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Background and Objective: Emerging evidence has uncovered that long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) exert biofunctions on cellular mineralization and bone formation. In this study, we aimed to identify lncRNA–mRNA expression profiles and expression patterns, and explore their underlying biofunctions during cementoblast mineralization. Materials and Methods: Cementoblasts were cultured in mineralized medium for 0, 7, and 14 days. We used quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blot (WB) to detect expression levels of osteocalcin (OCN), bone sialoprotein (BSP), and Osterix (Osx). Alkaline phosphatase (ALP) staining and alizarin red staining (ARS) were conducted to detect ALP activity and number of mineralized nodule. Total RNA was extracted from cells and used for high‐throughput sequencing. EBSeq package was applied to analyze differentially expressed genes. Mfuzz R package was used to identify gene expression patterns. The weighted gene co‐expression network analysis (WGCNA) was performed to explore co‐expressed mRNAs of differentially expressed lncRNAs (DElncRNAs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were adopted by Clusterprofile R package. Results: Cementoblasts were successfully induced by osteogenic medium. Compared with those on day 0, 384 DElncRNAs and 4255 differentially expressed mRNAs (DEmRNAs), respectively, were found on day 7. Meanwhile, 645 DElncRNAs and 4717 DEmRNAs were detected on day 14. Both DElncRNAs and DEmRNAs were classified into six clusters with different expression patterns. DEmRNAs and co‐expressed mRNA of DElncRNAs were predominantly related to cell process, binding, phosphatidylinositol‐3 kinase (PI3K)‐Akt signaling pathway, hypoxia‐inducible factor‐1 (HIF‐1) signaling pathway, mitogen‐activated protein kinase (MAPK) signaling pathway, and hippo signaling pathway. Conclusion: The results demonstrated that both noncoding and coding RNAs were involved in the process of mineralization in cementoblasts, which may provide a new database for further study. [ABSTRACT FROM AUTHOR]

Hypoxia often occurs in inflammatory tissues, such as tissues affected by periodontitis and apical periodontitis lesions. Mitochondrial biogenesis can be disrupted in hypoxia. Peroxisome proliferator‐activated receptor gamma coactivator‐1 alpha (PGC‐1α) is a core factor required for mitochondrial biogenesis. Cementoblasts are root surface lining cells that play an integral role in cementum formation. There is a dearth of research on the effect of hypoxia on cementoblasts and underlying mechanisms, particularly in relation to mitochondrial biogenesis during the hypoxic process. In this study, we found that the expression of hypoxia inducible factor‐1α was elevated in apical periodontitis tissues in vivo. In contrast, periapical lesions exhibited a reduction of PGC‐1α expression. For in vitro experiments, cobalt chloride (CoCl2) was used to induce hypoxia. We observed that CoCl2‐induced hypoxia suppressed the mineralization ability and mitochondrial biogenesis of cementoblasts, accompanied by abnormal mitochondria morphology. Furthermore, we found that CoCl2 blocked the p38 pathway, while it activated the Erk1/2 pathway, with the former upregulating the expression of PGC‐1α, while the latter reversed the effects. Overall, our findings demonstrate that mitochondrial biogenesis, especially via PGC‐1α, is impaired during cementogenesis in the context of CoCl2‐induced hypoxia, dependent on the mitogen‐activated protein kinase signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Catch‐up fat in adults (CUFA) caused by rapid nutrition promotion after undernutrition plays an important role in the epidemic of insulin resistance (IR)‐related diseases in developing societies. Insulin resistance is considered to be closely associated with reduced testosterone levels and cognitive function. However, the effects of CUFA on testosterone levels and cognitive function are unclear in males. Objectives: To investigate the changes in testosterone levels and cognitive function in CUFA in male humans and rats, and explore their probable relationship and mechanisms in rats. Materials and methods: The blood testosterone levels, fasting glucose, and blood insulin (FINS) were measured in subpopulation 1 (27 CUFA individuals, 61 controls without CUFA) aged 40–50 years to show the characteristics of sex hormone levels and the metabolic status in CUFA men. Cognitive Flexibility Inventory was conducted in subpopulation 2 (54 CUFA individuals, 214 controls) over 20 years to investigate the associations between sex hormone levels, cognitive function, and CUFA. Male rats (n = 27) were randomly allocated to the NC group (normal chow controls), RN group (CUFA, refeeding after caloric restriction), and RT group (RN with testosterone intramuscular injected while refeeding). The blood testosterone levels, intraperitoneal insulin tolerance test (IPITT), and FINS were measured, and the attentional set‐shifting task test (ASST) for the assessment of cognitive function was performed in these animals. Insulin signaling pathway, N‐methyl‐d‐aspartate receptors subtype 2A (NR2A) and 2B (NR2B) expression levels were determined in the rat cerebral cortex. Results: The total testosterone levels decreased (medium [inter‐quartile ranges], 13.43 [9.87–18.96] vs. 15.58 [13.37–24.96], p = 0.036), and HOMA‐IR (Homeostatic Model Assessment for Insulin Resistance) elevated (1.61 [1.08–2.33] vs. 1.24 [0.87–1.87], P = 0.037) in CUFA men in subpopulation 1. Additionally, cognitive impairment was observed in CUFA men in subpopulation 2. Moreover, our results indicated decreases in total and free testosterone levels, elevations in visceral lipid accumulation, FINS, HOMA‐IR, blood glucose, and the area under the curve after IPITT, increases in the number of trials required to achieve the criterion of the first reversal of discrimination (R1) in ASST, and downregulation of IRS‐1 mRNA expression, AKT phosphorylation, and the NR2A and NR2B expression in brain tissue in male CUFA rats. Notably, testosterone supplementation improved visceral lipid accumulation and IR‐related metabolic disorders, cognitive dysfunction, decreases in IRS‐1 mRNA expression, Akt phosphorylation, and NR2A and NR2B expression in brain tissue in male CUFA rodents. Discussion and Conclusion: CUFA was characterized by reduced testosterone levels, metabolic abnormalities, and cognitive dysfunction in males, and testosterone supplementation attenuated these changes, as well as the alteration in insulin signaling and NR2A and NR2B expression in male CUFA rodents. Herein, we tentatively put forward that CUFA in males induces low testosterone, consequently promoting metabolic abnormalities and cognitive impairment probably mediated by defects in insulin signaling and NR2A, NR2B pathway in brain tissue. [ABSTRACT FROM AUTHOR]

Summary: This paper presents a robust neural network–based control scheme to deal with the problem of tracking and stabilization simultaneously for a wheeled mobile robot subject to parametric uncertainties, external disturbances, and input saturation. At first, a new error‐state transformation scheme is designed by introducing some auxiliary variables as an additional virtual control signals to reduce the adverse effect caused by the underactuation. These variables can change their structures for different desired trajectories to be tracked. Then, a robust control law is proposed combining with a kinematic controller and a dynamic controller, while a three‐layer neural network system is applied to approximate model uncertainties. Stability analysis via the Lyapunov theory shows that the proposed controller can make tracking errors converge to bounded neighborhoods of the origin. Finally, some simulation results are illustrated to verify the effectiveness of the proposed control strategy. [ABSTRACT FROM AUTHOR]

The article presents the case -control study focused on obesity and cardiovascular risk. It mentions that Asia is a threat of metabolic disorders related to increased cardiovascular risk. It mentions that the consumption increment of fat in China as in North America. It mentions that the epidemic of metabolic disorders in Asia is related to the process from undernutrition.