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Recently, research has proven that food products containing chemical preservatives have a harmful effect on health and cause major health risks, so it was necessary to provide a safe alternative for consumers, and this is why the demand by consumers for food products free from harmful chemical preservatives has increased and one of these products is shrimp popcorn. Replacing chemical preservatives with natural ones is not an easy thing, so the food industry is highly interested in studying natural extracts well, studying their activity as antioxidants and antimicrobials, and evaluating their efficiency in preserving new food products while maintaining product quality and consumer preferences. Thus, the aim of the study was to evaluate two plant extracts (ginger and rosemary) and study their effects on the shelf life and quality of the shrimp popcorn product. Three different concentrations (0.02, 0.2, and 0.5%) of both aqueous ginger and rosemary extracts were applied to shrimp popcorn and their impact on shelf life was assessed through determination of TBARS, DNPH, TVB-N, TMA, PV, pH value, WHC, aerobic plate count, coliform count, yeast and mold count and compared with negative control and positive control (BHT) through a storage period of 12 days and at 4°C. The treatment with aqueous extract of ginger and rosemary showed a results superior to that of the synthetic preservative with a lower TBARS value, carbonyl content, total volatile basic nitrogen, Tri-methylamine value, peroxide value and aerobic plate count at 12 days of storage with mean values of (1.50, 0.95, 1.02, 0.85, 0.79, 0.91, 0.61 and 0.53 mg MDA/Kg), (19.31, 10.52, 15.61, 11.28, 8.39, 10.65, 7.32, and 4.51 nmol carbonyl content/mg protein), (39.48, 31.52, 35.41, 20.22, 13.45, 23.27, 12.38, and 9.15 mg/100 g), (12.38, 10.38, 11.45, 6.85, 2.31, 9.31, 3.20, and 1.56 mg/kg), (25.71, 16.37, 19.65, 15.90, 13.37, 17.18, 11.68, and 9.01 mg /100g muscle), and (3.8x105, 2.2x104, 3.5x104, 2.1x10³, 3.3x10³, 2.5x104, 2.1x10³, and 1.5x10³ CFU/g) respectively for (negative control, positive control (BHT), 0.02%GE, 0.2%GE, 0.5%GE, 0.02%RE, 0.2%RE, 0.5%RE). These findings show that the ginger extract at the level of 0.2 and 0.5% and rosemary extract at level of 0.2 and 0.5% were very effective against lipid and protein oxidation, and a powerful antimicrobial in shrimp popcorn product and promising natural antioxidant and antimicrobial replacing the chemical preservatives in food processing. [ABSTRACT FROM AUTHOR]

Despite the availability of a wide range of oral nutritional supplements (ONS) offerings, individuals with malnutrition are still struggling to meet their nutritional targets. A new concentrated and high-protein energy-dense ONS (≥2.1 kcal/mL;32 g protein/200 mL) with high-quality protein (60% whey protein) has emerged as a pivotal formula to reach the patient's energy-protein requirements, enhance compliance, and maximize stimulation of muscle protein synthesis, key factors driving better nutritional, functional, and clinical outcomes. The purpose of this article is to provide our clinical experience using this new nutritionally concentrated ONS as a therapeutic strategy for patients with DRM. Three clinical cases have been examined using new assessment procedures and a new form of nutritional therapy, and their impact on the nutritional and functional outcomes in patients with moderate-to-severe DRM. A tailored individualized nutritional interventions improved anthropometric, biochemical, and functional outcomes (Case 1,2, and 3) assessed using hand grip strength, bioimpedance and muscle ultrasound, and as well as good gastrointestinal tolerance (Case 1) and compliance to the ONS in patients with DRM (Case 1,2,3). The use of this novel high-protein energy-dense formula with high-quality protein source (≥2.1 kcal/mL; 32 g protein/200 mL; 60% whey protein) overcome common practical challenges in the medical nutrition therapy of patients with DRM, either because these patients require a highly concentrated formulation to meet nutritional requirements due to loss of appetite, lack of interest in food, and high caloric-protein needs due to disease, and a large quantity and quality of protein to optimize muscle recovery due to sarcopenia, common in patients with moderate-severe malnutrition. [ABSTRACT FROM AUTHOR]

The nutritional profile, protein identification of Rhynchophorus phoenicis larvae protein concentrate (Rp PC) were evaluated, as well as its emulsifying properties at different pH levels. Rp PC larvae was prepared from defatted insect flour through alkaline solubilization (pH 9.0) followed by acid precipitation (pH 4.5). The composition of Rp PC consisted of 70.66 g/100 g of proteins, 10.30 g/100 g of lipids (including triacylglycerols and free fatty acids at 3.09 g/100 g and 4.87 g/100 g, respectively), and 11.30 g/100 g of water. The amino acid profile of Rp PC showed high nutritional value, with 38.33 g/100 g of indispensable amino acids. Similarly, the polyunsaturated fatty acid content was 1.14 g/100 g, with an excellent n-6/n-3 ratio of 2.98. Among the identified proteins, some were muscle proteins while others were allergens. In terms of functional properties, Rp PC exhibited maximum solubility of 84.6 ± 2.0 g/100 g protein at pH 10.0, and minimum solubility of 11.6 ± 0.7 g/100 g protein at pH 4.0. Rp PC was able to form oil-in-water emulsions with monomodal particle size distributions and volume-weighted average diameters ranging from 2.2 ± 0.1 µm (at pH 9.0) to 4.8 ± 1.6 µm (at pH 5.0). Rp PC allowed for the stabilization of oil-in-water emulsions for at least 24 h at pH 7.0 and 9.0. Proteins extracted from Rhynchophorus phoenicis larvae at alkaline pH exhibited valuable nutritional and emulsifying properties, suggesting that Rp PC could be used as an emulsifying agent or in the formulation of new food products. [ABSTRACT FROM AUTHOR]

Harpiosquillid mantis shrimp (Harpiosquilla raphidea) (HMS) without and with beheading pretreated with pulsed electric field (PEF) (15 kV/cm, 800 pulses, 5 min) were soaked in chitooligosaccharide (COS) solution at varying concentrations (0, 1 and 2%, w/v) for 20 min and stored for 3 days in iced water. Changes in the trypsin activity, color, texture, protein pattern, TCA soluble peptide content, histological images, protein secondary structure and microbial load were monitored during the storage. The beheaded HMS pretreated with PEF and soaked in 2% COS solution showed the maximum efficacy in inhibiting trypsin activity and proteolysis, thus retaining muscle proteins, especially myosin heavy chain, actin and troponin T as well as shear force up to day 3. Pronounced muscle destruction in the whole HMS was displayed by a decreased mean grey index and fiber gapping. Such changes were lowered by the beheading and PEF/2% COS treatment (2% COS-BH). Nevertheless, no marked change in the secondary structure including α-helix, β-sheets, β-turns and random coil were observed among any of the samples. The microbiological analysis revealed that the total viable count (TVC) was below 6 log CFU/g till day 2 in all samples. Nonetheless, the 2% COS-BH sample had the lowest psychrophilic bacterial count and Enterobacteriaceae count at day 3, compared to the others. Thus, the combination of the prior PEF and 2% COS treatment of beheaded HMS could effectively inhibit proteases, retard the microbial growth and maintain the quality of HMS stored in iced water. [ABSTRACT FROM AUTHOR]

Due to nonspecific pathological changes and the rapid degradation of insulin in postmortem blood samples, the identification of the cause of death during insulin overdose has always been a difficulty in forensic medicine. At present, there is a lack of studies on the toxicological changes and related mechanisms of an insulin overdose, and the specific molecular markers of insulin overdose are still unclear. In this study, an animal model of insulin overdose was established, and 24 SD rats were randomly divided into a control group, insulin overdose group, and a recovery group (n = 8). We detected the biochemical changes and analyzed the toxicological mechanism of an insulin overdose. The results showed that after insulin overdose, the rats developed irregular convulsions, Eclampsia, Opisthotonos, and other symptoms. The levels of glucose, glycogen, and C-peptide in the body decreased significantly, while the levels of lactate, insulin, and glucagon increased significantly. The decrease in plasma K+ was accompanied by the increase in skeletal muscle K+. The PI3K-AKT signaling pathway was significantly activated in skeletal muscle, and the translocation of GLUT4/Na+-K+-ATPase to sarcolemma was significantly increased. Rare glycogenic hepatopathy occurred in the recovery group after insulin overdose. Our study showed that insulin overdose also plays a role in skeletal muscle cells, mainly through the PI3K-Akt signaling pathway. Therefore, the detection of signaling pathway proteins of the skeletal muscle cell membrane GLUT4 and Na+-K+-ATPase has a certain auxiliary diagnostic value for forensic insulin overdose identification. Glycogen detection in the liver and skeletal muscle is important for the diagnosis of insulin overdose, but it still needs to be differentiated from other causes of death. Skeletal muscle has great potential for insulin detection, and the ratio of insulin to the C-peptide (I:C) can determine whether an exogenous insulin overdose is present. [ABSTRACT FROM AUTHOR]

Obscurin is a giant sarcomeric protein expressed in striated muscles known to establish several interactions with other proteins of the sarcomere, but also with proteins of the sarcoplasmic reticulum and costameres. Here, we report experiments aiming to better understand the contribution of obscurin to skeletal muscle fibers, starting with a detailed characterization of the diaphragm muscle function, which we previously reported to be the most affected muscle in obscurin (Obscn) KO mice. Twitch and tetanus tension were not significantly different in the diaphragm of WT and Obscn KO mice, while the time to peak (TTP) and half relaxation time (HRT) were prolonged. Differences in force-frequency and force-velocity relationships and an enhanced fatigability are observed in an Obscn KO diaphragm with respect to WT controls. Voltage clamp experiments show that a sarcoplasmic reticulum's Ca2+ release and SERCA reuptake rates were decreased in muscle fibers from Obscn KO mice, suggesting that an impairment in intracellular Ca2+ dynamics could explain the observed differences in the TTP and HRT in the diaphragm. In partial contrast with previous observations, Obscn KO mice show a normal exercise tolerance, but fiber damage, the altered sarcomere ultrastructure and M-band disarray are still observed after intense exercise.

The tumor suppressor p53 is thought to play a key role in the maintenance of cell size and homeostasis, but relatively little is known about its role in skeletal muscle. Based on its ability to suppress cell growth, we hypothesized that inhibiting the function of wild-type p53 through the overexpression of a dominant-negative p53 mutant (DDp53) could result in muscle fiber hypertrophy. To test this hypothesis, we electroporated adult rat tibialis anterior muscles with DDp53 and collected the tissue three weeks later. We confirmed successful overexpression of DDp53 on a histological and biochemical level and found pronounced changes to muscle architecture, metabolism, and molecular signaling. Muscle mass, fiber cross-sectional area, and fiber diameter significantly decreased with DDp53 overexpression. We found histopathological changes in DDp53 transfected muscle which were accompanied by increased levels of proteins that are associated with membrane damage and repair. In addition, DDp53 decreased oxidative phosphorylation complex I and V protein levels, and despite its negative effects on muscle mass and fiber size, caused an increase in muscle protein synthesis as assessed via the SUnSET technique. Interestingly, the increase in muscle protein synthesis was concomitant with a decrease in phospho-S6K1 (Thr389). Furthermore, the muscle wasting in the DDp53 electroporated leg was accompanied by a decrease in global protein ubiquitination and an increase in proteasome activity. In conclusion, overexpression of a dominant-negative p53 mutant in skeletal muscle results in decreased muscle mass, myofiber size, histological muscle damage, a metabolic phenotype, and perturbed homeostasis between muscle protein synthesis and degradation.

The molecular responses to acute resistance exercise are well characterized. However, how cellular signals change over time to modulate chronic adaptations to more prolonged exercise training is less well understood. We investigated anabolic signaling and muscle protein synthesis rates at several time points after acute and chronic eccentric loading. Adult rat tibialis anterior muscle was stimulated for six sets of ten repetitions, and the muscle was collected at 0 h, 6 h, 18 h and 48 h. In the last group of animals, 48 h after the first exercise bout a second bout was conducted, and the muscle was collected 6 h later (54 h total). In a second experiment, rats were exposed to four exercise sessions over the course of 2 weeks. Anabolic signaling increased robustly 6 h after the first bout returning to baseline between 18 and 48 h. Interestingly, 6 h after the second bout mTORC1 activity was significantly lower than following the first bout. In the chronically exercised rats, we found baseline anabolic signaling was decreased, whereas myofibrillar protein synthesis (MPS) was substantially increased, 48 h after the last bout of exercise. The increase in MPS occurred in the absence of changes to muscle fiber size or mass. In conclusion, we find that anabolic signaling is already diminished after the second bout of acute resistance type exercise. Further, chronic exposure to resistance type exercise training results in decreased basal anabolic signaling but increased overall MPS rates.

This editorial published in the journal Frontiers in Physiology provides a historical perspective on the classification and discovery of unconventional myosins, which are molecular motors involved in cellular movement. It discusses the identification of the first unconventional myosin, myosin I, in 1973 and subsequent research that led to the discovery of other unconventional myosins. The document includes articles and reviews on specific unconventional myosins, such as myosin Va and myosin 5c, and their roles in cellular processes. The editorial also highlights recent research on different isoforms of unconventional myosins, including myosin VI and class-18 myosins, and their functions in various cellular structures and processes. The article concludes by acknowledging the contributions of researchers in the field and providing a historic perspective on the discovery of unconventional myosins. [Extracted from the article]

Neuromuscular disorders comprise a diverse group of human inborn diseases that arise from defects in the structure and/or function of the muscle tissue - encompassing the muscle cells (myofibres) themselves and their extracellular matrix - or muscle fibre innervation. Since the identification in 1987 of the first genetic lesion associated with a neuromuscular disorder - mutations in dystrophin as an underlying cause of Duchenne muscular dystrophy - the field has made tremendous progress in understanding the genetic basis of these diseases, with pathogenic variants in more than 500 genes now identified as underlying causes of neuromuscular disorders. The subset of neuromuscular disorders that affect skeletal muscle are referred to as myopathies or muscular dystrophies, and are due to variants in genes encoding muscle proteins. Many of these proteins provide structural stability to the myofibres or function in regulating sarcolemmal integrity, whereas others are involved in protein turnover, intracellular trafficking, calcium handling and electrical excitability - processes that ensure myofibre resistance to stress and their primary activity in muscle contraction. In this Review, we discuss how defects in muscle proteins give rise to muscle dysfunction, and ultimately to disease, with a focus on pathologies that are most common, best understood and that provide the most insight into muscle biology.

Human trophoblast stem cells (hTSC) can be isolated from first trimester placenta but not from term placenta. Here we demonstrate that villous cytotrophoblasts (vCTB) from term placenta can be reprogrammed into induced trophoblastic stem-like cells (iTSC) by introducing sets of transcription factors. The iTSCs express TSC markers such as GATA3, TEAD4 and ELF5, and are multipotent, validated by their differentiation into both extravillous trophoblasts (EVT) and syncytiotrophoblasts (STB) in vitro and in vivo. The iTSC can be passaged indefinitely in vitro without slowing of growth. The transcriptome profile of these cells closely resembles the profile of hTSC isolated from first trimester placentae but different from the term placental vCTB from which they originated. The ability to reprogram cells from term placenta into iTSC will allow study of early gestation events which impact placental function later in gestation, including preeclampsia and spontaneous preterm birth.

Adolescent idiopathic scoliosis (AIS) is the predominant orthopedic disorder in children, affecting 1–3% of the global population. Research in this field has tried to delineate the genetic factors behind scoliosis and its association with heredity since AIS is considered a polygenic disease and has different genetic and epigenetic factors. The current study conducted a narrative review of the literature, focusing on biomarkers in the pathophysiology of muscle in AIS patients. Articles were collected from Scopus, Pubmed, and Web of Science. The key screening parameters were scoliosis classification, sampling, and the biomarkers evaluated. This review emphasizes potential key mechanisms and molecular regulators in muscle tissue. While there has been limited focus on the proteins contributing to muscle changes in AIS, significant attention has been given to genomic studies of single-nucleotide polymorphisms, particularly in LBX1. Despite these efforts, the exact causes of AIS remain elusive, with several theories suggesting genetic and hormonal factors. This review identified critical protein biomarkers such as Gi-protein alpha subunits, fibrillin-1 and -2, and various differentially expressed proteins, which may be linked to muscle alterations in AIS. This field of research is still limited due to a lack of homogeneity in the distinction of patients by groups and curve severity. Although the pathophysiology of AIS is still unclear, molecular research is important to guide the treatment of AIS before achieving skeletal maturity, thus avoiding serious problems associated with posture changes and low quality of life. In the future, a more comprehensive synergy between orthopedic and molecular research might ameliorate the diagnosis and treatment of AIS patients. [ABSTRACT FROM AUTHOR]

Simple Summary: Epithelial ovarian cancer (EOC) is the fifth-leading cause of cancer-related deaths in women worldwide and the most lethal gynecologic malignancy. Seventy-five percent of patients are diagnosed at an advanced stage, accompanied by extensive pelvic and abdominal metastases, and thus have a poor prognosis. We first screened for critical genes in EOC in the GEO database. LLGL2 was upregulated in ovarian cancer tissue, while low expression of LLGL2 was significantly associated with a more advanced stage and a higher grade of EOC and a poorer survival of patients, implying that LLGL2 may function as a tumor suppressor gene. Our data demonstrated that overexpression of LLGL2 inhibited the ovarian cancer cell migration and invasion abilities in vivo and in vitro. Mechanistically, LLGL2 altered the intracellular localization and function of ACTN1 by interacting with ACTN1 and regulating cytoskeleton remodeling to inhibit the invasion and metastasis of ovarian cancer cells. Epithelial ovarian cancer is the most lethal gynecological malignant tumor. Although debulking surgery, chemotherapy, and PARP inhibitors have greatly improved survival, the prognosis for patients with advanced EOC without HRD is still poor. LLGL2, as a cell polarity factor, is involved in maintaining cell polarity and asymmetric cell division. In the study of zebrafish development, LLGL2 regulated the proliferation and migration of epidermal cells and the formation of cortical F-actin. However, the role of LLGL2 in ovarian cancer has not been described. Our study found, through bioinformatics analysis, that low expression of LLGL2 was significantly associated with a more advanced stage and a higher grade of EOC and a poorer survival of patients. Functional experiments that involved LLGL2 overexpression and knockdown showed that LLGL2 inhibited the migration and invasion abilities of ovarian cancer cells in vitro, without affecting their proliferation. LLGL2-overexpressing mice had fewer metastatic implant foci than the controls in vivo. Mechanistically, immunoprecipitation combined with mass spectrometry analysis suggested that LLGL2 regulated cytoskeletal remodeling by interacting with ACTN1. LLGL2 altered the intracellular localization and function of ACTN1 without changing its protein and mRNA levels. Collectively, we uncovered that LLGL2 impaired actin filament aggregation into bundles by interacting with ACTN1, which led to cytoskeleton remodeling and inhibition of the invasion and metastasis of ovarian cancer cells. [ABSTRACT FROM AUTHOR]

Simple Summary: Greasyback shrimp (Metapenaeus ensis) is a highly sought-after shrimp species in the market. However, there is a lack of studies investigating the optimal dietary protein level for greasyback shrimp, which hampers the development of shrimp farming for this species. Therefore, this study aimed to explore the effects of dietary protein levels on various aspects of growth, antioxidant capacity, digestive enzyme activity, and gene expression related to muscle growth and protein synthesis in juvenile greasyback shrimp. The ultimate goal was to determine the optimal protein requirement for these shrimp. The findings revealed that the appropriate dietary protein level for juvenile greasyback shrimp is 38.59%, as determined by the broken-line regression analysis of the specific growth rate (SGR). These results serve as a foundation for the development of formulated diets tailored for greasyback shrimp. An 8-week feeding trial was conducted to assess the effects on growth, antioxidant capacity, digestive enzyme activity, and gene expression related to muscle growth and protein synthesis of juvenile greasyback shrimp (Metapenaeus ensis) using five experimental diets containing 29.37%, 34.30%, 39.11%, 44.05%, and 49.32% of protein. The results demonstrated that juvenile greasyback shrimp consuming 39.11%, 44.05%, and 49.32% dietary protein had a significantly higher final body weight (FBW), weight gain (WG), feed conversion ratio (FCR), and specific growth rate (SGR) than other groups (p < 0.05). The protein efficiency ratio (PER) showed a significantly quadratic pattern with increasing dietary protein levels (p < 0.05). The highest trypsin and pepsin activities were observed in the group with a protein level of 44.05% (p < 0.05). Relatively higher superoxide dismutase (SOD) activity was found in groups with protein levels of 39.11% (p < 0.05). Alkaline phosphatase (AKP) and catalase (CAT) activity showed a significantly linear increasing pattern with increasing protein intake up to 44.05%, and then decreased gradually (p < 0.05). Compared to the dietary 29.37% protein level, the expression levels of myogenic regulatory factors (mef2α, mlc, and myf5) and mTOR pathway (mtor, s6k, akt, and pi3k)-related genes were significantly up-regulated in muscle with 39.11%, 44.05%, and 49.32% dietary protein levels (p < 0.05). The AAR pathway (gcn2, eif2α, and atf4)-related gene expression levels were significantly lower in muscles with 39.11%, 44.05%, and 49.32% protein levels than in other groups (p < 0.05). Based on the broken-line regression analysis of SGR, the estimated appropriate dietary protein requirement for juvenile greasyback shrimp is 38.59%. [ABSTRACT FROM AUTHOR]

Hyperhomocysteinemia is a main risk factor for phenotypic modulation of vascular smooth muscle cells (VSMCs) and atherosclerosis. Phenotypic switching and proliferation of VSMCs are related to the progression of vascular inflammation. Chrysanthemum coronarium L. is a leafy vegetable with various biological functions, such as antioxidative, anti-inflammatory, and antiproliferative effects. In this study, we aimed to identify the mechanisms underlying the therapeutic and preventive effects of C. coronarium L. extract (CC) in regulating homocysteine (Hcy)-induced vascular inflammation in human aortic VSMCs. CC did not exhibit cytotoxicity and inhibited Hcy-stimulated VSMC proliferation and migration. In addition, CC promoted Hcy-induced expression of VSMC contractile phenotype proteins, including alpha-smooth muscle actin, calponin, and smooth muscle 22α. CC also decreased Hcy-induced accumulation of reactive oxygen species and expression of inflammatory markers nicotinamide adenine dinucleotide phosphate oxidase-4 and soluble epoxide hydrolase. These results showed that CC attenuates Hcy-induced inflammatory responses, highlighting its potential as a therapeutic or preventive target for Hcy-induced vascular inflammation. [ABSTRACT FROM AUTHOR]

The unprecedented surge of developing meat analogues and other alternative protein products in the past few years has occurred amidst numerous technological challenges. The creation of fibril structure and flavour from non-muscle proteinaceous sources to mimic fresh and processed meat requires a clear understanding of the fundamental differences between muscle and alternative proteins. Currently, plant-based meat alternatives are dominating the alternative market; mycoprotein-based products have also gained a market share, while algae and insects are other emerging sources of alternative proteins. Both traditional and novel processing technologies and innovative ingredient formulations are being developed to transform nonmuscle proteins into fibrous or particle structures that microscopically resemble muscle. However, the production of meat analogues generally entails ultra-processing and ultra-formulation, which could compromise nutritional value and safety. Therefore, to sustain the alternative protein market, scientists and entrepreneurs must methodically examine and understand inherent differences that separate alternative proteins from muscle proteins. An intuitive knowledge base is essential to designing new approaches to overcome technical challenges. In doing so, food scientists and entrepreneurs must be keenly cognisant that animal meat products are unique; the quality and sensorial attributes of meat can only be simulated but not replicated. [ABSTRACT FROM AUTHOR]

Amyotrophic Lateral Sclerosis (ALS) is the most common motor neuron disease, still incurable. The disease is highly heterogenous both genetically and phenotypically. Therefore, developing efficacious treatments is challenging in many aspects because it is difficult to predict the rate of disease progression and stratify the patients to minimize statistical variability in clinical studies. Moreover, there is a lack of sensitive measures of therapeutic effect to assess whether a pharmacological intervention ameliorates the disease. There is also urgency of markers that reflect a molecular mechanism dysregulated by ALS pathology and can be rescued when a treatment relieves the condition. Here, we summarize and discuss biomarkers tested in multicentered studies and across different laboratories like neurofilaments, the most used marker in ALS clinical studies, neuroinflammatory-related proteins, p75ECD, p-Tau/t-Tau, and UCHL1. We also explore the applicability of muscle proteins and extracellular vesicles as potential biomarkers. • Amyotrophic Lateral Sclerosis (ALS) is the most common motor neuron disease. • There is an urgent need to identify biomarkers for ALS. • Neurofilaments show very good performances for diagnosis and prognosis. • Other markers are under analysis across multiple laboratories for validation. [ABSTRACT FROM AUTHOR]

Summary: Rapid softening of texture is a major problem associated with quality loss and consumer rejection of harpiosquillid mantis shrimp (Harpiosquilla raphidea) (HMS). Effects of endogenous proteases in muscles and digestive tract on protein degradation and softening were investigated. Scanning electron microscopic and histological images indicated drastic destruction of muscle during iced storage. Based on autolysis, maximal activity was found at pH 8.5 and 55 °C, and serine proteases including trypsin were dominant. Cathepsin B and L + B in muscle were altered throughout storage, while trypsin remained constant in HMS meat for 1–3 days. Firmness and toughness decreased and coincided with augmented degradation of myofibrillar proteins and collagen. Trypsin from the digestive tract was contaminated into the abdomen during iced storage, therefore inducing drastic hydrolysis of muscle proteins. This phenomenon caused the undesirable pasty/mushy texture associated with the loss in firmness and toughness of meat within 3 days of storage. [ABSTRACT FROM AUTHOR]

Cardiac fibrosis contributes to adverse ventricular remodeling and is associated with loss of miR-29b. Overexpression of miR-29b via plasmid or intravenous injection of microRNA mimic has blunted fibrosis, but these are inefficient and non-targeted delivery strategies. In this study, we tested the hypothesis that delivery of microRNA-29b (miR-29b) using ultrasound-targeted microbubble cavitation (UTMC) of miR-29b-loaded microbubbles would attenuate cardiac fibrosis and preserve left ventricular (LV) function. Lipid microbubbles were loaded with miR-29b mimic (miR-29b-MB) or negative control (NC) mimic (NC-MB), placed with cardiac fibroblasts (CFs) and treated with pulsed ultrasound. Cells were harvested to measure downstream fibrotic mediators. Mice received angiotensin II (ANG II) infusion causing afterload increase and direct ANG II-induced cardiac fibrosis. UTMC of miRNA-loaded microbubbles was administered to the heart at days 0, 3 and 7. Serial echocardiography was performed, and hearts were harvested on day 10. UTMC treatment of CFs with miR-29b-MB increased miR-29b and decreased fibrotic transcripts compared with NC-MB treatment. In vivo UTMC + NC-MB led to increased LV mass, reduction in cardiac function and increase in fibrotic markers, demonstrating ANGI II-induced adverse cardiac remodeling. Mice treated with UTMC + miR-29b-MB had preservation of cardiac function, downregulation of cardiac fibrillin and trends of lower COL1A1, COL1A2 and COL3 mRNA and decreased cardiac α-smooth muscle protein. UTMC-mediated delivery of miR-29b mimic blunts expression of fibrosis markers and preserves LV function in ANG II-induced cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Rathor, Richa, Sukanya Srivastava, and Geetha Suryakumar. A comparative biochemical study between L-carnosine and β-alanine in amelioration of hypobaric hypoxia-induced skeletal muscle protein loss. High Alt Med Biol. 24:302–311, 2023. Background: Carnosine (CAR; β-alanyl-L-histidine), a biologically active dipeptide is known for its unique pH-buffering capacity, metal chelating activity, and antioxidant and antiglycation property. β-Alanine (ALA) is a nonessential amino acid and used to enhance performance and cognitive functions. Hypobaric hypoxia (HH)-induced muscle protein loss is regulated by multifaceted signaling pathways. The present study investigated the beneficial effects of CAR and ALA against HH-associated muscle loss. Methodology: Simulated HH exposure was performed in an animal decompression chamber. Gastric oral administration of CAR (50 mg·kg−1) and ALA (450 mg·kg−1) were given daily for 3 days and at the end of the treatment, hindlimb skeletal muscle tissue was excised for western blot and biochemical assays. Results: Cosupplementation of CAR and ALA alone was able to ameliorate the hypoxia-induced inflammation, oxidative stress (FOXO), ER stress (GRP-78), and atrophic signaling (MuRF-1) in the skeletal muscles. Creatinine phospho kinase activity and apoptosis were also decreased in CAR- and ALA-supplemented rats. However, CAR showed enhanced protection in HH-induced muscle loss as CAR supplementation was able to enhance protein concentration, body weight, and decreased the protein oxidation and ALA administration was not able to restore the same. Conclusions: Hence, the present comprehensive study supports the fact that CAR (50 mg·kg−1) is more beneficial as compared with ALA (450 mg·kg−1) in ameliorating the hypoxia-induced skeletal muscle loss. [ABSTRACT FROM AUTHOR]

Critical torque (CT) represents the highest oxidative steady state for intermittent knee extensor exercise, but the extent to which it is influenced by skeletal muscle mitochondria and sex is unclear. Vastus lateralis muscle biopsy samples were collected from 12 females and 12 males –matched for relative maximal oxygen uptake normalized to fat‐free mass (FFM) (F: 57.3 (7.5) ml (kg FFM)−1 min−1; M: 56.8 (7.6) ml (kg FFM)−1 min−1; P = 0.856) – prior to CT determination and performance fatiguability trials. Males had a lower proportion of myosin heavy chain (MHC) I isoform (40.6 (18.4)%) compared to females (59.5 (18.9)%; P = 0.021), but MHC IIa and IIx isoform distributions and protein markers of mitochondrial content were not different between sexes (P > 0.05). When normalized to maximum voluntary contraction (MVC), the relative CT (F: 42.9 (8.3)%; M: 37.9 (9.0)%; P = 0.172) and curvature constant, W′ (F: 26.6 (11.0) N m s (N m)−1; M: 26.4 (6.5) N m s (N m)−1; P = 0.962) were not significantly different between sexes. All protein biomarkers of skeletal muscle mitochondrial content, as well as the proportion of MHC I isoform, positively correlated with relative CT (0.48 < r < 0.70; P < 0.05), and the proportion of MHC IIx isoform correlated positively with relative W′ (r = 0.57; P = 0.007). Indices of performance fatiguability were not different between males and females for MVC‐ and CT‐controlled trials (P > 0.05). Greater mitochondrial protein abundance was associated with attenuated declines in potentiated twitch torque for exercise at 60% MVC (P < 0.05); however, the influence of mitochondrial protein abundance on performance fatiguability was reduced when exercise was prescribed relative to CT. Whether these findings translate to whole‐body exercise requires additional research. Key points: The quadriceps critical torque represents the highest intensity of intermittent knee extensor exercise for which an oxidative steady state is attainable, but its relationship with skeletal muscle mitochondrial protein abundance is unknown.Matching males and females for maximal oxygen uptake relative to fat‐free mass facilitates investigations of sex differences in exercise physiology, but studies that have compared critical torque and performance fatiguability during intermittent knee extensor exercise have not ensured equal aerobic fitness between sexes.Skeletal muscle mitochondrial protein abundance was correlated with critical torque and fatigue resistance for exercise prescribed relative to maximum voluntary contraction but not for exercise performed relative to the critical torque.Differences between sexes in critical torque, skeletal muscle mitochondrial protein abundance and performance fatiguability were not statistically significant.Our results suggest that skeletal muscle mitochondrial protein abundance may contribute to fatigue resistance by influencing the critical intensity of exercise. [ABSTRACT FROM AUTHOR]

Superficial discolored spots on Atlantic salmon (Salmo salar) fillets are a serious quality problem for commercial seafood farming. Previous reports have proposed that the black spots (called melanized focal changes (MFCs)) may be melanin, but no convincing evidence has been reported. In this study, we performed chemical characterization of MFCs and of red pigment (called red focal changes (RFCs)) from salmon fillets using alkaline hydrogen peroxide oxidation and hydroiodic acid hydrolysis. This revealed that the MFCs contain 3,4-dihydroxyphenylalanine (DOPA)-derived eumelanin, whereas the RFCs contain only trace amounts of eumelanin. Therefore, it is probable that the black color of the MFCs can be explained by the presence of eumelanin from accumulated melanomacrophages. For the red pigment, we could not find a significant signature of either eumelanin or pheomelanin; the red color is probably predominantly hemorrhagic in nature. However, we found that the level of pigmentation in RFCs increased together with some melanogenic metabolites. Comparison with a "mimicking experiment", in which a mixture of a salmon homogenate + DOPA was oxidized with tyrosinase, suggested that the RFCs include conjugations of DOPAquinone and/or DOPAchrome with salmon muscle tissue proteins. In short, the results suggest that melanogenic metabolites in MFCs and RFCs derive from different chemical pathways, which would agree with the two different colorations deriving from distinct cellular origins, namely melanomacrophages and red blood cells, respectively. [ABSTRACT FROM AUTHOR]

Calcium binding to troponin, with subsequent displacement of its linked tropomyosin molecule on the thin filament surface, cooperates with myosin binding to actin in the contractile regulation of striated muscle. The intertwined role of these systems is studied in the present issue of JGP by Ishii et al. (https://doi.org/10.1085/jgp.202313414). A particularly interesting feature of the paper, except for studying both skeletal and cardiac muscle proteins, is that the experiments unlike most other similar studies are performed at physiological temperature (35--40°C). [ABSTRACT FROM AUTHOR]

The transcription factor Ftz‐f1 has multiple functions in insect development in a spatial‐temporal line. One of these roles is in the insect ovaries, specifically in the regulation of steroidogenic enzymes production. We studied the function of F in Blattella germanica oogenesis, as it shows two moments of high expression in ovaries: before the imaginal moult, and just before ovulation in the adult. Injecting dsftz‐f1 into adult females, either just after the imaginal moult or just prior to choriogenesis, prevented oviposition, with differences between the two approaches. In 3‐day‐old adult females treated with dsftz‐f1 just after the emergence, the expression of ftz‐f1 was not modified, but the steroidogenic genes increased their expression. ftz‐f1 transcript levels in the ovaries of 5‐day‐old dsftz‐f1‐treated females were significantly depleted, and the expression levels of the same steroidogenic genes began to decrease. These results suggest that Ftz‐f1 regulates the expression of steroidogenic genes in B. germanica, with phm possibly being a key target. Ftz‐f1 has a different temporal function in the cytoskeleton of follicular cells of the basal ovarian follicles. Early in the gonadotrophic cycle, Ftz‐f1 promotes the expression of genes related to the cytoskeleton and muscle proteins, while at the end of the cycle it maintains the expression levels of these genes, thus ensuring correct ovulation. [ABSTRACT FROM AUTHOR]

[Objectives] This study was conducted to investigate the effects of Astragalus membranaceus in different groups on energy metabolism and CNTF protein expression in skeletal muscle of exercise-induced fatigue rats. [Methods] Thirty-five clean male SD rats were randomly divided into a normal group, and low-, meddle- and high-dose groups of A. membranaceus aqueous solution, with 7 rats in each group. The low-dose, medium-dose and high-dose groups were given by gavage at 0. 65, 1.3 and 2. 6 g/kg, respectively, while the normal group and the model group were given normal food and water. The weight of rats was observed. The contents of serum urea, lactate, muscle glycogen, liver glycogen and CNTF expression were detected. [Results] After modeling, compared with the normal group, the serum lactate and urea contents of rats in the model group significantly increased (P <0.01), while the muscle glycogen content (P <0.01) and liver glycogen content (P <0.05) of the skeletal muscle significantly decreased. Compared with the model group, the low-, meddle- and high-dose groups of A. membranaceus significantly reduced the levels of lactate and urea in serum (P <0. 01), while the levels of muscle glycogen and liver glycogen in the skeletal muscle significantly increased (P<0. 01, P <0. 05). [Conclusions] This study provides a good research foundation for the treatment of exercise-induced fatigue using traditional Chinese herb A. membranaceus in modem clinical practice. [ABSTRACT FROM AUTHOR]

In this study, the effect of modified atmosphere packaging with different gas mixtures on texture and muscle properties of Pacific white shrimp (Litopenaeus vannamei) during refrigerated storage was studied via texture profile, water holding capacity (WHC), protein properties (Ca2+-ATPase, TCA-soluble peptides, myofibrillar/sarcoplasmic protein content), and microbial counts. The results showed that the antibacterial effect of Modified atmosphere packaging (MAP) was correlated with the increase of CO2 with the presence of low level of O2. Though MAP without O2 had a higher whiteness value but also had higher bacterial counts and total volatile basic nitrogen (TVB-N) values compared with other MAP-groups. In general, a gas composition of 80% CO2 + 5%O2 + 15% N2 treatment had lowest microbial counts and reduced TVB-N values by 22.85% in comparison with the control on day 10. However, MAP was found to have a complicated impact on muscle protein and texture of shrimp. 60% CO2 + 5% O2 + 35% N2 and 40% CO2 + 5% O2 + 55% N2 had an advantage in maintaining springiness and the content of myofibrillar/sarcoplasmic proteins. The correlation analysis showed that WHC had stronger relationship with springiness, resilience, myofibrillar protein content. Therefore, regarding the texture and protein properties, the concentration of CO2 in MAP for Pacific white shrimp should not be higher than 60%. [ABSTRACT FROM AUTHOR]

Myopathy is the most common side effect of statins, but it has not been addressed effectively. In anticipation of its wider use as a small molecule to complement the current COVID-19 management, a pharmacological solution to statin-associated muscle symptoms (SAMS) is warranted. Statins act by suppressing the mevalonate pathway, which in turn affects the downstream synthesis of isoprenoids required for normal physiological functions. CoQ10 and geranylgeraniol (GG) syntheses are reduced by statin use. However, CoQ10 supplementation has not been shown to reverse SAMS. GG is an obligatory substrate for CoQ10 synthesis, an endogenous nutrient critical for skeletal muscle protein synthesis. Multiple studies showed GG supplementation is effective in reversing SAMS. This opinion paper proposes employing GG to prevent SAMS in pleiotropic statin use, including usage in the post-COVID-19 pandemic era. [ABSTRACT FROM AUTHOR]

Sporadic inclusion body myositis (sIBM) is an idiopathic inflammatory myopathy with invasion of CD8 T cells in muscle and aggregation of proteins in the sarcoplasm. TDP-43 and p62 are two proteins that aggregate in affected muscle, and have been suggested as specific markers for sIBM over other inflammatory myopathies. TDP-43 is also mislocalised from the nucleus to the sarcoplasm in sIBM. It is not clear if inflammation precedes protein aggregation in sIBM. This study investigated if exposure to cytotoxic inflammatory cells caused TDP-43 and p62 aggregation or TDP-43 mislocalisation in cultured myotubes. TALL-104 coculture was highly cytotoxic to myotubes after 24 h. Secretion of IFNγ and TNFα were higher in cocultures compared to monocultured TALL-104 cells, indicating activation. TALL-104 cells attached to and infiltrated myotubes. There was no effect of TALL-104 coculture on TDP-43 or p62 sarcoplasmic aggregate size or frequency. However, there was decreased localisation of TDP-43 to the nucleus with TALL-104 coculture compared to control. In an in vitro setting, cytotoxic immune cells did not cause TDP-43 or p62 sarcoplasmic aggregation, suggesting cellular cytotoxicity may not trigger aggregation of these proteins. However TALL-104 coculture influenced TDP-43 localisation, suggesting cytotoxic immune cells may contribute to TDP-43 localisation shifts which is observed in sIBM. [ABSTRACT FROM AUTHOR]

Simple Summary: To understand the bionetworks involved in intestinal gastric cancer (IGC), an integrative approach to investigate omics data is essential; otherwise, a broad comprehension of IGC molecular networks cannot be achieved. Thus, an integrative analysis of high-throughput data from the expression of major biological molecules (mRNAs, microRNAs, and proteins) was performed to identify key components in the development of IGC, which had not been performed until now. Through the identification of regulatory circuits based on the interaction of microRNA/mRNA/proteins, we were able to identify different mechanisms of gene regulation impacting similar biological functions and key regulators (hubs) in IGC development. Besides their good potential as diagnostic, prognostic, and tumor development biomarkers, hub expression was related to relevant aspects of IGC patient clinicopathology, where we found hub interactions operating together to impact clinical outcomes. This approach will help us better understand the biological and clinical relevance of complex molecular bionetwork in IGC. Intestinal gastric cancer (IGC) carcinogenesis results from a complex interplay between environmental and molecular factors, ultimately contributing to disease development. We used integrative bioinformatic analysis to investigate IGC high-throughput molecular data to uncover interactions among differentially expressed genes, microRNAs, and proteins and their roles in IGC. An integrated network was generated based on experimentally validated microRNA-gene/protein interaction data, with three regulatory circuits involved in a complex network contributing to IGC progression. Key regulators were determined, including 23 microRNA and 15 gene/protein hubs. The regulatory circuit networks were associated with hallmarks of cancer, e.g., cell death, apoptosis and the cell cycle, the immune response, and epithelial-to-mesenchymal transition, indicating that different mechanisms of gene regulation impact similar biological functions. Altered expression of hubs was related to the clinicopathological characteristics of IGC patients and showed good performance in discriminating tumors from adjacent nontumor tissues and in relation to T stage and overall survival (OS). Interestingly, expression of upregulated hub hsa-mir-200b and its downregulated target hub gene/protein CFL2 were related not only to pathological T staging and OS but also to changes during IGC carcinogenesis. Our study suggests that regulation of CFL2 by hsa-miR-200b is a dynamic process during tumor progression and that this control plays essential roles in IGC development. Overall, the results indicate that this regulatory interaction is an important component in IGC pathogenesis. Also, we identified a novel molecular interplay between microRNAs, proteins, and genes associated with IGC in a complex biological network and the hubs closely related to IGC carcinogenesis as potential biomarkers. [ABSTRACT FROM AUTHOR]

It is well-known that the postprandial muscle protein synthetic response to protein ingestion is regulated on various levels, including dietary protein digestion and amino acid (AA) absorption, splanchnic AA retention, the availability of dietary protein–derived AA in the circulation, delivery of AA to the muscle, uptake of AA by the muscle, and intramuscular signaling. AA availability after consumption of dairy products is primarily determined by the rate of gastric emptying of milk proteins, which is mainly linked to coagulation of milk proteins in the stomach. Caseins form gastric coagula, which make their gastric emptying and subsequent postprandial aminoacidemia notably slower than that of whey proteins. Only recently, the role of processing, food structure, preservation and matrix on coagulation herein has been getting attention. In this review we describe various processes, that affect gastric coagulation of caseins and therewith control gastric emptying, such as the conversion to caseinate, heat treatment in the presence of whey proteins, conversion to stirred yoghurt and enzymatic hydrolysis. Modulating product characteristics by processing can be very useful to steer the gastric behavior of protein, and the subsequent digestion and AA absorption and muscle anabolic response to maintain or increase muscle mass. [ABSTRACT FROM AUTHOR]

Objective: To study the protective effect of cannabidiol (CBD) on rats with pulmonary fibrosis and explore the possible mechanism of the use of CBD in the treatment of pulmonary fibrosis. Methods: Sixty SD rats were randomly divided into the normal control group, model group, prednisone group, CBD low, medium and high dose groups (12, 36, 108 mg/kg, ig),10 rats in each group. Except for the normal control group, the other 5 groups were all induced by tracheal injection of bleomycin to rat models of pulmonary fibrosis. After modeling, the rats were given intragastric administration once a day for 28 consecutive days and samples were taken. The degree of pulmonary edema was detected; the pathological changes of lung tissue were observed by HE and Masson staining; tumor necrosis factor a (TNF-a), interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and lung tissue superoxide dismutase (SOD), malondialdehyde (MDA), hydroxyproline (HYP) contents were measured by ELISA, transforming growth factor-ß1 (TGF-ß1) and a-smooth muscle protein (a-SMA) concentration were detected by immunocytochemical method, real-time fluorescent quantitative PCR (qRT-PCR) method was used to detect the mRNA expression levels of TGF-ß1,a-SMA, Nrf2 and nuclear transcription factor-κB p65 (NF-κB p65). Results: The lung organ coefficient and W/D value were significantly decreased in the CBD administration group (P<0.05); medium and high doses of CBD could reduce the number of collagen fibers and fibroblasts; the pulmonary fibrosis in the low, medium, and high dose groups of CBD was significantly lower. The levels of TNF-a, IL-1ß, and IL-6 in rat serum, as well as MDA and HYP in lung tissue, were significantly lower compared to the model group. Additionally, the level of SOD was significantly increased (P<0.05); The expression of a-SMA was decreased compared with the model group (P<0.05); the contents of TGF-ß1, a-SMA and NF-κB p65 mRNA in lung tissue decreased, and the expression level of Nrf2 mRNA increased (P<0.05). Especially, the high-dose group had the most significant effect. Conclusion: CBD can significantly reduce the degree of pulmonary fibrosis in rats, and its potential mechanism may be related to inhibiting inflammatory response, enhancing antioxidant capacity and inhibiting the protein expression of TGF -ß1 and a-SMA. [ABSTRACT FROM AUTHOR]

Glucocorticoids, commonly used to manage inflammatory diseases, can induce muscle atrophy by accelerating the breakdown of muscle proteins. This research delves into the influence of Prolyl-hydroxyproline (Pro-Hyp), a collagen-derived peptide, on muscle atrophy induced with dexamethasone (DEX), a synthetic glucocorticoid, in mouse C2C12 skeletal myotubes. Exposure to DEX (10 μM) for 6 days resulted in a decrease in myotube diameter, along with elevated mRNA and protein levels of two muscle-atrophy-related ubiquitin ligases, muscle atrophy F-box (MAFbx, also known as atrogin-1) and muscle ring finger 1 (MuRF-1). Remarkably, treatment with 0.1 mM of Pro-Hyp mitigated the reduction in myotube thickness caused by DEX, while promoting the phosphorylation of Akt, mammalian target of rapamycin (mTOR), and forkhead box O3a (Foxo3a). This led to the inhibition of the upregulation of the ubiquitin ligases atrogin-1 and MuRF-1. These findings indicate the potential significance of Pro-Hyp as a promising therapeutic target for countering DEX-induced muscle atrophy. [ABSTRACT FROM AUTHOR]

Objectives AECAs are detected in multiple forms of vasculitis or vasculopathy, including JDM. High levels of tropomyosin alpha-4 chain (TPM4) gene expression in cutaneous lesions and TPM4 protein expression in some endothelial cells (ECs) have been proven. Furthermore, the presence of autoantibodies to tropomyosin proteins have been discovered in DM. We therefore investigated whether anti-TPM4 autoantibodies are an AECA in JDM and are correlated with clinical features of JDM. Methods The expression of TPM4 protein in cultured normal human dermal microvascular ECs was investigated by Western blotting. Plasma samples from 63 children with JDM, 50 children with polyarticular JIA (pJIA) and 40 healthy children (HC) were tested for the presence of anti-TPM4 autoantibodies using an ELISA. Clinical features were compared between JDM patients with and without anti-TPM4 autoantibodies. Results Autoantibodies to TPM4 were detected in the plasma of 30% of JDM, 2% of pJIA (P  < 0.0001) and 0% of HC (P  < 0.0001). In JDM, anti-TPM4 autoantibodies were associated with the presence of cutaneous ulcers (53%; P  = 0.02), shawl sign rash (47%; P  = 0.03), mucous membrane lesions (84%; P  = 0.04) and subcutaneous edema (42%; P  < 0.05). Anti-TPM4 autoantibodies significantly correlated with the use of intravenous steroids and IVIG therapy in JDM (both P  = 0.01). The total number of medications received was higher in patients with anti-TPM4 autoantibodies (P  = 0.02). Conclusion Anti-TPM4 autoantibodies are detected frequently in children with JDM and are novel myositis-associated autoantibodies. Their presence correlates with vasculopathic and other cutaneous manifestations of JDM that may be indicative of more refractory disease. [ABSTRACT FROM AUTHOR]

Background: A precise determination of time since death plays a major role in forensic routine. Currently available techniques for estimating the postmortem interval (PMI) are restricted to specific time periods or cannot be applied for individual case-specific reasons. During recent years, it has been repeatedly demonstrated that Western blot analysis of postmortem muscle protein degradation can substantially contribute to overcome these limitations in cases with different background. Enabling to delimit time points at which certain marker proteins undergo distinct degradation events, the method has become a reasonable new tool for PMI delimitation under various forensic scenarios. However, additional research is yet required to improve our understanding of protein decomposition and how it is affected by intrinsic and extrinsic factors. Since there are temperature limits for proteolysis, and investigators are confronted with frozen corpses, investigation of the effects of freezing and thawing on postmortem protein decomposition in the muscle tissue is an important objective to firmly establish the new method. It is also important because freezing is often the only practical means to intermittently preserve tissue samples from both true cases and animal model research. Methods: Sets of dismembered pig hind limbs, either freshly detached non-frozen, or thawed after 4 months of freeze-storage (n = 6 each), were left to decompose under controlled conditions at 30 °C for 7 days and 10 days, respectively. Samples of the M. biceps femoris were regularly collected at predefined time points. All samples were processed via SDS-PAGE and Western blotting to identify the degradation patterns of previously characterized muscle proteins. Results: Western blots show that the proteins degrade predictably over time in precise patterns that are largely unaffected by the freeze-and-thaw process. Investigated proteins showed complete degradation of the native protein band, partly giving rise to degradation products present in distinct time phases of the decomposition process. Conclusion: This study provides substantial new information from a porcine model to assess the degree of bias that freezing and thawing induces on postmortem degradation of skeletal muscle proteins. Results support that a freeze–thaw cycle with prolonged storage in frozen state has no significant impact on the decomposition behavior. This will help to equip the protein degradation–based method for PMI determination with a robust applicability in the normal forensic setting. [ABSTRACT FROM AUTHOR]

Following burns a sustained catabolic stress response is activated, resulting in skeletal muscle wasting. A better understanding of the underlying mechanisms of postburn skeletal muscle wasting is essential for the development of preventive and/or therapeutic strategies. Six weeks old female rats underwent a sham, 10% or 40% total body surface area scald burn. Ten days post-injury, severely burned animals gained significantly less weight compared to sham treated and minor burned animals, reflected in a significantly lower ratio of muscle to total body weight for Soleus (SOL) and Extensor Digitorum Longus (EDL) in the severely burned group. Postburn, total fiber number was significantly lower in EDL, while in SOL the amount of type1 fibers significantly increased and type2 fibers significantly decreased. No signs of mitochondrial dysfunction (COX/SDH) or apoptosis (caspase-3) were found. In SOL and EDL, eEF2 and pAKT expression was significantly lower after severe burn. MURF1,2,3 and Atrogin-1 was significantly higher in SOL, whilst in EDL MURF1,2,3 was significantly lower postburn. In both muscles, FOXO3A was significantly lower postburn. This study identified postburn changes in muscle anthropomorphology and proteins involved in pathways regulating protein synthesis and breakdown, with more pronounced catabolic effects in SOL. • Muscle wasting characteristics are dependent of fiber type 10 days postburn. • In the early flow phase postburn anabolic signaling is diminished in SOL and EDL. • Catabolic signaling is more pronounced in SOL 10 days postburn. • No sign of apoptosis and mitochondrial dysfunction was found 10 days postburn. [ABSTRACT FROM AUTHOR]

Regular exercise leads to many adaptations, including changes to protein abundance, which serve to blunt subsequent homeostatic threats generated by future skeletal muscle contractions. The exercise biology field has developed its own dogma, which proposes that transient changes in mRNA after a single session of exercise can provide insights into both the direction and magnitude of protein changes likely to occur following training. However, there are examples of contraction-induced changes in mRNA without any subsequent change in encoded proteins, and, conversely, proteins with increased abundance in response to exercise training without a corresponding change in respective mRNA levels. We propose an alternative view that there is not always a direct relationship between exercise-induced changes in mRNA levels and the abundance of proteins they encode. The ability of skeletal muscle to adapt to repeated contractile stimuli is one of the most intriguing aspects of physiology. The molecular bases underpinning these adaptations involve increased protein activity and/or expression, mediated by an array of pre- and post-transcriptional processes, as well as translational and post-translational control. A longstanding dogma assumes a direct relationship between exercise-induced increases in mRNA levels and subsequent changes in the abundance of the proteins they encode. Drawing on the results of recent studies, we dissect and question the common assumption of a direct relationship between changes in the skeletal muscle transcriptome and proteome induced by repeated muscle contractions (e.g., exercise). [ABSTRACT FROM AUTHOR]

Myofibrillar proteins are the most important proteins of muscle and their gelation properties have a decisive effect on the sensory quality of meat products. Due to the unique structural characteristics, plant polyphenols can interact with myofibrillar proteins during heat-induced gelation formation with the structural change and cross-linking of protein, which affects the gelation formation and gelation properties. In this article, the process and mechanism of the improvement of gelation formation of myofibrillar proteins based on plant polyphenols in the normal-ion strength system, low-ion strength system, and oxidative system were reviewed, aiming to provide a novel insight into the improvement of gelation properties of gel-type meat products based on environmental-friendly methods. [ABSTRACT FROM AUTHOR]

Leptin is critically compromised in the major common forms of obesity. Skeletal muscle is the main effector tissue for energy modification that occurs as a result of the effect of endocrine axes, such as leptin signaling. Our study was carried out using skeletal muscle from a leptin-deficient animal model, in order to ascertain the importance of this hormone and to identify the major skeletal muscle mechanisms affected. We also examined the therapeutic role of melatonin against leptin-induced muscle wasting. Here, we report that leptin deficiency stimulates fatty acid β-oxidation, which results in mitochondrial uncoupling and the suppression of mitochondrial oxidative damage; however, it increases cytosolic oxidative damage. Thus, different nutrient-sensing pathways are disrupted, impairing proteostasis and promoting lipid anabolism, which induces myofiber degeneration and drives oxidative type I fiber conversion. Melatonin treatment plays a significant role in reducing cellular oxidative damage and regulating energy homeostasis and fuel utilization. Melatonin is able to improve both glucose and mitochondrial metabolism and partially restore proteostasis. Taken together, our study demonstrates melatonin to be a decisive mitochondrial function-fate regulator in skeletal muscle, with implications for resembling physiological energy requirements and targeting glycolytic type II fiber recovery. [ABSTRACT FROM AUTHOR]

Objective: This study tested the hypothesis that expression of insulin‐like growth factor 1 (IGF‐1) protein and mRNA splice variants is lower in skeletal muscle of humans with obesity who have a lower mixed‐muscle protein fractional synthesis rate (MMP‐FSR) when compared with individuals without obesity. Methods: The study included nine participants with obesity (OB, mean [SD], BMI = 35 [3] kg/m2, MMP‐FSR = 0.06%/h [0.02%/h]) and nine participants without obesity (W‐OB, BMI = 24 [3] kg/m2, MMP‐FSR = 0.08%/h [0.02%/h]; for both BMI and MMP‐FSR p < 0.05). MMP‐FSR and mitochondrial protein FSR were measured following an overnight fast. Results: Along with lower MMP‐FSR, OB participants displayed lower mitochondrial protein FSR (p = 0.03) compared with W‐OB participants. Expression of IGF‐1 (p = 0.04) and IGF‐1 receptor (p < 0.01) proteins was lower in muscle of OB participants. In addition, OB participants had lower (p < 0.05) mRNA expression of IGF1 variants Eb and Ec. This study demonstrates that lower protein synthesis in muscle of humans with obesity occurs concurrently with lower expression of muscle IGF‐1 and IGF‐1 receptor proteins, as well as lower mRNA expression of the IGF1 splice variants. Conclusions: These findings indicate that lower protein synthesis observed in muscle of humans with obesity may result from diminished muscle IGF1 gene expression. [ABSTRACT FROM AUTHOR]

Biopolymers derived from seafood processing byproducts are used to prepare active and biodegradable films as the packaging of food products. These films possess bioactivities to enhance the shelf life of packed foods by proactively releasing antimicrobial/antioxidative agents into the foods and providing sufficient barrier properties. Seafood processing byproducts are an eminent source of valuable compounds, including biopolymers and bioactive compounds. These biopolymers, including collagen, gelatin, chitosan, and muscle proteins, could be used to prepare robust and sustainable food packaging with some antimicrobial agents or antioxidants, for example, plant extracts rich in polyphenols or essential oils. These active packaging are not only biodegradable but also prevent the deterioration of packed foods caused by spoilage microorganisms as well as chemical deterioration. Seafood discards have a promising benefit for the development of environmentally friendly food packaging systems via the appropriate preparation methods or techniques. Therefore, the green packaging from seafood leftover can be better exploited and replace the synthetic counterpart. [ABSTRACT FROM AUTHOR]

Advances in scanning capillary microscopy (SCM) in studies of living objects have generated interest in this technique: over its 30 years of existence, more than 300 articles and numerous reviews describing the development of SCM have been published. The growth of dendrites and axons and the dynamics of actin in living cells have been visualized, changes in the volumes of nerve cells during migration have been measured, changes in the structure of the cell membrane during endocytosis of nanoparticles have been studied, the topography and stiffness of living fibroblasts have been assessed, and more. The uniqueness of the method lies not only in its provision of contactless three-dimensional visualization of living cells in their natural environment with nanometer spatial resolution, but also in the opportunity of using capillaries as sensors for reactive oxygen species, various neurotransmitters, and growth factors, as well as for assessing concentrations, etc., which opens up opportunities for addressing a variety of tasks in biomedicine. [ABSTRACT FROM AUTHOR]

The importance of various markers such as Sclerostin, Dickkopf-1 (DKK-1), Irisin, receptor activator of NF-kB ligand (RANKL), and Vitamin D have been well studied in bone metabolism. Additionally, inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and Interleukin 6 (IL-6) have been shown to hinder muscle protein synthesis, leading to the loss of muscle and strength. However, a research gap exists in understanding their role in muscle function and physical activity. Therefore, this study aims to explore the serum levels of Sclerostin, DKK-1, Irisin, IL-6, RANKL, Vitamin D, and TNF-α and assess their relationships with upper- and lower-body strength in young adults. In this study, 38 college-aged students (18–23 years), males and females, participated and completed the protocols. The participants' lower and upper body strength were assessed by the vertical jump test (Just Jump, Probotic, AL) with a Tendo FitroDyne (Tendo Sports Machines, Trencin, Slovak Republic) and handgrip (HG) dynamometry (Takei Scientific Instruments, Yashiroda, Japan), respectively. Fasting morning blood samples were analyzed for serum levels of biomarkers by ELISA. The results indicate significant sex differences in Sclerostin, DKK-1, Irisin, and Vitamin D levels (p < 0.05). Furthermore, a positive association was observed between Sclerostin, DKK-1, and Vitamin D, with lower body muscle performance variables (p < 0.05). Conversely, a significant negative correlation was observed between TNF-α and lower-body muscle performance variables (p < 0.05). The results suggest that these markers may have a distinct effect on muscle performance, underscoring the need for further investigation to elucidate the concept of muscle–bone crosstalk. [ABSTRACT FROM AUTHOR]

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Although several reports have hypothesized that exercise may increase skeletalmuscle protein lactylation, empirical evidence in humans is lacking. Thus, we adopted a multifaceted approach to examine if acute and subchronic resistance training (RT) altered skeletal muscle protein lactylation levels. Inmice, we also sought to examine if surgical ablation-induced plantaris hypertrophy coincided with increases in muscle protein lactylation. To examine acute responses, participants' blood lactate concentrations were assessed before, during, and after eight sets of an exhaustive lower body RT bout (n = 10 trained college-agedmen). Vastus lateralis biopsies were also taken before, 3-h post, and 6-h post-exercise to assess muscle protein lactylation. To identify training responses, another cohort of trained college-aged men (n = 14) partook in 6 weeks of lower-body RT (3x/week) and biopsies were obtained before and following the intervention. Five-month-old C57BL/6 mice were subjected to 10 days of plantaris overload (OV, n = 8) or served as age-matched sham surgery controls (Sham, n = 8). Although acute resistance training significantly increased blood lactate responses ~7.2-fold (p < 0.001), cytoplasmic and nuclear protein lactylation levels were not significantly altered at the post-exercise time points, and no putative lactylation-dependent mRNA was altered following exercise. Six weeks of RT did not alter cytoplasmic protein lactylation (p = 0.800) despite significantly increasing VLmuscle size (+3.5%, p=0.037), and again, no putative lactylation-dependent mRNA was significantly affected by training. Plantaris muscles were larger in OV versus Sham mice (+43.7%, p < 0.001). However, cytoplasmic protein lactylation was similar between groups (p = 0.369), and nuclear protein lactylation was significantly lower in OV versus Sham mice (p < 0.001). The current null findings, along with other recent null findings in the literature, challenge the thesis that lactate has an appreciable role in promoting skeletalmuscle hypertrophy. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate if home-based resistance training compared with centerbased resistance training was associated with better preservation of muscle mass and strength in older individuals, 6 months after the interventions ended. One hundred four healthy older individuals (>65 years) who had completed 1 year of either home-based lightintensity training with daily whey protein supplementation (LITW), center-based heavy resistance training with whey protein supplementation (HRTW), or daily whey protein supplementation alone (WHEY) returned for follow-up measurement 6 months after the interventions. Measures of muscle mass, strength, and power were assessed at the end of intervention as well as at follow-up. Furthermore, we compared changes in these parameters between subjects who continued resistance training (≥1 weekly training session) during follow-up (CONT) with those who stopped (STOP). Resistance training continuation during follow-up did not differ between HRTW and LITW (41 vs. 41%, P = 1.0) but was higher for both groups compared with WHEY (18%, P = 0.04-0.05). However, no between-group differences were observed between LITW/HRTW/WHEY in changes in muscle mass, strength, or power during follow-up. STOPwas associatedwith a poorer preservation of quadriceps cross-sectional area comparedwithCONT (-1.7 cm² [-0.4 to 23.0], P = 0.01, effect size: 0.79). No effect of training continuation was observed on changes in muscle strength and power. In conclusion,maintenance of muscle mass and strength is not superior after home-based resistance training comparedwith center-based training. However, training continuation seems crucial for the maintenance of muscle mass, irrespective of the training intervention. [ABSTRACT FROM AUTHOR]

Simple Summary: Control of tissue growth is an important component of cancer treatment, but understanding how to do this effectively is still in the early stages. Tissue growth typically involves both complex interacting signal transduction networks as well as mechanical interactions within and between cells, and how they interact to control growth is an open problem. Herein we begin the process of how to understand the interactions by focusing on tissue growth in the fruit fly Drosophila melanogaster. A model of the Hippo pathway, which is one of the primary growth-control pathways, is integrated with a description of the mechanical behavior of cells in wing-disc tissue to predict how mechanics and signaling interact, and a number of significant insights and predictions have emerged from the analysis of the model. Drosophila melanogaster has emerged as an ideal system for studying the networks that control tissue development and homeostasis and, given the similarity of the pathways involved, controlled and uncontrolled growth in mammalian systems. The signaling pathways used in patterning the Drosophila wing disc are well known and result in the emergence of interaction of these pathways with the Hippo signaling pathway, which plays a central role in controlling cell proliferation and apoptosis. Mechanical effects are another major factor in the control of growth, but far less is known about how they exert their control. Herein, we develop a mathematical model that integrates the mechanical interactions between cells, which occur via adherens and tight junctions, with the intracellular actin network and the Hippo pathway so as to better understand cell-autonomous and non-autonomous control of growth in response to mechanical forces. [ABSTRACT FROM AUTHOR]

Endurance exercise alters amino acid (AA) metabolism that necessitates greater AA intake in the post exercise recovery period to support recovery. Thus, daily AA ingestion during a period of endurance training may affect the metabolically active plasma free AA pool, which is otherwise maintained during periods of inadequate protein intake by the breakdown of skeletal muscle proteins. Nine endurance-trained males completed a 4-day running protocol (20 km, 5 km, 10 km and 20 km on days 1–4, respectively) on three occasions with a controlled diet providing different protein intakes [0.94(LOW), 1.20(MOD) or 1.83gprotein kgbody mass−1 day−1 (HIGH)]. Urine collected over 24 h on day-4 and plasma collected after an overnight fast on day-5 were analyzed for free AA (plasma) and 3-methylhistidine (3MH; plasma and urine), a marker of myofibrillar protein breakdown. There was an effect of protein intake (HIGH > MOD/LOW; P < 0.05) on fasted plasma essential AA, branched chain AA and 3MH but no effect on 24-h urinary 3-MH excretion. Consuming a previously determined optimal daily protein intake of 1.83 g kg−1 day−1 during endurance training maintains fasted plasma free AA and may attenuate myofibrillar protein catabolism, although this latter effect was not detected in 24-h urinary excretion. The maintenance of the metabolically active free plasma AA pool may support greater recovery from exercise and contribute to the previously determined greater whole-body net protein balance in this athletic population. TRN: NCT02801344 (June 15, 2016). [ABSTRACT FROM AUTHOR]

Non-venomous snakes commonly evolve natural resistance to venom to escape predators. Sinonatrix annularis serum has been shown to inhibit Deinagkistrodon acutus venom-induced hemorrhage and upregulation of serum CK, CK-MB, LDH, AST and ALT levels. Using TMT-labeled proteomics analysis, 168 proteins were found to be altered significantly in the envenomed gastrocnemius muscle and categorized into pathways such as complement and coagulation cascades, leukocyte transendothelial migration, and JAK/STAT signaling. These alterations were mitigated by S. annularis serum. Subsequently, a novel metalloproteinase inhibitor, SaMPI, was isolated from S. annularis serum by two-step chromatography. It showed strong antidotal effects against D. acutus envenomation, including inhibition of subcutaneous bleeding caused by crude venom and DaMP (a metalloproteinase derived from D. acutus) activity in a 1:1 ratio. Histology and immunoblotting analyses demonstrated that SaMPI mitigated myonecrosis, reduced neutrophil infiltration and local inflammatory factor release, and retarded JAK/STAT and MAPK signaling activation. Analysis of the SaMPI gene cloned by 5′-RACE revealed a shared sequence identity of 58–79% with other SVMP inhibitors. These findings demonstrate the protective effects of SaMPI and indicate its potential value as a candidate for viper bite adjuvant therapy. [Display omitted] • Snake envenomation ug-regulated 154 proteins in gastrocnemius muscle of mice. • Snake venom metalloproteinase activates IFN-JAK/STAT signaling pathway. • A novel metalloproteinase inhibitor, SaMPI, was isolated from snake S. annularis. • SaMPI mitigated envenoming symptoms evoked by D.acutus venom. [ABSTRACT FROM AUTHOR]