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Background. Mesenchymal stem cells (MSCs) differentiate into osteocytes, adipocytes, and chondrocytes. Resveratrol and bone morphogenetic protein 9 (BMP9) are known osteogenic induction factors of MSCs, but the effect of both resveratrol and BMP9 on osteogenesis is unknown. Herein, we explored whether resveratrol cooperates with BMP9 to improve osteogenic induction. Methods. The osteogenic induction of resveratrol and BMP9 on C3H10T1/2 cells was evaluated by detecting the staining and activity of the early osteogenic marker alkaline phosphatase (ALP). In addition, the late osteogenic effect was measured by the mRNA and protein levels of osteogenic markers, such as osteopontin (OPN) and osteocalcin (OCN). To assess the bone formation function of resveratrol plus BMP9 in vivo, we transplanted BMP9-infected C3H10T1/2 cells into nude mice followed by intragastric injection of resveratrol. Western blot (WB) analysis was utilized to elucidate the mechanism of resveratrol plus BMP9. Results. Resveratrol not only enhanced osteogenic induction alone but also improved BMP9-induced ALP at 3, 5, and 7 d postinduction. Both the early osteogenic markers (ALP, Runx2, and SP7) and the late osteogenic markers (OPN and OCN) were significantly increased when resveratrol was combined with BMP9. The fetal limb explant culture further verified these results. The in vivo bone formation experiment, which involved transplanting BMP9-overexpressing C3H10T1/2 cells into nude mice, also confirmed that resveratrol synergistically enhanced the BMP9-induced bone formation function. Resveratrol phosphorylated adenosine monophosphate- (AMP-) activated protein kinase (AMPK) and stimulated autophagy, but these effects were abolished by inhibiting AMPK and Beclin1 using an inhibitor or siRNA. Conclusions. Resveratrol combined with BMP9 significantly improves the osteogenic induction of C3H10T1/2 cells by activating AMPK and autophagy. [ABSTRACT FROM AUTHOR]

This study proposes a green, low-cost, and robust method to synthesize spherical calcium hydroxide (CH) nanoparticles based on the co-precipitation of Ca2+ and OH− in the presence of tannic acid (TA), an inexpensive plant-derived polyphenol. It has been found that the morphology and crystalline phase of the produced CH nanoparticles can be controlled by TA. With the increasing dosage of TA, the crystallinity of the CH particles reduces, changing from well crystallization to amorphous phases. Experimental evidence suggests that complexion reaction took place between TA and Ca2+, which gave the Ca2+ a strong bond effect. As a result, the nucleation and growth of CH were significantly affected. CH nanoparticles with sizes of about 50 nm have been successfully synthesized by using 0.3% or more TA. [ABSTRACT FROM AUTHOR]

Oxidative stress induces bone loss and osteoporosis, and epigallocatechin-3-gallate (EGCG) may be used to combat these diseases due to its antioxidative property. Herein, oxidative stress in human bone marrow-derived mesenchymal stem cells (BM-MSCs) was induced by H2O2, resulting in an adverse effect on their osteogenic differentiation. However, this H2O2-induced adverse effect was nullified when the cells were treated with EGCG. In addition, treatment of BM-MSCs with EGCG alone also resulted in the enhancement of osteogenic differentiation of BM-MSCs. After EGCG treatment, expressions of β-catenin and cyclin D1 were upregulated, suggesting that the Wnt pathway was involved in the effects of EGCG on the osteogenic differentiation of BM-MSCs. This was also confirmed by the fact that the Wnt pathway inhibitor, Dickkopf-1 (DKK-1), can nullify the EGCG-induced enhancement effect on BM-MSC’s osteogenic differentiation. Hence, our results suggested that EGCG can reduce the effects of oxidative stress on Wnt pathway in osteogenic cells, which supported a potentially promising therapy of bone disorders induced by oxidative stress. Considering its positive effects on BM-MSCs, EGCG may also be beneficial for stem cell-based bone repair. [ABSTRACT FROM AUTHOR]

Oxidative stress induces bone loss and osteoporosis, and epigallocatechin-3-gallate (EGCG) may be used to combat these diseases due to its antioxidative property. Herein, oxidative stress in human bone marrow-derived mesenchymal stem cells (BM-MSCs) was induced by H2O2, resulting in an adverse effect on their osteogenic differentiation. However, this H2O2-induced adverse effect was nullified when the cells were treated with EGCG. In addition, treatment of BM-MSCs with EGCG alone also resulted in the enhancement of osteogenic differentiation of BM-MSCs. After EGCG treatment, expressions of β-catenin and cyclin D1 were upregulated, suggesting that the Wnt pathway was involved in the effects of EGCG on the osteogenic differentiation of BM-MSCs. This was also confirmed by the fact that the Wnt pathway inhibitor, Dickkopf-1 (DKK-1), can nullify the EGCG-induced enhancement effect on BM-MSC’s osteogenic differentiation. Hence, our results suggested that EGCG can reduce the effects of oxidative stress on Wnt pathway in osteogenic cells, which supported a potentially promising therapy of bone disorders induced by oxidative stress. Considering its positive effects on BM-MSCs, EGCG may also be beneficial for stem cell-based bone repair. [ABSTRACT FROM AUTHOR]

Explicit finite element programme LS-DYNA was used to simulate a long-span steel reticulated shell under blast loading to investigate the structural dynamic responses in this paper. The elaborate finite element model of the Kiewitt-8 single-layer reticulated shell with span of 40 m subjected to central blast loading was established and all the process from the detonation of the explosive charge to the demolition, including the propagation of the blast wave and its interaction with structure was reproduced. The peak overpressure from the numerical analysis was compared with empirical formulas to verify the credibility and applicability of numerical simulation for blast loading. The dynamic responses of the structure under blast loading with different TNT equivalent weights of explosive and rise-span ratios were obtained. In addition, the response types of Kiewitt-8 single-layer reticulated shell subjected to central explosive blast loading were defined. [ABSTRACT FROM AUTHOR]

Myofascial trigger point (MTrP), an iconic characteristic of myofascial pain syndrome (MPS), can induce cerebral cortex changes including altered cortical excitability and connectivity. The corresponding characteristically reactive cortex is still ambiguous. Seventeen participants with latent MTrPs underwent functional near-infrared spectroscopy (fNIRS) to collect cerebral oxygenation hemoglobin (Δ[oxy-Hb]) signals. The Δ[oxy-Hb] signals of the left/right prefrontal cortex (L/R PFC), left/right motor cortex (L/R MC), and left/right occipital lobe (L/R OL) of the subjects were measured using functional near-infrared spectroscopy (fNIRS) in the resting state, nonmyofascial trigger point (NMTrP), state and MTrP state. The data investigated the latent MTrP-induced changes in brain activity and effective connectivity (EC) within the nonsensory cortex. The parameter wavelet amplitude (WA) was used to describe cortical activation, EC to show brain network connectivity, and main coupling direction (mCD) to exhibit the dominant connectivity direction in different frequency bands. An increasing trend of WA and a decreasing trend of EC values were observed in the PFC. The interregional mCD was primarily shifted from a unidirectional to bidirectional connection, especially from PFC to MC or OL, when responding to manual stimulation during the MTrP state compared with resting state and NMTrP state in the intervals III, IV, and V. This study demonstrates that the nonsensory cortex PFC, MC, and OL can participate in the cortical reactions induced by stimulation of a latent MTrP. Additionally, the PFC shows nonnegligible higher activation and weakened regulation than other brain regions. Thus, the PFC may be responsible for the central cortical regulation of a latent MTrP. This trial is registered with ChiCTR2100048433. [ABSTRACT FROM AUTHOR]

The 7050 aluminum alloy orifice plate is extruded and strengthened by the cold expansion process of slotted bushing holes. A three-dimensional finite element model was established for cold expansion strengthening of holes, and the residual stress distribution of 7050 aluminum alloy orifice plates is studied after cold expansion. The influence of different relative extrusion amounts and different sample thicknesses on the residual stress around the sample hole was analyzed, and the relationship between the extrusion amounts and the thicknesses of the substrate and the residual stress was obtained by analysis. The research results indicate that the cold expansion process of slotted bushing holes can enhance the residual stress distribution around the hole and form a strong residual stress layer. As the amounts of extrusion increase, the residual stress tends to increase, reaching the maximum when the amounts of extrusion are 4%. The residual stress on the surface of the extrusion inlet increases with the increase in the thickness of the substrate. Within the range of 3%-4% of the extrusion amounts, with the continuous increase of the extrusion amounts, the fatigue life has been substantially enhanced, and the number of fatigue life is more than 3 times that of the empty plate fatigue test. [ABSTRACT FROM AUTHOR]