Association of radio polar cap brightening with bright patches and coronal holes

Radio-bright regions near the solar poles are frequently observed in Nobeyama Radioheliograph (NoRH) maps at 17 GHz, and often in association with coronal holes. However, the origin of these polar brightening has not been established yet. We propose that small magnetic loops are the source of these bright patches, and present modeling results that reproduce the main observational characteristics of the polar brightening within coronal holes at 17 GHz. The simulations were carried out by calculating the radio emission of the small loops, with several temperature and density profiles, within a 2D coronal hole atmospheric model. If located at high latitudes, the size of the simulated bright patches are much smaller than the beam size and they present the instrument beam size when observed. The larger bright patches can be generated by a great number of small magnetic loops unresolved by the NoRH beam. Loop models that reproduce bright patches contain denser and hotter plasma near the upper chromosphere and lower corona. On the other hand, loops with increased plasma density and temperature only in the corona do not contribute to the emission at 17 GHz. This could explain the absence of a one-to-one association between the 17 GHz bright patches and those observed in extreme ultraviolet. Moreover, the emission arising from small magnetic loops located close to the limb may merge with the usual limb brightening profile, increasing its brightness temperature and width.Comment: 8 pages, 6 figures, 1 table. Accepted for publication in The Astrophysical Journa

Spinal motoneuron synaptic plasticity after axotomy in the absence of inducible nitric oxide synthase

<p>Abstract</p> <p>Background</p> <p>Astrocytes play a major role in preserving and restoring structural and physiological integrity following injury to the nervous system. After peripheral axotomy, reactive gliosis propagates within adjacent spinal segments, influenced by the local synthesis of nitric oxide (NO). The present work investigated the importance of inducible nitric oxide synthase (iNOS) activity in acute and late glial responses after injury and in major histocompatibility complex class I (MHC I) expression and synaptic plasticity of inputs to lesioned alpha motoneurons.</p> <p>Methods</p> <p><it>In vivo </it>analyses were carried out using C57BL/6J-iNOS knockout (iNOS^-/-) and C57BL/6J mice. Glial response after axotomy, glial MHC I expression, and the effects of axotomy on synaptic contacts were measured using immunohistochemistry and transmission electron microscopy. For this purpose, 2-month-old animals were sacrificed and fixed one or two weeks after unilateral sciatic nerve transection, and spinal cord sections were incubated with antibodies against classical MHC I, GFAP (glial fibrillary acidic protein - an astroglial marker), Iba-1 (an ionized calcium binding adaptor protein and a microglial marker) or synaptophysin (a presynaptic terminal marker). Western blotting analysis of MHC I and nNOS expression one week after lesion were also performed. The data were analyzed using a two-tailed Student's <it>t </it>test for parametric data or a two-tailed Mann-Whitney <it>U </it>test for nonparametric data.</p> <p>Results</p> <p>A statistical difference was shown with respect to astrogliosis between strains at the different time points studied. Also, MHC I expression by iNOS^-/-microglial cells did not increase at one or two weeks after unilateral axotomy. There was a difference in synaptophysin expression reflecting synaptic elimination, in which iNOS^-/-mice displayed a decreased number of the inputs to alpha motoneurons, in comparison to that of C57BL/6J.</p> <p>Conclusion</p> <p>The findings herein indicate that iNOS isoform activity influences MHC I expression by microglial cells one and two weeks after axotomy. This finding was associated with differences in astrogliosis, number of presynaptic terminals and synaptic covering of alpha motoneurons after lesioning in the mutant mice.</p

Regeneração medular: a ação do neurotrophin-3 sobre a lesão medular de ratos

OBJECTIVE: For many years, it was believed that medullary regeneration could not occur, although currently there are many trials using neurotrophic factors, stem cells, fetal medulla grafts, peripheral nerve grafts, and antibodies against myelin-associated proteins that demonstrate the existence of the possibility of spinal cord regeneration. The purpose of this study was to investigate the action of neurotrophin-3, a novel neurotrophic factor. METHODS: The New York University impactor, a standardized device for delivery of spinal cord injuries was used on 33 rats, which were divided into 2 groups: a control group receiving distilled water intraperitoneally and a treatment group receiving neurotrophin-3 intraperitoneally. RESULTS: Using the Basso, Beattie, and Bresnahan scale, the locomotor recovery curve for the neurotrophin-3 treated group was superior to that of the control group (P < 0.05); the administration of neurotrophin-3 was associated with the absence of deaths, while the control group showed a 28.5% (P = 0.026) mortality rate. Other parameters (hematuria rate and histological analysis) showed no significant differences. CONCLUSIONS: Based on these results, it appears that a strong relationship exists between the use of neurotrophin-3 in rats with spinal cord injury and better functional recovery.OBJETIVO: Por muitos anos acreditou-se que a regeneração medular não fosse factível. Atualmente porém, existem várias experiências utilizando fatores neurotróficos, células troncos, enxerto de medula fetal, enxerto de nervo periférico e anticorpos contra proteínas associadas a mielina que sugerem o contrário. Esta pesquisa estudou a ação de um dos mais novos neurotróficos, o Neurotrophin-3. MÉTODOS: As lesões medulares foram realizadas através do New York University impator, método experimental de produção de lesão medular padronizada. Foram utilizados 33 ratos divididos em 2 grupos. Um grupo controle com administração intraperitoneal de água destilada e um grupo tratamento, tratado com Neurotrophin-3 por via intraperitoneal. RESULTADOS: Observamos que a curva de recuperação locomotora, segundo a escala de Basso, Beattie e Bresnahan, do grupo Neurotrophin-3 foi superior à do grupo controle (p < 0,05); a administração de Neurotrophin-3 determinou ausência de mortes no grupo tratamento, enquanto o grupo controle apresentou taxa de mortalidade de 28,5% (p = 0,026). Os outros parâmetros (taxa de hematúria e análise histológica) não apresentaram diferenças estatisticamente significantes. CONCLUSÕES: Existe forte relação entre a aplicação de Neurotrophin-3 em ratos com lesão medular e melhor recuperação funcional

Associação entre características de desempenho de tilápia-do-nilo ao longo do período de cultivo.

O objetivo deste trabalho foi estimar as herdabilidades e a estrutura de correlações genéticas entre as características de desempenho de tilápia-do-nilo (Oreochromis niloticus) da linhagem GIFT, em diferentes estágios do ciclo de produção. As tilápias foram cultivadas em tanques - rede. Mediu-se ganho em peso diário total, peso vivo e ganho em peso diário, em quatro períodos, com intervalos de aproximadamente 30 dias. Foram realizadas análises unicaracter para as medidas, em todas as biometrias e, nas análises bicaracter, as medidas de mesma característica foram combinadas duas a duas e com o ganho em peso diário total. As estimações de herdabilidade variaram de 0,15 a 0,11 para peso vivo, 0,16 a 0,09 para ganho em peso diário e 0,17 a 0,12 para ganho em peso diário total, nas análises unicaracter. Os valores estimados de correlação genética para peso vivo e ganho em peso diário, associados ao ganho em peso diário total, variaram entre 0,37 a 0,98 e 0,74 a 0,8 respectivamente. A forte associação genética estimada entre peso vivo em biometrias intermediárias e ganho em peso diário total sugere que a seleção para velocidade de crescimento pode ser realizada de forma precoce

Glatiramer Acetate Treatment Increases Stability Of Spinal Synapses And Down Regulates Mhc I During The Course Of Eae.

The recent discovery that the major histocompatibility complex of class I (MHC I) expression has a role in the synaptic elimination process, represented an insight into understanding the cross talk between neurons. In the present study, the possibility that glatiramer acetate (GA) treatment influences the MHC class I expression and the synaptic plasticity process in the spinal cord during the course of EAE was investigated. C57BL/6J mice were induced to EAE and submitted to treatment either with a placebo solution or with GA (0.05 mg/animal, subcutaneously, on a daily basis). All the animals were sacrificed at the peak disease (14 days after induction) or at the point of recovery of the clinical signs (21 days after induction). The spinal cords were removed and submitted to immunohistochemical examination, Western blotting and transmission electron microscopy analysis. The results showed that GA treatment was able to decrease synaptic loss during the course of EAE, which correlates with the downregulation of the MHC I complex. The present results reinforce the neuroprotective role of GA treatment, by reducing synaptic loss during the course of the disease. Such action may be associated with the recently described role of MHC I regulation during the synaptic plasticity process.71188-20

Can Pacing Be Regulated by Post-Activation Potentiation? Insights from a Self-Paced 30 km Trial in Half-Marathon Runners

[EN] Purpose Given the co-existence of post-activation potentiation (PAP) and fatigue within muscle, it is not known whether PAP could influence performance and pacing during distance running by moderating fatigue. The aim of this study was to assess the influence of PAP on pacing, jumping and other physiological measures during a self-paced 30 km trial. Methods Eleven male endurance-trained runners (half-marathon runners) volunteered to participate in this study. Runners participated in a multi-stage 30 km trial. Before the trial started, determination of baseline blood lactate (bLa) and countermovement jump (CMJ) height was performed. The self-paced 30 km trial consisted of 6 × 5 km splits. At the end of each 5 km split (60 s break), data on time to complete the split, CMJ height, Rating of Perceived Exertion (RPE) and blood lactate were collected while heart rate was continuously monitored. Results There was a significant decrease in speed (e.g. positive pacing strategy after the 4th split, p<0.05) with a progressive increase in RPE throughout the trial. Compared with baseline, CMJ height was significantly (p<0.05) greater than baseline and was maintained until the end of the trial with an increase after the 5th split, concomitant with a significant reduction in speed and an increase in RPE. Significant correlations were found between ΔCMJ and ΔSPEED (r = 0.77 to 0.87, p<0.05) at different time points as well as between RPE and speed (r = -0.61 to -0.82, p<0.05). Conclusion Our results indicates that fatigue and potentiation co-exist during long lasting endurance events, and that the observed increase in jump performance towards the end of the trial could be reflecting a greater potentiation potentially perhaps counteracting the effects of fatigue and preventing further reductions in speed.We would like to thank Nova Biomedical for their donation for lactate analyzers and the athletes for their enthusiastic participation

Novel capsular depolymerases-based strategy to kill multidrug-resistant pathogenic bacteria

Multidrug resistant pathogens represent one of the greatest threats to human health of the new millennium. ESKAPE bacterial pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and other Enterobacteriaceae species) are the leading group among these socalled superbugs, which rapidly acquire resistances to several (and sometimes all) available antibiotics and cause a variety of nosocomial infections (e.g. bacteraemia and wound infections). Our research has been leading an innovative approach based on bacteriophage-derived enzymes (called capsular depolymerases) against A. baumannii (see video at ref 1). Previously, we found that some bacteriophages (i.e. viruses that specifically infect bacteria) acquired the ability to infect different Acinetobacter hosts through acquisition of different capsular depolymerases (2). These enzymes located at the bacteriophage tails bind and degrade specific bacterial capsules types (2). Recently, recombinantly expressed capsular depolymerases showed to be active in several environment conditions, non-nontoxic to mammalian cells and able to make A. baumannii fully susceptible to host complement effect, namely in i) Galleria mellonella caterpillar, ii) murine and iii) human serum models (3, 4). A single intraperitoneal injection of depolymerase protect 60% of mice from dead, with significant reduction of proinflammatory cytokine profile (4). We show that capsular depolymerases fit the new trend of antimicrobials needed, as they are highly specific, stable and refractory to resistance as they do not kill bacteria per se, instead they remove bacterial surface polysaccharides, diminishing bacterial virulence and exposing them to the host immune system. This innovative antimicrobial approach can be applied to other pathogenic bacteria.info:eu-repo/semantics/publishedVersio

The Role of Hepatocyte Growth Factor (HGF) in Insulin Resistance and Diabetes

In obesity, insulin resistance (IR) and diabetes, there are proteins and hormones that may lead to the discovery of promising biomarkers and treatments for these metabolic disorders. For example, these molecules may impair the insulin signaling pathway or provide protection against IR. Thus, identifying proteins that are upregulated in IR states is relevant to the diagnosis and treatment of the associated disorders. It is becoming clear that hepatocyte growth factor (HGF) is an important component of the pathophysiology of IR, with increased levels in most common IR conditions, including obesity. HGF has a role in the metabolic flux of glucose in different insulin sensitive cell types; plays a key role in β-cell homeostasis; and is capable of modulating the inflammatory response. In this review, we discuss how, and to what extent HGF contributes to IR and diabetes pathophysiology, as well as its role in cancer which is more prevalent in obesity and diabetes. Based on the current literature and knowledge, it is clear that HGF plays a central role in these metabolic disorders. Thus, HGF levels could be employed as a biomarker for disease status/progression, and HGF/c-Met signaling pathway modulators could effectively regulate IR and treat diabetes