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Hydrogen production using novel catalysts is regarded as one of the most needed technology for the future economic needs and water splitting to give H _2 gas, which is a challenging task for large-scale production. This work reports the synthesis of Meso-Cu-BTC metal organic framework and further used for understanding its role in electrochemical hydrogen evolution reaction (HER) in 1 M NaOH solution. Meso-Cu-BTC electrocatalyst showed a less overpotential of 89.32 mV and an onset potential of 25 mV with an appreciable current density. Results show a low Tafel slope of 33.41 mVdec ^−1 and long-term durability. Thus, the overall results show that Meso-Cu-BTC acted as a good candidate for electrocatalysis towards hydrogen evolution.

This article reports microstructural, morphological, optical, and photoresponse characteristics of pure and zirconium-doped V2O5 nanorods (Zr:V2O5; Zr at. 1, 3, 5, and 7 wt%) that were synthesized via the wet precipitation method. Undoubtedly, under experimental conditions, a growth mechanism has been proposed which explains morphological evolution. The microstructural analysis confirmed that the prepared samples showed a broad peak consistent with the V2O5 orthorhombic structure, and the absences of other reflections in this pattern ensure the phase purity. The optimized average crystallite size is determined by using Scherrer's equation from the most influential (002) peak of diffraction, which has coincided with those calculated by the TEM micrograph. SEM images showed agglomerated particles on the surfaces owing to an increase in the Zr-doping levels. The outcomes of Raman and XPS indicate that Zr doping can facilitate the generation of V5+ and oxygen vacancy. The recorded UV-DRS spectra reveal the redshifts, and the estimated optical bandgap (Eg) was decreasing with increasing Zr amount, which is further confirmed by PL studies. We used the nebulizer spray technique, a cost-effective, sophisticated, and effective way to formulate an n-ZrxV2O5/p-Si photodetector. The formulated n-ZrxV2O5/p-Si photodetector has good photoconducting behavior. [ABSTRACT FROM AUTHOR]

In the present work, Nickel doped Molybdenum trioxide (NixMoO3) where Ni = X (X = 5, 10, and 15%) nanoparticles (NPs) were synthesized by a wet chemical method. These nano crystals are structurely analysized by X-ray diffraction and confirm the formation of orthorhombic structure in both MoO3 and Ni-doped MoO3 samples. The impact of Ni doping on crystallite size, micro strain, and texture co efficient are obtained from XRD pattern. The morphology studies of FE-SEM and HR-TEM show that the presence of one dimensional (1D) nanorods with an average diameter of particle size around 28–32 nm and the compositional stoichiometry is confirmed by EDAX technique. The functional group and the vibrational mode of metal oxide (Mo = O) are confirmed by FT-IR spectra. The photocatalytic activities of pure and Ni-doped MoO3 are attributed to the degradation efficiency under UV–Visible light irradiation. The result shows that these structure exhibits promising degradation of Methylene blue (MB) is calculated along with the kinetic study, cyclic efficiency, and growth mechanism. The ability of the catalysts generates electron-hole pairs which create free radicals and also help to undergo the secondary reactions. The MoO3 and Ni-doped MoO3 samples normally reveal better results against in antibacterial activity such as Escherichia Coli (E. Coli) and Staphylococcus aureus (S. aureus) bacteria. Overall, the results demonstrate that the doping of Ni2+ ions inside the MoO3 matrix enhances the performance in antibacterial activity. Highlights: Ni decorated MoO3 nanorods of various concentrations (5, 10 & 15%) have been investigated. Morphological, structural & optical properties of Ni incorporation of MoO3 nanorods are studied by various experimental parameters. Degradation rate constant is found through the pseudo-first-order kinetic model. Recycle test and photocatalytic mechanisim are studied under UV-Visible light irradiation. The bacteria strain observes through disc diffusion technique. [ABSTRACT FROM AUTHOR]

Manganese oxide (Mn2O3) nanoparticles have been synthesized in co-precipitation method and followed by annealing of the samples at 200°C, 400°C and 600°C at 10 hours. The prepared samples are characterized with X-ray diffraction (XRD), scanning electron microscopy (SEM), energy dispersive analysis of X-ray spectroscopy (EDAX), UV-visible spectroscopy and vibrating-sample magnetometer (VSM). The XRD spectra reveals that the body centred cubic structure of Mn2O3 powder was obtained. Annealing temperature proliferates the crystallite sizes from 31 to 81nm are calculated by Scherer's formula. The SEM image unveils that the materials have an irregular nano-stick like morphology. Optical properties are appraised by UV-visible spectroscopy; band gap values deceased with increasing annealing treatment. Low annealing temperature treatment sample shows high transmittance in visible region. FT-IR studies shows that the number of surface hydroxyl group dwindle with the enhance of annealing temperature. The magnetization (VSM) is conducted to the sample and the saturation magnetization (Ms) is 38.73emu/g. [ABSTRACT FROM AUTHOR]

Loss of function of the Retinoblastoma gene (RB1) due to mutations is commonly seen in human osteosarcomas. One of the Rb1 gene functions is to facilitate cell fate from mesenchymal stem cells to osteoblasts and prevent adipocyte differentiations. In this study, we demonstrate that a stable reduction of Rb1 expression (RbKD) in murine osteoblasts causes them to express higher levels of PPAR-ɣ and other adipocyte-specific transcription factors while retaining high expression of osteoblast-specific transcription factors, Runx2/Cbfa1 and SP7/Osterix. Inhibition of gap junctional intercellular communication (GJIC) in osteoblasts is another mechanism that causes osteoblasts to transdifferentiate to adipocytes. We found that preosteoblasts exposed to osteoblast differentiating media (DP media) increased GJIC. RbKD cells showed reduced GJIC along with a reduction in expression of Cx43, the protein that mediates GJIC. Other membrane associated adhesion protein Cadherin 11 (Cad11) was also decreased. Since PPAR-ɣ is increased with Rb1 loss, we wondered if the reduction of this transcription factor would reverse the changes observed. Reduction of PPAR-ɣ in control osteoblasts slightly increased bone-specific expression and reduced adipocytic expression as expected along with an increase in Cad11 and Cx43 expression. GJIC remained high and was unaffected by a reduction in PPAR-ɣ in control cells. Knockdown of PPAR-ɣ in RbKD cells reduced adipocyte gene expression, while osteoblast-specific expression showed improvement. Cx43, Cad11 and GJIC remained unaffected by PPAR-ɣ reduction. Our observations suggest that increased PPAR-ɣ that happens with Rb1 loss only affects osteoblast-adipocyte-specific gene expression but does not completely reverse Cx43 gene expression or GJIC. Therefore, these effects may represent independent events triggered by Rb1loss and/or the differentiation process.

Dental pulp stem cells (DPSCs) and stem cells from human exfoliated deciduous teeth (SHED) are a source of mesenchymal stem cells with the potential to differentiate into several cell types. We initially isolated SHED cells and compared their osteogenic capacity with commercially available DPSCs. Both cells exhibited similar capacities of growth and osteogenic differentiation. A fourfold to sixfold increase in endogenous microRNA26a (miR26a) expression during osteogenic differentiation of preosteoblasts and a similar but attenuated increase (twofold to fourfold) in differentiating SHED was observed, suggesting a role in the process. We, therefore, overexpressed miR26a in SHED to determine if the osteogenic differentiation capacity can be potentiated in vitro . SHED with a threefold increase in miR26a expression showed increased growth rate when compared with parent cells. When exposed to an osteogenic differentiating promoting medium, the miR26a overexpressing cells showed 100-fold increases in the expression of bone marker genes such as type 1 collagen, alkaline phosphatase, and Runx2. The mineralization capacity of these cells was also increased 15-fold. As miR26a targets regulate several bone-specific genes, we evaluated the effect of miR26a overexpression on established targets. We found a moderate decrease in SMAD1 and a profound decrease in PTEN expression. miR26a could potentiate its effect on osteoblast differentiation by its ability to inhibit PTEN and increase the viability of cells and their numbers, a process essential in osteoblast differentiation. Our studies suggest that the upregulation of miR26a can increase bone formation and may serve as an important target to further investigate its potential in tissue engineering applications.

In order to understand the role of the p53 tumor suppressor gene in microRNA expression during osteoblast differentiation, we used a screen to identify microRNAs that were altered in a p53-dependent manner. MicroRNAs from MC3T3-E1 preosteoblasts were isolated from day 0 (undifferentiated) and day 4 (differentiating) and compared to a p53 deficient MC3T3-E1 line treated similarly. Overall, one fourth of all the microRNAs tested showed a reduction of 0.6 fold, and a similar number of them were increased 1.7 fold with differentiation. P53 deficiency caused 40% reduction in expression of microRNAs in differentiating cells, while a small percent (0.03%) showed an increase. Changes in microRNAs were validated using real-time PCR and two microRNAs were selected for further analysis (miR-34b and miR-140). These two microRNAs were increased significantly during differentiation but showed a dramatic reduction in expression in a p53 deficient state. Stable expression of miR-34b and miR-140 in MC3T3-E1 cells resulted in decreases in cell proliferation rates when compared to control cells. There was a 4-fold increase in p53 levels with miR-34b expression and a less dramatic increase with miR-140. Putative target binding sites for bone specific transcription factors, Runx2 and Osterix, were found for miR-34b, while Runx2, beta catenin and type 1 collagen were found to be miR-140 targets. Western blot analyses and functional assays for the transcription factors Runx2, Osterix and Beta-catenin confirmed microRNA specific interactions. These studies provide evidence that p53 mediated regulation of osteoblast differentiation can also occur through specific microRNAs such as miR-34b and miR-140 that also directly target important bone specific genes., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Authors.)

Liposarcoma is a malignant soft tissue tumor that originates from adipose tissue and is one of the most frequently diagnosed soft tissue sarcomas in humans. There is great interest in identifying novel chemotherapeutic options for treating liposarcoma based upon molecular alterations in the cancer cells. The Aurora kinases have been identified as promising chemotherapeutic targets based on their altered expression in many human cancers and cellular roles in mitosis and cytokinesis. In this study, we investigated the effects of an Aurora kinase A inhibitor (MK-5108), an Aurora kinase B inhibitor (AZD1152-HQPA), and a pan-Aurora kinase inhibitor (AMG 900) on undifferentiated SW-872 and well-differentiated 93T449 human liposarcoma cells. Treatment of the SW-872 and 93T449 cells with MK-5108 (0-1000 nM), AZD1152-HQPA (0-1000 nM), and AMG 900 (0-1000 nM) for 72 h resulted in a dose-dependent decrease in the total viable cell number. Based upon the EC 50 values, the potency of the three Aurora kinase inhibitors in the SW-872 cells was as follows: AMG 900 (EC 50  = 3.7 nM) > AZD1152-HQPA (EC 50  = 43.4 nM) > MK-5108 (EC 50  = 309.0 nM), while the potency in the 93T449 cells was as follows: AMG 900 (EC 50  = 6.5 nM) > AZD1152-HQPA (EC 50  = 74.5 nM) > MK-5108 (EC 50  = 283.6 nM). The percentage of polyploidy after 72 h of drug treatment (0-1000 nM) was determined by propidium iodide staining and flow cytometric analysis. AMG 900 caused a significant increase in polyploidy starting at 25 nM in the SW-872 and 93T449 cells, and AZD1152-HQPA caused a significant increase starting at 100 nM in the SW-872 cells and 250 nM in the 93T449 cells. The Aurora kinase A inhibitor MK-5108 did not significantly increase the percentage of polyploid cells at any of the doses tested in either cell line. The expression of Aurora kinase A and B was evaluated in the SW-872 cells versus differentiated adipocytes and human mesenchymal stem cells by real-time RT-PCR and Western blot analysis. Aurora kinase A and B mRNA expression was significantly increased in the SW-872 cells versus the differentiated adipocytes and human mesenchymal stem cells. Western blot analysis revealed a ~ 48 kDa immunoreactive band for Aurora kinase A that was not present in the differentiated adipocytes or the human mesenchymal stem cells. A ~ 39 kDa immunoreactive band for Aurora kinase B was detected in the SW-872 cells, differentiated adipocytes, and human mesenchymal stem cells. A smaller immunoreactive band for Aurora kinase B was detected in the SW-872 cells but not in the differentiated adipocytes and human mesenchymal stem cells, and this may reflect the expression of a truncated splice variant of Aurora kinase B that has been associated with poor patient prognosis. The 93T449 cells demonstrated decreased expression of Aurora kinase A and B mRNA and protein compared to the SW-872 cells, and also expressed the truncated form of Aurora kinase B. The results of these in vitro studies indicate that Aurora kinase inhibitors should be further investigated as possible chemotherapeutic agents for human liposarcoma.

Osteoblasts and adipocytes originate from common mesenchymal progenitor cells and are controlled by specific transcription factors. While 1,25-dihydroxyvitamin D 3 (vitamin D) is known to be an important factor for osteoblast differentiation, there are conflicting reports regarding its effect on adipogenesis. In this study, we attempted to understand the effect of exposure of preosteoblasts (MC3T3-E1) to adipogenic media with and without vitamin D and determined the expression of adipogenic genes during this process. Our studies show that while transdifferentiation of preosteoblasts occurred on exposure to adipogenic media, the effect of vitamin D treatment was synergistic resulting in several hundred fold increase in adipocyte transcription factors C/EBPα and peroxisome proliferator-activated receptor-gamma ( P  < 0.001) along with an increase in markers of adipogenesis and accumulation of lipid droplets in cells. Vitamin D treatment was also accompanied by 100-fold to 700-fold increases in vitamin D receptor expression during the treatment period ( P  < 0.001). To determine how the effect of vitamin D might compare to other genetic manipulations that promote adipogenic differentiation, we stably knocked down retinoblastoma expression in MC3T3-E1 cells. Recent studies have suggested retinoblastoma (Rb1) tumor suppressor gene function to be critical to maintain osteoblasts function and inhibit adipocyte differentiation. We exposed MC3T3-E1 cells with reduced Rb1 expression to adipogenic media and found an increase in adipogenic differentiation when compared to cells with a full complement of Rb dosage. However, the extent of the change was not as dramatic as seen with vitamin D. These studies show that preosteoblasts are sensitive and respond to these manipulations that favor the adipocytic phenotype. While vitamin D is not known to directly affect targets in adipogenesis, our observations may have resulted from the malleability of preosteoblast genome in MC3T3-E1 cells, which allowed adipocyte specific gene expression under appropriate stimuli. Why this pathway is influenced and subverted by an anabolic bone factor such as vitamin D remains to be determined.

Segmental mechanics for the retraction of anterior teeth is often used in cases where maximum anchorage is required. There are few conventional methods for the attachment of T-loops to the anterior segment. This article highlights a very simple method for the attachment of T-loops to the anterior segment for their retraction during day-to-day clinical practice.