Drosophila motor neuron boutons remodel through membrane blebbing coupled with muscle contraction

Funding Information: We would like to thank Telmo Pereira from the Microscopy Facility for technical support, the Fly Facility at Nova Medical Research; CONGENTO: consortium for genetically tractable organisms. We thank the Developmental Studies Hybridoma Bank, Bloomington Drosophila Stock Center and VDRC for antibodies and fly stocks. This work was supported by PTDC-01778/2022- NeuroDev3D to R.O.T. GEMiNI and PTDC/BIA-COM/0151/2020 to C.S.M and European Research Council H2020-GA 810207-ARPCOMPLEXITY to E.R.G. A.R.F. is supported with a PhD scholarship from Fundação para a Ciência e Tecnologia, Portugal, reference SFRH/BD/144488/2019, and J.P.M. with a reference SFRH/BD/130920/2017. This work also supported by iNOVA4Health (UIDB/04462/2020 and UIDP/04462/2020), and LS4FUTURE (LA/P/0087/2020). Funding Information: We would like to thank Telmo Pereira from the Microscopy Facility for technical support, the Fly Facility at Nova Medical Research; CONGENTO: consortium for genetically tractable organisms. We thank the Developmental Studies Hybridoma Bank, Bloomington Drosophila Stock Center and VDRC for antibodies and fly stocks. This work was supported by PTDC-01778/2022- NeuroDev3D to R.O.T. GEMiNI and PTDC/BIA-COM/0151/2020 to C.S.M and European Research Council H2020-GA 810207-ARPCOMPLEXITY to E.R.G.. A.R.F. is supported with a PhD scholarship from Fundação para a Ciência e Tecnologia, Portugal, reference SFRH/BD/144488/2019, and J.P.M. with a reference SFRH/BD/130920/2017. This work also supported by iNOVA4Health (UIDB/04462/2020 and UIDP/04462/2020), and LS4FUTURE (LA/P/0087/2020). Publisher Copyright: © 2023, The Author(s).Wired neurons form new presynaptic boutons in response to increased synaptic activity, however the mechanism(s) by which this occurs remains uncertain. Drosophila motor neurons (MNs) have clearly discernible boutons that display robust structural plasticity, being therefore an ideal system in which to study activity-dependent bouton genesis. Here, we show that in response to depolarization and in resting conditions, MNs form new boutons by membrane blebbing, a pressure-driven mechanism that occurs in 3-D cell migration, but to our knowledge not previously described to occur in neurons. Accordingly, F-actin is decreased in boutons during outgrowth, and non-muscle myosin-II is dynamically recruited to newly formed boutons. Furthermore, muscle contraction plays a mechanical role, which we hypothesize promotes bouton addition by increasing MN confinement. Overall, we identified a mechanism by which established circuits form new boutons allowing their structural expansion and plasticity, using trans-synaptic physical forces as the main driving force.publishersversionpublishe

Therapeutic Options Targeting Oxidative Stress, Mitochondrial Dysfunction and Inflammation to Hinder the Progression of Vascular Complications of Diabetes

Type 2 diabetes mellitus is a leading cause of morbidity and mortality worldwide, given its serious associated complications. Despite constant efforts and intensive research, an effective, ubiquitous treatment still eludes the scientific community. As such, the identification of novel avenues of research is key to the potential discovery of this evasive “silver bullet.” We focus on this review on the matter of diabetic injury to endothelial tissue and some of the pivotal underlying mechanisms, including hyperglycemia and hyperlipidemia evoked oxidative stress and inflammation. In this sense, we revisited the most promising therapeutic interventions (both non-pharmacological and antidiabetic drugs) targeting oxidative stress and inflammation to hinder progression of vascular complications of diabetes. This review article gives particular attention to the relevance of mitochondrial function, an often ignored and understudied organelle in the vascular endothelium. We highlight the importance of mitochondrial function and number homeostasis in diabetic conditions and discuss the work conducted to address the aforementioned issue by the use of various therapeutic strategies. We explore here the functional, biochemical and bioenergetic alterations provoked by hyperglycemia in the endothelium, from elevated oxidative stress to inflammation and cell death, as well as loss of tissue function. Furthermore, we synthetize the literature regarding the current and promising approaches into dealing with these alterations. We discuss how known agents and therapeutic behaviors (as, for example, metformin, dietary restriction or antioxidants) can restore normality to mitochondrial and endothelial function, preserving the tissue’s function and averting the aforementioned complications

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Novel precoded relay-assisted algorithm for cellular systems

Cooperative schemes are promising solutions for cellular wireless systems to improve system fairness, extend coverage and increase capacity. The use of relays is of significant interest to allow radio access in situations where a direct path is not available or has poor quality. A data precoded relay-assisted scheme is proposed for a system cooperating with 2 relays, each equipped with either a single antenna or 2-antenna array. However, because of the half-duplex constraint at the relays, relaying-assisted transmission would require the use of a higher order constellation than in the case when a continuous link is available from the BS to the UT. This would imply a penalty in the power efficiency. The simple precoding scheme proposed exploits the relation between QPSK and 16-QAM, by alternately transmitting through the 2 relays, achieving full diversity, while significantly reducing power penalty. Analysis of the pairwise error probability of the proposed algorithm with a single antenna in each relay is derived and confirmed with numerical results. We show the performance improvements of the precoded scheme, relatively to equivalent distributed SFBC scheme employing 16-QAM, for several channel quality scenarios. Copyright © 2010 Sara Teodoro, et al.European project CODIVPortuguese project CADWINPortuguese project AGILEFC

Blueberry consumption challenges hepatic mitochondrial bioenergetics and elicits transcriptomics reprogramming in healthy wistar rats

An emergent trend of blueberries’ (BB) “prophylactic” consumption, due to their phytochemicals’ richness and well-known health-promoting claims, is widely scaled-up. However, the benefits arising from BB indiscriminate intake remains puzzling based on incongruent preclinical and human data. To provide a more in-depth elucidation and support towards a healthier and safer consumption, we conducted a translation-minded experimental study in healthy Wistar rats that consumed BB in a juice form (25 g/kg body weight (BW)/day; 14 weeks’ protocol). Particular attention was paid to the physiological adaptations succeeding in the gut and liver tissues regarding the acknowledged BB-induced metabolic benefits. Systemically, BB boosted serum antioxidant activity and repressed the circulating levels of 3-hydroxybutyrate (3-HB) ketone bodies and 3-HB/acetoacetate ratio. Moreover, BB elicited increased fecal succinic acid levels without major changes on gut microbiota (GM) composition and gut ultra-structural organization. Remarkably, an accentuated hepatic mitochondrial bioenergetic challenge, ensuing metabolic transcriptomic reprogramming along with a concerted anti-inflammatory pre-conditioning, was clearly detected upon long-term consumption of BB phytochemicals. Altogether, the results disclosed herein portray a quiescent mitochondrial-related metabolomics and hint for a unified adaptive response to this nutritional challenge. The beneficial or noxious consequences arising from this dietary trend should be carefully interpreted and necessarily claims future research.info:eu-repo/semantics/publishedVersio

Para o estudo da evolução do ensino e da formação em administração educacional em Portugal

Estudos sobre a evolução do ensino de disciplinas, na formação de professores em Portugal, são recentes. O controle burocrático centralizado reteve as dimensões do controle político-administrativo. De certo modo, protegeu a esfera educativa das influências modernizantes, do capitalismo industrial e das lógicas mercantis e gerencialistas. Defendeu a educação do domínio político, da intervenção de movimentos sociais, das propagandas de ideais democráticos e da cidadania. A utilização da designação "Administração educacional" ilustra as dificuldades sentidas, ao longo dos últimos anos, em termos da construção acadêmica de uma área, seja pela falta de tradição, seja pelos antecedentes históricos.In Portugal, studies about the evolution of disciplines teaching in the teachers formation are recent. The centralized bureaucratic control has held back the dimensions of politic administrative control. In a certain way, it has protected the education against the new-fashioned influences, manufacturing capitalism, and mercantile and managerial logics. This centralized bureaucratic control has also profected the education against the politic dominion, the intervention of social movements, the advertising of democratic ideals, and against the citizenship. The use of the term "Educational administration" shows the difficulties met by the searchers along the latest years, since there is no tradiction nor historic antecedence

Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging

SummaryEver since eukaryotes subsumed the bacterial ancestor of mitochondria, the nuclear and mitochondrial genomes have had to closely coordinate their activities, as each encode different subunits of the oxidative phosphorylation (OXPHOS) system. Mitochondrial dysfunction is a hallmark of aging, but its causes are debated. We show that, during aging, there is a specific loss of mitochondrial, but not nuclear, encoded OXPHOS subunits. We trace the cause to an alternate PGC-1α/β-independent pathway of nuclear-mitochondrial communication that is induced by a decline in nuclear NAD+ and the accumulation of HIF-1α under normoxic conditions, with parallels to Warburg reprogramming. Deleting SIRT1 accelerates this process, whereas raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse in a SIRT1-dependent manner. Thus, a pseudohypoxic state that disrupts PGC-1α/β-independent nuclear-mitochondrial communication contributes to the decline in mitochondrial function with age, a process that is apparently reversible