Insects collected from an alpine-subalpine region in SE British Columbia

Insects were caught in a subalpine area of southeastern British Columbia. The list consists of 23 spp. and 37 genera, in families of five orders. The insects were collected during July and August, 1975 as part of a larger study of the ecology of mountain caribou in the Poplar Creek area, north of Nelson, B.C

Editorial: Myokines, Adipokines, Cytokines in Muscle Pathophysiology.

[No abstract available

Editorial: myokines, adipokines, cytokines in muscle pathophysiology

Individual striated muscle fibers communicate in both a paracrine and endocrine fashion and are also involved in the crosstalk with other tissues and organs such as the adipose tissue, immune system, liver, pancreas, bones, and brain (Delezie andHandschin, 2018). The striatedmuscle, which accounts for 40% of bodymass, presents high biosynthetic activity, and extensive vascularization, features that endorse current thinking that muscle is the largest endocrine system of the body (Benatti and Pedersen, 2015). There are hundreds of muscle secretory products, collectively known as myokines, including proteins, miRNA, and exosomes (Barone et al., 2016). Muscle secretion is significantly affected by muscle contraction (Son et al., 2018) due to the activation of mechanotransduction pathways (Coletti et al., 2016a). It has been suggested that the adipose tissue is also an endocrine organ, producing adipokines- leptin, and other hormones, in addition to cytokines (Galic et al., 2010). The inflammatory infiltrate in fat depots affects the course of several diseases, including cancer (Batista et al., 2012; Sawicka and Krasowska, 2016; Neto et al., 2018; Opatrilova et al., 2018), and an extensive review on the role of adipokines in disease has been published elsewhere (Orzechowski et al., 2014). Myokines, adipokines, and cytokines are major therapeutic targets in both muscular and non-muscular diseases (Lindegaard et al., 2013;Manole et al., 2018), and understanding of their role in tissue crosstalk represents a subject of great interest in current biology.We have therefore chosen to address this paradigm within this Frontiers special issue on “Myokines, Adipokines, Cytokines in Muscle Pathophysiology.

Tumor microenvironment autophagic processes and cachexia: the missing link?

Cachexia is a syndrome that affects the entire organism and presents a variable plethora of symptoms in patients, always associated with continuous and involuntary degradation of skeletal muscle mass and function loss. In cancer, this syndrome occurs in 50% of all patients, while prevalence increases to 80% as the disease worsens, reducing quality of life, treatment tolerance, therapeutic response, and survival. Both chronic systemic inflammation and immunosuppression, paradoxically, correspond to important features in cachexia patients. Systemic inflammation in cachexia is fueled by the interaction between tumor and peripheral tissues with significant involvement of infiltrating immune cells, both in the peripheral tissues and in the tumor itself. Autophagy, as a process of regulating cellular metabolism and homeostasis, can interfere with the metabolic profile in the tumor microenvironment. Under a scenario of balanced autophagy in the tumor microenvironment, the infiltrating immune cells control cytokine production and secretion. On the other hand, when autophagy is unbalanced or dysfunctional within the tumor microenvironment, there is an impairment in the regulation of immune cell’s inflammatory phenotype. The inflammatory phenotype upregulates metabolic consumption and cytokine production, not only in the tumor microenvironment but also in other tissues and organs of the host. We propose that cachexia-related chronic inflammation can be, at least, partly associated with the failure of autophagic processes in tumor cells. Autophagy endangers tumor cell viability by producing immunogenic tumor antigens, thus eliciting the immune response necessary to counteract tumor progression, while preventing the establishment of inflammation, a hallmark of cachexia. Comprehensive understanding of this complex functional dichotomy may enhance cancer treatment response and prevent/mitigate cancer cachexia. This review summarizes the recent available literature regarding the role of autophagy within the tumor microenvironment and the consequences eliciting the development of cancer cachexia

Mesenchymal stem cells as promoters, enhancers, and playmakers of the translational regenerative medicine

Since their first isolation and characterization by Friedenstein et al. in 1974, mesenchymal stem cells (MSCs) were proven essential for tissue regeneration and homeostasis. Over the years, thanks to a better understanding of the molecular mechanisms underlying the therapeutic effects of MSCs, several approaches with MSC-based therapies have been proposed, in order to treat different human diseases. In this light, MSCs are currently being tested in preclinical in vivo settings as well as in early-stage clinical trials for their ability to modulate immune responses, fostering wound healing and tissue regeneration of various tissue types and organs, including the skin, bone, cartilage, brain, muscle, and tendons

Human cachexia induces changes in mitochondria, autophagy and apoptosis in the skeletal muscle

Cachexia is a wasting syndrome characterized by the continuous loss of skeletal muscle mass due to imbalance between protein synthesis and degradation, which is related with poor prognosis and compromised quality of life. Dysfunctional mitochondria are associated with lower muscle strength and muscle atrophy in cancer patients, yet poorly described in human cachexia. We herein investigated mitochondrial morphology, autophagy and apoptosis in the skeletal muscle of patients with gastrointestinal cancer-associated cachexia (CC), as compared with a weight-stable cancer group (WSC). CC showed prominent weight loss and increased circulating levels of serum C-reactive protein, lower body mass index and decreased circulating hemoglobin, when compared to WSC. Electron microscopy analysis revealed an increase in intermyofibrillar mitochondrial area in CC, as compared to WSC. Relative gene expression of Fission 1, a protein related to mitochondrial fission, was increased in CC, as compared to WSC. LC3 II, autophagy-related (ATG) 5 and 7 essential proteins for autophagosome formation, presented higher content in the cachectic group. Protein levels of phosphorylated p53 (Ser46), activated caspase 8 (Asp384) and 9 (Asp315) were also increased in the skeletal muscle of CC. Overall, our results demonstrate that human cancer-associated cachexia leads to exacerbated muscle-stress response that may culminate in muscle loss, which is in part due to disruption of mitochondrial morphology, dysfunctional autophagy and increased apoptosis. To the best of our knowledge, this is the first report showing quantitative morphological alterations in skeletal muscle mitochondria in cachectic patients

Rbm24 displays dynamic functions required for myogenic differentiation during muscle regeneration

Skeletal muscle has a remarkable capacity of regeneration after injury, but the regulatory network underlying this repair process remains elusive. RNA-binding proteins play key roles in the post-transcriptional regulation of gene expression and the maintenance of tissue homeostasis and plasticity. Rbm24 regulates myogenic differentiation during early development, but its implication in adult muscle is poorly understood. Here we show that it exerts multiple functions in muscle regeneration. Consistent with its dynamic subcellular localization during embryonic muscle development, Rbm24 also displays cytoplasm to nucleus translocation during C2C12 myoblast differentiation. In adult mice, Rbm24 mRNA is enriched in slow-twitch muscles along with myogenin mRNA. The protein displays nuclear localization in both slow and fast myofibers. Upon injury, Rbm24 is rapidly upregulated in regenerating myofibers and accumulates in the myonucleus of nascent myofibers. Through satellite cell transplantation, we demonstrate that Rbm24 functions sequentially to regulate myogenic differentiation and muscle regeneration. It is required for myogenin expression at early stages of muscle injury and for muscle-specific pre-mRNA alternative splicing at late stages of regeneration. These results identify Rbm24 as a multifaceted regulator of myoblast differentiation. They provide insights into the molecular pathway orchestrating the expression of myogenic factors and muscle functional proteins during regeneration

Terahertz detection by epitaxial-graphene field-effect-transistors on silicon carbide

We report on room temperature detection of terahertz radiation by means of antenna-coupled field effect transistors (FETs) fabricated using epitaxial graphene grown on silicon carbide. The achieved photoresponsivity (similar to 0.25 V/W) and noise equivalent power (similar to 80 nW/root Hz) result from the combined effect of two independent detection mechanisms: over-damped plasma wave rectification and thermoelectric effects, the latter ascribed to the presence of carrier density junctions along the FET channel. The calculated plasmonic and thermoelectric response reproduces qualitatively well the measured photovoltages; the experimentally observed sign-switch demonstrates the stronger contribution of plasmonic detection compared to the thermoelectric one. These results unveil the potential of plasmonic detectors exploiting epitaxial graphene on silicon carbide for fast large area imaging of macroscopic samples

Stable non-standard imprecise probabilities

Stability arises as the consistency criterion in a betting interpretation for hyperreal imprecise previsions, that is imprecise previsions (and probabilities) which may take infinitesimal values. The purpose of this work is to extend the notion of stable coherence introduced in [8] to conditional hyperreal imprecise probabilities. Our investigation extends the de Finetti-Walley operational characterisation of (imprecise) prevision to conditioning on events which are considered "practically impossible" but not "logically impossible"