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Parkinson's disease (PD) is one of the most widespread neurodegenerative diseases. PD is associated with progressive loss of substantia nigra dopaminergic neurons, including various motor symptoms (e.g., bradykinesia, rigidity, and resting tremor), as well as non-motor symptoms (e.g., cognitive impairment, constipation, fatigue, sleep disturbance, and depression). PD involves multiple biological processes, including mitochondrial or lysosomal dysfunction, oxidative stress, insulin resistance, and neuroinflammation. Metabolic syndrome (MetS), a collection of numerous connected cerebral cardiovascular conditions, is a common and growing public health problem associated with many chronic diseases worldwide. MetS components include central/abdominal obesity, systemic hypertension, diabetes, and atherogenic dyslipidemia. MetS and PD share multiple pathophysiological processes, including insulin resistance, oxidative stress, and chronic inflammation. In recent years, MetS has been linked to an increased risk of PD, according to studies; however, the specific mechanism remains unclear. Researchers also found that some related metabolic therapies are potential therapeutic strategies to prevent and improve PD. This article reviews the epidemiological relationship between components of MetS and the risk of PD and discusses the potentially relevant mechanisms and recent progress of MetS as a risk factor for PD. Furthermore, we conclude that MetS-related therapies are beneficial for the prevention and treatment of PD. [ABSTRACT FROM AUTHOR]

A multi-case study approach was used in this study to investigate how parents and children collaborated with each other when they learned to program in MSWLogo together. Three parent-child pairs were observed directly in a five-day computer camp. Each pair was assigned a total of 33 programming tasks to work on. The observation focused on how parents interacted with their children while they tried to solve the tasks together. Findings from this study indicated that, despite different patterns of interactions exhibited in the three pairs, parent-child collaboration in programming naturally fell into a special form of "pair programming" in which the parent and the child in each pair took the roles of "the reviewer" and "the driver" respectively. As such, children wrote programs in a more systematic and disciplined manner instead of resorting to trial-and-error and tinkering; children spent more time on analysis and design which were considered essential to successful problem solving; the programs they produced were more compact, well-structured, and contained fewer errors. Moreover, children tended to reflect on their solutions more often than if they learned alone. The interviews conducted after the camp revealed that the participating parents and children alike found great pleasure in learning to program collaboratively. In addition, the parents felt that the collaboration enabled them to gain a better understanding of their children and develop a closer parent-child relationship. (Contains 5 tables and 1 figure.)

The problems of parallel two-sided assembly lines balancing (TALB) are nonpolynomial (NP-hard) problems that belong to the field of combinatorial optimization. In most cases, these problems can be resolved with algorithms. To this end, this research adopts colored Petri nets (CPN) and a minimal spanning tree (MST) to address the type I problems for two-sided assembly line balancing problem (TALBP). This research proposes a three-step method. In the first step, a reachability tree chart is built to show potential tasks order assignment. In the second step, the color firing mechanism is employed to determine if the colored conditions are satisfied. The final step uses a MST and a least-time prioritized rule to select the proper tasks for assignment efficiently. These steps will be performed repetitively until all the tasks are properly assigned. Since the whole assignment process is based on graphical and paradigm methods, it can be adopted to lessen the burdens of complex calculations. The end of the research will present the comparison results between the examples from the literature and the method proposed in this research. As indicated by the research findings, employing CPN and an MST for TALBPs (type-I) can obtain even favorable and consistent results over legacy methods, and further optimize workstation design and enhance balance efficiency. [ABSTRACT FROM AUTHOR]

The nutritional level of vitamin D may affect musculoskeletal health. We have reported that vitamin D is a pivotal protector against tissue injuries by suppressing local renin‐angiotensin system (RAS). This study aimed to explore the role of the vitamin D receptor (VDR) in the protection against muscle atrophy and the underlying mechanism. A cross‐sectional study on participants (n = 1034) in Shanghai (China) was performed to analyze the association between vitamin D level and the risk of low muscle strength as well as to detect the circulating level of angiotensin II (Ang II). In animal studies, dexamethasone (Dex) was applied to induce muscle atrophy in wild‐type (WT) and VDR‐null mice, and the mice with the induction of muscle atrophy were treated with calcitriol for 10 days. The skeletal muscle cell line C2C12 and the muscle satellite cells were applied in in vitro studies. The increased risk of low muscle strength was correlated to a lower level of vitamin D (adjusted odds ratio [OR] 0.58) accompanied by an elevation in serum Ang II level. Ang II impaired the myogenic differentiation of C2C12 myoblasts as illustrated by the decrease in the area of myotubes and the downregulation of myogenic factors (myosin heavy chain [MHC] and myogenic differentiation factor D [MyoD]). The phenotype of muscle atrophy induced by Dex and Ang II was aggravated by VDR ablation in mice and in muscle satellite cells, respectively, and mediated by RAS and its downstream phosphatidylinositol 3‐kinase/protein kinase B/forkhead box O1 (PI3K/Akt/FOXO1) signaling. Calcitriol treatment exhibited beneficial effects on muscle function as demonstrated by the increased weight‐loaded swimming time, grip strength, and fiber area, and improved fiber type composition via regulating ubiquitin ligases and their substrates MHC and MyoD through suppressing renin/Ang II axis. Taken together, VDR protects against skeletal muscle atrophy by suppressing RAS. Vitamin D could be a potential agent for the prevention and treatment of skeletal muscle atrophy. © 2021 American Society for Bone and Mineral Research (ASBMR). [ABSTRACT FROM AUTHOR]