Odgaardphelps5031

So far, surface electromyography (sEMG) has been the method of choice to detect and evaluate muscle fatigue. However, recent advancements in non-cryogenic quantum sensors, such as optically pumped magnetometers (OPMs), enable interesting possibilities to flexibly record biomagnetic signals. Yet, a magnetomyographic investigation of muscular fatigue is still missing. Here, we simultaneously used sEMG (4 surface electrode) and OPM-based magnetomyography (OPM-MMG, 4 sensors) to detect muscle fatigue during a 3 × 1-min isometric contractions of the left rectus femoris muscle in 7 healthy participants. Both signals exhibited the characteristic spectral compression distinctive for muscle fatigue. OPM-MMG and sEMG slope values, used to quantify the spectral compression of the signals, were positively correlated, displaying similarity between the techniques. Additionally, the analysis of the different components of the magnetic field vector enabled speculations regarding the propagation of the muscle action potentials (MAPs). Altogether these results show the feasibility of the magnetomyographic approach with OPMs and propose a potential alternative to sEMG for the study of muscle fatigue.Background/Aims It is widely known that the imbalance between reactive oxygen species (ROS)/antioxidants and mitochondrial function could play a pivotal role in aging and in the physiopathology of viral infections. Here, we correlated the plasma oxidants/antioxidants levels of the elderly admitted to a long-term care (LTC) unit with clinical data in relation to flu-like disease/COVID-19. Moreover, in vitro we examined the effects of plasma on cell viability, ROS release and mitochondrial function. Materials and Methods In 60 patients admitted to LTC unit for at least 1 year at moderate or high care load, demographic and clinical variables were taken. Blood samples were collected for the evaluations of oxidants/antioxidants, as thiobarbituric acid reactive substances, 8-hydroxy-2-deoxyguanosine, 8-isoprostanes, superoxide dismutase activity, glutathione, and vitamin D. In vitro, human umbilical vascular endothelial cells (HUVEC) were used to examine the effects of plasma on viability, ROS release and mitochondrial membrane potential. Results The results obtained showed that the redox state of the elderly was quite balanced; mitochondrial membrane potential of HUVEC was reduced by about 20%, only. Also, the correlation analysis evidenced the association between mitochondrial function and the patients' outcomes. Interestingly, lower levels of mitochondrial membrane potential were found in the elderly who had symptoms suggestive of COVID-19 or with a confirmed diagnosis of COVID-19. Conclusion The results of this study highlight the importance of mitochondrial function in the tendency to get a flu-like syndrome like COVID-19 in the elderly admitted to LTC unit. This information could have clinical implications for the management of old population.The stellate ganglion (SG) of the autonomic nervous system plays important role in cardiovascular diseases (CDs). Myocardial infarction (MI) is associated with sustained increasing cardiac sympathetic nerve activity. Expressions and functions of proteins in SG tissue after MI are remaining unclear. This study is to explore the expression characteristics of proteins in SGs associated with MI. Japanese big-ear white rabbits (n = 22) were randomly assigned to the control group and MI group. The MI model was established by left anterior descending coronary artery ligation and confirmed by serum myocardial enzymes increasing 2,3,5-triphenyltetrazolium (TTC) staining and echocardiography. The expressions of proteins in rabbit SGs after MI were detected using tandem mass tags (TMT) quantitative proteomic sequencing. There were 3,043 credible proteins were predicted in rabbit SG tissues and 383 differentially expressed proteins (DEPs) including 143 upregulated and 240 downregulated proteins. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the DEPs involved in adrenergic signaling in cardiomyocytes, positive regulation of ERK1 and ERK2 cascade, and other biological processes. Three kinds of proteins directly correlated to CDs were selected to be validated by the subsequent western blot experiment. This study first identified the characterization of proteins in rabbit SG after MI, which laid a solid foundation for revealing the mechanism of roles of SG on the MI process.Anticipation is the act of using information about the past and present to make predictions about future scenarios. As a concept, it is predominantly associated with the psychology of the human mind; however, there is accumulating evidence that diverse taxa without complex neural systems, and even biochemical networks themselves, can respond to perceived future conditions. Although anticipatory processes, such as circadian rhythms, stress priming, and cephalic responses, have been extensively studied over the last three centuries, newer research on anticipatory genetic networks in microbial species shows that anticipatory processes are widespread, evolutionarily old, and not simply reserved for neurological complex organisms. Overall, data suggest that anticipatory responses represent a unique type of biological processes that can be distinguished based on their organizational properties and mechanisms. Unfortunately, an empirically based biologically explicit framework for describing anticipatory processes does not currently exist. This review attempts to fill this void by discussing the existing examples of anticipatory processes in non-cognitive organisms, providing potential criteria for defining anticipatory processes, as well as their putative mechanisms, and drawing attention to the often-overlooked role of anticipation in the evolution of physiological systems. Ultimately, a case is made for incorporating an anticipatory framework into the existing physiological paradigm to advance our understanding of complex biological processes.[This corrects the article DOI 10.3389/fphar.2021.757666.].[This corrects the article DOI 10.3389/fphar.2021.758792.].Liver kinase B1 (LKB1) is known to shape the regulation of macrophage function by participating in multiple processes including cell metabolism, growth, and polarization. However, whether LKB1 also affects the functional plasticity of macrophages in atherosclerosis has not attracted much attention. Abnormal macrophage function is a pathophysiological hallmark of atherosclerosis, characterized by the formation of foam cells and the maintenance of vascular inflammation. Mounting evidence supports that LKB1 plays a vital role in the regulation of macrophage function in atherosclerosis, including affecting lipid metabolism reprogramming, inflammation, endoplasmic reticulum stress, and autophagy in macrophages. Thus, decreased expression of LKB1 in atherosclerosis aggravates vascular injury by inducing excessive lipid deposition in macrophages and the formation of foam cells. To systematically understand the role and potential mechanism of LKB1 in regulating macrophage functions in atherosclerosis, this review summarizes the relevant data in this regard, hoping to provide new ideas for the prevention and treatment of atherosclerosis.[This corrects the article DOI 10.3389/fphar.2021.753727.].Malignant mesothelioma (MMe) is a rare neoplasm with few therapeutic options available. The landscape of effective therapy for this disease remained unchanged in the last two decades. Recently, however, the introduction of Immune Checkpoint Inhibitors (ICIs) led to small, but nevertheless, promising improvements. However, many efforts are still needed to radically improve the prognosis of MMe. In this review, we analyze all those therapeutic strategies for MMe that are still in a preclinical or early clinical phase of development. In particular, we focus on novel antiangiogenic drugs and their possible combination with immunotherapy. Furthermore, we describe also more complex strategies such as microRNA-loaded vectors, oncolytic viruses, and engineered lymphocytes.Cervical cancer is one of the most common malignant tumors among women in the world. In clinical practice, Hedyotis diffusa has pharmacological effects in treating cervical cancer, but its components are relatively complex, and the mechanism of Hedyotis diffusa in treating cervical cancer is still unclear. In this work, the potential active components and mechanism of Hedyotis diffusa in the treatment of cervical cancer were explored by means of network pharmacology. By constructing its active ingredient-target network, and enriching and analyzing the targets, we found the key targets and their effective components (beta-Sitosterol and Quercetin) that play a therapeutic role. Finally, we evaluated the prognostic value of the core target genes through survival analysis. Our work initially explored the therapeutic mechanism of cervical cancer, which lays a theoretical foundation for further exploring its pharmacological action and its clinical application.Obesity is a life-threatening metabolic disorder necessitating urgent development of safe and effective therapy. Currently, limited such therapeutic measures are available for obesity. The present study was designed to develop a novel, safe and effective herbal therapy for the management of obesity. A polyherbal formulation (18KHT01) was developed by homogeneously mixing a specific proportion of crude Quercus acutissima (acorn jelly powder), Camellia sinensis (dry leaf buds), and Geranium thunbergii (dry aerial part) along with Citrus limon (fruit juice). Synergistic antioxidant, antiadipogenic, and anti-obesity activities were evaluated by in vitro as well as in vivo studies. In vitro experiments revealed strong synergistic antioxidant and anti-adipogenic activities of 18KHT01. Molecular assessment of 18KHT01 showed significant down-regulation of vital adipogenic factors such as PPARγ, C/EBPα, aP2, SREBP-1c, FAS, and LPL. Based on the results of the preliminary toxicity study, 75 and 150 mg/kg, twice daily doses of 18KHT01 were administered to evaluate anti-obesity activity in diet-induced obese (DIO) C57BL/6J mice model. The major obesity-related parameters such as body weight, weight gain, food efficiency ratio, as well as serum lipid profile were significantly reduced by 18KHT01 with potential synergism. Also, the high-fat diet-induced insulin resistance was suggestively alleviated by the formulation, and thus ameliorated fasting blood glucose. Histological evaluation of liver and white adipose tissue revealed that the significant reduction of fat depositions and thus reduction of these tissue weights. Synergy evaluation experiments exhibited that the 18KHT01 offered strong synergism by improving efficacy and reducing the toxicity of its ingredients. Overall results evidenced the 18KHT01 as a safe and potent anti-obesity herbal therapy.Presently, there is a lack of effective disease-modifying drugs for the treatment of Alzheimer's disease (AD). Uncaria rhynchophylla (UR) and its predominant active phytochemicals alkaloids have been studied to treat AD. This study used a novel network pharmacology strategy to identify UR alkaloids against AD from the perspective of AD pathophysiological processes and identified the key alkaloids for specific pathological process. The analysis identified 10 alkaloids from UR based on high-performance liquid chromatography (HPLC) that corresponded to 127 targets correlated with amyloid-β (Aβ) pathology, tau pathology and Alzheimer disease pathway. Based on the number of targets correlated with AD pathophysiological processes, angustoline, angustidine, corynoxine and isocorynoxeine are highly likely to become key phytochemicals in AD treatment. Among the 127 targets, JUN, STAT3, MAPK3, CCND1, MMP2, MAPK8, GSK3B, JAK3, LCK, CCR5, CDK5 and GRIN2B were identified as core targets. Based on the pathological process of AD, angustoline, angustidine and isocorynoxeine were identified as the key UR alkaloids regulating Aβ production and corynoxine, isocorynoxeine, dihydrocorynatheine, isorhynchophylline and hirsutine were identified as key alkaloids that regulate tau phosphorylation.