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There is a growing body of evidencethat indicates that the aging of the brain results from the decline of energy metabolism. In particular, the neuronal metabolism of glucose declines steadily, resulting in a growing deficit of adenosine triphosphate (ATP) production-which, in turn, limits glucose access. This vicious circle of energy metabolism at the cellular level is evoked by a rising deficiency of nicotinamide adenine dinucleotide (NAD) in the mitochondrial salvage pathway and subsequent impairment of the Krebs cycle. A decreasing NAD level also impoverishes the activity of NAD-dependent enzymes that augments genetic errors and initiate processes of neuronal degeneration and death.This sequence of events is characteristic of several brain structures in which neurons have the highest energy metabolism. Neurons of the cerebral cortex and basal ganglia with long unmyelinated axons and these with numerous synaptic junctions are particularly prone to senescence and neurodegeneration. Unfortunately, functional deficits of neurodegeneration are initially well-compensated, therefore, clinical symptoms are recognized too late when the damages to the brain structures are already irreversible. Therefore, future treatment strategies in neurodegenerative disorders should focus on energy metabolism and compensation age-related NAD deficit in neurons. This review summarizes the complex interrelationships between metabolic processes on the systemic and cellular levels and provides directions on how to reduce the risk of neurodegeneration and protect the elderly against neurodegenerative diseases.Mesenchymal stem cells (MSCs) are multipotent stem cells that can be isolated from various tissues in the adult body. MSCs should be characterized by three criteria for regenerative medicine. MSCs must (1) adhere to plastic surfaces, (2) express specific surface antigens, and (3) differentiate into mesodermal lineages, including chondrocytes, osteoblasts, and adipocytes, in vitro. Interestingly, MSCs have immunomodulatory features and secrete trophic factors and immune receptors that regulate the microenvironment in host tissue. These specific and unique therapeutic properties make MSCs ideal as therapeutic agents in vivo. Specifically, pre-clinical and clinical investigators generated inflammatory and fibrotic diseases models, and then transplantation of MSCs into diseases models for therapeutic effects investigation. In this review, we characterize MSCs from various tissues and describe their applications for treating various inflammation and fibrotic diseases.In this study, structural characterization, electrical properties and energy storage performance of plasticized polymer electrolytes based on polyvinyl alcohol/methylcellulose/ammonium thiocyanate (PVA/MC-NH4SCN) were carried out. An X-ray diffraction (XRD) study displayed that the plasticized electrolyte system with the uppermost value of direct current (DC) ionic conductivity was the most amorphous system. The electrolyte in the present work realized an ionic conductivity of 2.903 × 10-3 Scm-1 at room temperature. The main charge carrier in the electrolyte was found to be the ions with the ionic transference number (tion) of 0.912, compared to only 0.088 for the electronic transference number (telec). The electrochemical stability potential window of the electrolyte is 2.1 V. The specific capacitance was found to reduce from 102.88 F/g to 28.58 F/g as the scan rate increased in cyclic voltammetry (CV) analysis. The fabricated electrochemical double layer capacitor (EDLC) was stable up to 200 cycles with high efficiency. The specific capacitance obtained for the EDLC by using charge-discharge analysis was 132.7 F/g at the first cycle, which is slightly higher compared to the CV plot. The equivalent series resistance (ESR) increased from 58 to 171 Ω throughout the cycles, which indicates a good electrolyte/electrode contact. Ions in the electrolyte were considered to have almost the same amount of energy during the conduction process as the energy density is approximately at 14.0 Wh/kg throughout the 200 cycles. The power density is stabilized at the range of 1444.3 to 467.6 W/kg as the EDLC completed the cycles.This study evaluated the impact of fermented milk maceration on fermented lamb loin without nitrate to obtain peptides with high activity against oxidative changes (ABTS, DPPH, reducing power) as well as a favorable fatty acid profile, including CLA content. Additionally, an attempt was made to evaluate the influence of the lamb breed on the assessed properties. Raw loins (m. selleck inhibitor Longissimus dorsi) obtained from sheep of three polish breeds-Wrzosówka, Uhruska, and Świniarka-and fermented products were tested. The fermented loins obtained after 14 days of processing were characterized by pH and water activity values in the ranges, respectively, 4.76-5.12 and 0.902-0.915. The maceration of meat in a fermented milk has caused greater acidification of the meat during fermentation. Statistical analysis indicated that treatment was the factor with significant effect on peptide content; no effect of animal breed was found. The peptide content isolated from raw meat ranged from 2.90 to 4.31 mg g-1 of sample, while in fermented meat products it was significant higher (11.59-16.37 mg g-1 of product). The antioxidant properties of peptides were positively correlated with peptides content. The maceration in fermented milk resulted in a statistically significant increase of ABTS value in case of fermented lamb loin of Świniarka breed. The raw meat and fermented meat products form the Świniarka lamb breed were characterized by the highest content of the total CLA isomers. The main CLA isomer found was cis9-trans11 (rumenic acid), followed by cis9-cis11, trans9-trans11, and trans10-cis12. The rumenic acid content was higher than, respectively, 87% and 80-88% of total CLA isomers in case of raw meat and fermented lamb loins of three breeds.Lumpy skin disease is an important economic disease of cattle that is controlled by vaccination. This paper presents an investigation into the role of the lumpy skin disease virus (LSDV) superoxide dismutase (SOD) homologue on growth and histopathology of the virus both in vitro and in vivo. SOD homologue knock-out and knock-in recombinants (nLSDV∆SOD-UCT and nLSDVSODis-UCT, respectively) were constructed and compared to the Neethling vaccine (nLSDV) for growth in a permissive bovine cell line as well as on fertilized chick chorioallantoic membranes (CAMs). The infected CAMs were scored for histological changes. Deletion of the SOD homologue from LSDV reduced virus growth both in Madin-Darby bovine kidney (MDBK) cells as well as on CAMs. Furthermore, the knockout virus showed reduced inflammation in CAMs and more ballooning degeneration. A pilot experiment was performed in cattle to compare the lesions produced by the different LSDV constructs in the same animal. One animal developed a larger lesion to nLSDV∆SOD-UCT compared to both nLSDVSODis-UCT and nLSDV.
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