Avaliação preliminar de substrato padrão europeu de Biobed contra dois solos brasileiros na degradação de resíduos pontuais de agrotóxicos.

Com o objetivo de encontrar alternativas no descarte de resíduos da lavagem de tratores e pulverizadores para reduzir o dano ao ambiente, foram testados 19 reatores, sendo 8 com turfa + palha de trigo + solo agrícola (SPT), 4 com Latossolo puro e 4 com Nitossolo puro

Single cell analysis reveals the involvement of the long non-coding RNA Pvt1 in the modulation of muscle atrophy and mitochondrial network

Long non-coding RNAs (lncRNAs) are emerging as important players in the regulation of several aspects of cellular biology. For a better comprehension of their function, it is fundamental to determine their tissue or cell specificity and to identify their subcellular localization. In fact, the activity of lncRNAs may vary according to cell and tissue specificity and subcellular compartmentalization. Myofibers are the smallest complete contractile system of skeletal muscle influencing its contraction velocity and metabolism. How lncRNAs are expressed in different myofibers, participate in metabolism regulation and muscle atrophy or how they are compartmentalized within a single myofiber is still unknown. We compiled a comprehensive catalog of lncRNAs expressed in skeletal muscle, associating the fiber-type specificity and subcellular location to each of them, and demonstrating that many lncRNAs can be involved in the biological processes de-regulated during muscle atrophy. We demonstrated that the lncRNA Pvt1, activated early during muscle atrophy, impacts mitochondrial respiration and morphology and affects mito/autophagy, apoptosis and myofiber size in vivo. This work corroborates the importance of lncRNAs in the regulation of metabolism and neuromuscular pathologies and offers a valuable resource to study the metabolism in single cells characterized by pronounced plasticity

Effects of Tenebrio molitor larvae meal inclusion in rainbow trout feed: myogenesis-related gene expression and histomorphological features

The effects of Tenebrio molitor larvae meal (TM) dietary inclusion in rainbow trout diet were evaluated on muscular growth using gene expression and histomorphological features of liver, spleen, kidney, anterior and posterior gut through histopathological analyses. Two hundred fifty-two grow-out rainbow trout were fed four experimental diets containing increasing levels of TM: 0% (TM0), 5% (TM25), 10% (TM50), and 20% (TM100) corresponding to different levels of fish meal replacement (0, 25, 50, and 100%, respectively). Muscular growth was evaluated analysing the expression of various genes involved in different steps of myogenesis. Among the analysed genes, only MyoD expression resulted significantly higher in fish fed TM100 compared to fish fed TM0. The gut histomorphology was not affected by TM dietary inclusion and villus height differs from anterior and posterior segments regardless of the fed diet. Histopathological alterations were observed in all the sampled organs for all the dietary treatments; however, dietary TM inclusion did not influence either development or severity of the observed histopathological changes. The results obtained confirmed the safe utilisation of TM as an alternative protein source in rainbow trout diets and highlighted the necessity to deepen the studies of TM effect on the myogenesis process, especially at a molecular level.Highlights Rainbow trout can effectively be fed with a TM protein source. Total FM substitution by TM (TM100) decreased MyoD gene expression. Increasing TM dietary inclusion did not influence gut histomorphology

Global warming-related response after bacterial challenge in Astroides calycularis, a Mediterranean thermophilic coral

A worldwide increase in the prevalence of coral diseases and mortality has been linked to ocean warming due to changes in coral-associated bacterial communities, pathogen virulence, and immune system function. In the Mediterranean basin, the worrying upward temperature trend has already caused recurrent mass mortality events in recent decades. To evaluate how elevated seawater temperatures affect the immune response of a thermophilic coral species, colonies of Astroides calycularis were exposed to environmental (23 °C) or elevated (28 °C) temperatures, and subsequently challenged with bacterial lipopolysaccharides (LPS). Using immunolabeling with specific antibodies, we detected the production of Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-kB), molecules involved in coral immune responses, and heat shock protein 70 (HSP70) activity, involved in general responses to thermal stress. A histological approach allowed us to characterize the tissue sites of activation (epithelium and/or gastroderm) under different experimental conditions. The activity patterns of the examined markers after 6 h of LPS stimulation revealed an up-modulation at environmental temperature. Under warmer conditions plus LPS-challenge, TLR4-NF-kB activation was almost completely suppressed, while constituent elevated values were recorded under thermal stress only. An HSP70 up-regulation appeared in both treatments at elevated temperature, with a significantly higher activation in LPS-challenge colonies. Such an approach is useful for further understanding the molecular pathogen-defense mechanisms in corals in order to disentangle the complex interactive effects on the health of these ecologically relevant organisms related to global climate change

Dysfunctional mitochondria accumulate in a skeletal muscle knockout model of Smn1, the causal gene of spinal muscular atrophy

The approved gene therapies for spinal muscular atrophy (SMA), caused by loss of survival motor neuron 1 (SMN1), greatly ameliorate SMA natural history but are not curative. These therapies primarily target motor neurons, but SMN1 loss has detrimental effects beyond motor neurons and especially in muscle. Here we show that SMN loss in mouse skeletal muscle leads to accumulation of dysfunctional mitochondria. Expression profiling of single myofibers from a muscle specific Smn1 knockout mouse model revealed down-regulation of mitochondrial and lysosomal genes. Albeit levels of proteins that mark mitochondria for mitophagy were increased, morphologically deranged mitochondria with impaired complex I and IV activity and respiration and that produced excess reactive oxygen species accumulated in Smn1 knockout muscles, because of the lysosomal dysfunction highlighted by the transcriptional profiling. Amniotic fluid stem cells transplantation that corrects the SMN knockout mouse myopathic phenotype restored mitochondrial morphology and expression of mitochondrial genes. Thus, targeting muscle mitochondrial dysfunction in SMA may complement the current gene therapy