged plots with no access by honey bees or any other pollinator. Monitoring visits by honey bees to soybean flowers indicated consistent visits in open and caged plots with a beehive, and larger numbers of honey bees were observed visiting soybeans at 11 am. The average yield for the three years revealed a significant increase when honey bees had access to flowers: 5,565 kg/ha for caged plots with honey bees and 5,201 for open plots, compared to caged plots without honey bee hives, which yielded 4,926 kg/ha. The yield increase was mainly associated with the occurrence of more 3 and 4-seeded pods, a larger number of seeds/pod and seed weight, as well as a smaller number of pods with zero or one seed observed in treatments with the presence of honey bees, compared to the caged plots without beehives.

AbstractBrazil is the leading soybean producing country in the world, and soybean is the major crop of Brazilian agriculture, spread over 36 million hectares during the 2020/21 season, producing almost 125 million tons. The honey bee, Apis melliferaLinnaeus, 1758 (Hymenoptera: Apidae), and other bees are known as soybean flowers visitors, being potential pollinators of the crop, normally resulting in higher soybean yields. Over the last ten years, it has been observed an increasing interest of both beekeepers and soybean growers, to place honey bee colonies close to soybean fields, using the crop as a forage source. In the majority of the reports of soybeans growers, an increase of the soybean yield was observed when following this practice, while a small number claimed no yield modification. The purpose of the present work was to study the effect of visits of individuals of A. melliferato soybean flowers and the consequent pollination on soybean productivity, when there is a constraint to the expression of the potential crop yield. The experiments were set up in Londrina, Brazil, during the 2016/17 and 2019/20 crop seasons, in areas with known sub superficial compaction layers, preventing soybean roots from deepening in the soil, therefore restricting the absorption of water and nutrients by the plants. Treatments consisted of 1) open plots, resembling a typical grower field with free access of bees; 2) a caged plot with an A. melliferabeehive inside, and 3) a caged plot with no bees or any other potential pollinating insect inside. Results indicated no yield differences due to the pollination of soybean flowers by the bees, compared to the treatment with the absence of bee visit. Among the yield components, only pods with 1 or 2 seeds were lower on caged plots with bees on the 1stexperiment. No differences were detected for all others observed parameters on 1stand for all components on 2ndexperiments. Observations of the honey bee behavior demonstrated that only 27.9% of the bee visits to soybean flowers resulted in nectar hoarding, with a time lapse of 4.52 seconds for a visit to a single flower. When a flower was only tested (72.1%), without nectar collection, the average time of a honey bee visit was 1.38 seconds. New studies should be performed to verify if other biotic or abiotic stresses that depress soybean yield also prevent the expression of the benefit of bees’ pollination to soybean yield.

Grounded on public sensorization initiatives to monitor the Lisbon's mobility system as a whole, the Integrative Learning from Urban Data and Situational Context for City Mobility Optimization(ILU) research project was initially designed as a means of providing decision support tools for the city of Lisbon to advance towards sustainable mobility. This paper reviews a significant number of research outcomes developed in the scope of the ILU project that are aligned with the envisaged goal. These are comprehensively analyzed through an integrated framework to identify how different theories and methods anchored in data science and transport planning were applied to the different datasets of the public transport services, converging to build principles of urban mobility resilience. Lessons learned are potentially transferrable to other European cities.

The CoDEC (Connected Data for Effective Collaboration) project has developed standardised tools – an Asset Data Dictionary and associated Ontology – to support data integration between Building Information Modelling (BIM) and Asset Management Systems (AMS). CoDEC has also developed an OpenAPI (Application Protocol Interface) to enable automatic data connection between the two systems. Having developed the standardised process, the potential benefits offered for connecting and linking data have been shown in three pilot projects to demonstrate (1) how tunnel monitoring data can enrich BIM models of tunnels (2) how data from bridge sensors can be linked and visualised and (3) how highway data from a BIM model can be linked to GIS-based AMS for the operational phase. This paper describes the project outcomes.

•Entry-only AFC systems still challenge the inference of origin-destination matrices.•Analysis of the state-of-art principles granted a solid baseline for developing the estimation approach.•Assembling principles with machine learning methods enhanced the alighting estimation.•Novel clustering approach on entry-exit pairs showed promise in estimating passengers' stochastic behavior.•A hurdle for the estimation arises from trips involving boarding stops in the city periphery.

ABSTRACTPlasmodium falciparuminfection during pregnancy leads to abortions, stillbirth, low birth weight, and maternal mortality. Infected erythrocytes (IEs) accumulate in the placenta by adhering to chondroitin sulfate A (CSA) via var2CSA protein exposed on the P. falciparumIE membrane. Plasmodium bergheiIE infection in pregnant BALB/c mice is a model for severe placental malaria (PM). Here, we describe a transgenic P. bergheiparasite expressing the full-length var2CSA extracellular region (domains DBL1X to DBL6ε) fused to a P. bergheiexported protein (EMAP1) and characterize a var2CSA-based mouse model of PM. BALB/c mice were infected at midgestation with different doses of P. berghei-var2CSA (P. berghei-VAR) or P. bergheiwild-type IEs. Infection with 104P. berghei-VAR IEs induced a higher incidence of stillbirth and lower fetal weight than P. berghei. At doses of 105and 106IEs, P. berghei-VAR-infected mice showed increased maternal mortality during pregnancy and fetal loss, respectively. Parasite loads in infected placentas were similar between parasite lines despite differences in maternal outcomes. Fetal weight loss normalized for parasitemia was higher in P. berghei-VAR-infected mice than in P. berghei-infected mice. In vitroassays showed that higher numbers of P. berghei-VAR IEs than P. bergheiIEs adhered to placental tissue. Immunization of mice with P. berghei-VAR elicited IgG antibodies reactive to DBL1-6 recombinant protein, indicating that the topology of immunogenic epitopes is maintained between DBL1-6–EMAP1 on P. berghei-VAR and recombinant DBL1-6 (recDBL1-6). Our data suggested that impairments in pregnancy caused by P. berghei-VAR infection were attributable to var2CSA expression. This model provides a tool for preclinical evaluation of protection against PM induced by approaches that target var2CSA.

Oligodendrocytes are the myelinating cells of the central nervous system that constitute about 5 to 10% of the total glial population. These cells are responsible for myelin sheath production, which is essential not only for the rapid and efficient conduction of the electrical impulses along the axons, but also for preserving axonal integrity. Oligodendrocytes arise from oligodendrocyte progenitor cells that proliferate and differentiate just before and after birth, under a highly-regulated program. Both oligodendrocytes and their precursors are very susceptible to injury by several mechanisms, including excitotoxic damage, oxidative stress and inflammatory events. In this review, we will cover not only several important aspects of oligodendrocyte development and regulatory mechanisms involved in this process, but also some of the most important pathways of injury associated to oligodendrogenesis. Moreover, we will also address some neurological disorders along life journey that present impairment in oligodendrocyte function and in myelination during neurodevelopment, such as periventricular leukomalacia, hypoxia/ischemia and hyperbilirubinemia that in turn can potentiate the emergence of neurological and neurodegenerative diseases like schizophrenia, multiple sclerosis and Alzheimer’s disease.

Glycogen synthase kinase 3 (GSK-3) is a serine-threonine kinase discovered decades ago to have an important role in glycogen metabolism. Today, we know that this kinase is involved in the regulation of many cell functions, including insulin signaling, specification of cell fate during embryonic development, and the control of cell division and apoptosis. Insulin and TDZD-8 (4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione) are inhibitors of GSK-3 that have been shown to possess organ-protective effects in inflammatory-mediated organ injury models. We aimed to evaluate the cytoprotective effect of GSK-3 inhibition on rat models of liver ischemia-reperfusion and thermal injury. In the liver ischemia-reperfusion model, TDZD-8 and insulin were administered at 5 mgkg (i.v.) and 1.4 IUkg (i.v.), respectively, 30 min before induction of ischemia and led to the significant reduction of the serum concentration of aspartate aminotransferase, alanine aminotransferase, -glutamyltransferase, and lactate dehydrogenase. Beneficial effects were found to be independent from blood glucose levels. In the thermal injury model, TDZD-8 was administered at 5 mgkg (i.v.) 5 min before induction of injury and significantly reduced multiple organ dysfunction markers (liver, neuromuscular, and lung). In the lung, TDZD-8 reduced the histological signs of tissue injury, inflammatory markers (cytokines), and neutrophil chemotaxisinfiltration; reduced GSK-3, nuclear factor-B, and Akt activation; reduced caspase-3 and metalloproteinase-9 activation. Our study provides a new insight on the beneficial effects of GSK-3 inhibition on systemic inflammation and further elucidates the mechanism and pathway crosstalks by which TDZD-8 reduces the multiple organ injury elicited by thermal injury.

Bilirubin-induced neurologic dysfunction (BIND) and kernicterushas been used to describe moderate to severe neurologic dysfunction observed in children exposed to excessive levels of total serum bilirubin (TSB) during the neonatal period. Here we use a new mouse model that targets deletion of the Ugt1locus and the Ugt1a1gene in liver to promote hyperbilirubinemia-induced seizures and central nervous system toxicity. The accumulation of TSB in these mice leads to diffuse yellow coloration of brain tissue and a marked cerebellar hypoplasia that we characterize as kernicterus. Histologic studies of brain tissue demonstrate that the onset of severe neonatal hyperbilirubinemia, characterized by seizures, leads to alterations in myelination and glia reactivity. Kernicterus presents as axonopathy with myelination deficits at different brain regions, including pons, medulla oblongata, and cerebellum. The excessive accumulation of TSB in the early neonatal period (5 days after birth) promotes activation of the myelin basic protein (Mbp) gene with an accelerated loss of MBP that correlates with a lack of myelin sheath formation. These changes were accompanied by increased astroglial and microglial reactivity, possibly as a response to myelination injury. Interestingly, cerebellum was the area most affected, with greater myelination impairment and glia burden, and showing a marked loss of Purkinje cells and reduced arborization of the remaining ones. Thus, kernicterus in this model displays not only axonal damage but also myelination deficits and glial activation in different brain regions that are usually related to the neurologic sequelae observed after severe hyperbilirubinemia.

Companies throughout history consider that growth is one of their main goals and doing it profitably is another of the goals to be achieved. The question they face is how to keep the investor interested in making the balance between the payment of growing dividends and/or favouring gains on invested capital. This article presents a performance analysis of some large corporations with similar global presence and significant market share in the manufacturing of electrical and electronic equipment intended for infrastructure projects. To perform the analysis the survey has considered the financial data of three conglomerates published in the New York stock market considering a 20-year period to minimise the effects of any crisis. So the goal is to find a pattern in the performance of these successful companies that can serve as a model for extremely competitive markets.

Pregnancy-associated malaria is often associated with adverse pregnancy outcomes. Placental circulatory impairments are an intriguing and unsolved component of malaria pathophysiology.

Elevated levels of free bilirubin in the brain triggered by increased concentrations of unconjugated bilirubin (UCB) may cause adverse neurological outcomes. We aimed to evaluate: (i)the effects of UCB in neuronal apoptosis, oxidative stress and P-JNK1/2 expression; (ii) if UCB damages the neuritic tree and whether glycoursodeoxycholic acid (GUDCA), IL-10 or L-NAME are protective; (iii)the brain regional susceptibility to UCB-induced dendritic disruption.Rat cortical neurons with 3 days in vitro (DIV) were incubated with 50 microM UCB plus 100 microM HSA. After 4h, we evaluated apoptosis (caspase-3 activity), P-JNK1/2 and nNOS expression (Western blot) and nitrites (Griess reagent). Following 24h, neurite arborization (MAP-2 labeling) was evaluated. Cells were also incubated with 50 microM GUDCA, 10 ng/mL IL-10 or 100 microM L-NAME prior to UCB exposure. Neurons from hippocampus and cerebellum at 3 DIV were also exposed to UCB (24h) to assess neuritic arborization.UCB increased caspase-3 activity (1.5-fold, p< 0.01), P-JNK1/2 (1.3-fold, p< 0.01) and nNOS (1.2- fold, p< 0.01), as well as NO production (1.7-fold, p< 0.01). Moreover, UCB decreased neurite extension (0.8-fold, p< 0.05) and ramification (0.5-fold, p< 0.05), effects that were prevented by GUDCA (p< 0.05 vs UCB), IL-10 and L-NAME (extension, p< 0.05; ramification, p< 0.01 vs UCB). Hippocampus revealed the utmost reduction in neurite ramification (46%, p< 0.01) and extension (28%, p< 0.05).Neuronal dysfunction by UCB comprises several intracellular pathways involving oxidative injury and disruption of neurite arborization. Anti-oxidant and/or anti-inflammatory compounds prevent UCB-damage to neuronal network. Hippocampus reveals the higher neurotoxicty by UCB. Funding:FCT- PTDC/SAU-NEU/64385/2006.