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

Efficacy of Utilization of All-Plant-Based and Commercial Low-Fishmeal Feeds in Two Divergently Selected Strains of Rainbow Trout (Oncorhynchus mykiss): Focus on Growth Performance, Whole-Body Proximate Composition, and Intestinal Microbiome

The present study aimed to investigate the growth performance, whole-body proximate composition, and intestinal microbiome of rainbow trout strains when selected and non-selected for weight gain on all-plant protein diets. A 2x2 factorial design was applied, where a selected (United States) and a non-selected (ITA) rainbow trout strain were fed using either an all-plant protein (PP) or a commercial low-FM diet (C). Diets were fed to five replicates of 20 (PP) or 25 (C) fish for 105 days. At the end of the trial, growth parameters were assessed, and whole fish (15 pools of three fish/diet) and gut samples (six fish/diet) were collected for whole-body proximate composition and gut microbiome analyses, respectively. Independent of the administered diet, the United States strain showed higher survival, final body weight, weight gain, and specific growth rate when compared to the ITA fish (p < 0.001). Furthermore, decreased whole-body ether extract content was identified in the PP-fed United States rainbow trout when compared to the ITA strain fed the same diet (p < 0.001). Gut microbiome analysis revealed the Cetobacterium probiotic-like genus as clearly associated with the United States rainbow trout, along with the up-regulation of the pathway involved in starch and sucrose metabolism. In summary, the overall improvement in growth performance and, to a lesser extent, whole-body proximate composition observed in the selected rainbow trout strain was accompanied by specific, positive modulation of the intestinal microbiome

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