Search

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]

This paper studies earnings management using 363 closed-end mutual fund firm-years of data. Closed-end fund assets consist of unrestricted and restricted securities, and realized and unrealized income. While unrestricted securities are not subject to earnings management, restricted security values are largely discretionary. Managerial valuation of restricted securities is modeled as contingent on unrestricted returns relative to a performance benchmark. Four unrestricted performance regions are identified. Known multi-period compensation incentives become the basis for hypothesizing earnings management behaviors in the regions in the form of restricted security valuation. Across several benchmarks, the results are consistent with multi-period maximization rather than simpler single-period compensation maximization or income smoothing. Funds with extreme unrestricted performance show relatively larger income-decreasing earnings management, and funds with slightly-below benchmark returns show relatively larger income-increasing earnings management than those slightly above. These results clarify the relationship between complex earnings management behavior and managerial incentives. [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]

Abstract Background This study was undertaken to examine the relationship between the tumor suppressor gene p53 and the nuclear signaling protein beta-catenin during bone differentiation. Cross talk between p53 and beta-catenin pathways has been demonstrated and is important during tumorigenesis and DNA damage, where deregulation of beta catenin activates p53. In this study, we used estrogen treatment of osteoblasts as a paradigm to study the relationship between the two proteins during osteoblast differentiation. Results We exposed osteoblast-like ROS17/2.8 cells to 17-beta estradiol (E2), in a short term assay, and studied the cellular distribution and expression of beta-catenin. We found beta-catenin to be up regulated several fold following E2 treatment. Levels of p53 and its functional activity mirrored the quantitative changes seen in beta-catenin. Alkaline phosphatase, an early marker of osteoblast differentiation, was increased in a manner similar to beta-catenin and p53. In order to determine if there was a direct relationship between alkaline phosphatase expression and beta-catenin, we used two different approaches. In the first approach, treatment with LiCl, which is known to activate beta-catenin, caused a several fold increase in alkaline phosphatase activity. In the second approach, transient transfection of wild type beta-catenin into osteoblasts increased alkaline phosphatase activity two fold over basal levels, showing that beta catenin expression can directly affect alkaline phosphatase expression. However increase in beta catenin activity was not associated with an increase in its signaling activity through TCF/LEF mediated transcription. Immunofluorescence analyses of p53 and beta-catenin localization showed that E2 first caused an increase in cytosolic beta-catenin followed by the accumulation of beta-catenin in the nucleus. Nuclear p53 localization was detected in several cells. Expression of p53 was accompanied by distribution of beta-catenin to the cytoplasm and cell borders. A sub population of cells staining strongly for both proteins appeared to be apoptotic. Conclusion These results suggest that interactions between p53 and beta-catenin signaling pathways may play a key role in osteoblast differentiation and maintenance of tissue homeostasis.

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.)

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.

The tumor suppressor gene p53 is involved in a variety of cellular activities such as cellular stress responses, cell cycle regulation and differentiation. In our previous studies we have shown p53's transcription activating role to be important in osteoblast differentiation. There is still a debate in the literature as to whether p53 inhibits or promotes differentiation. We have found p53 heterozygous mice to show a p53 dependency on some bone marker gene expression that is absent in knockout mice. Mice heterozygous for p53 also show a higher incidence of osteosarcomas than p53 knockout mice. This suggests that p53 is able to modify the environment within osteoblasts. In this study we compare changes in gene expression resulting after either a transient or stable reduction in p53. Accordingly we reduced p53 levels transiently and stably in C2C12 cells, which are capable of both myoblast and osteoblast differentiation, and compared the changes in gene expression of candidate genes regulated by the p53 pathway. Using a PCR array to assay for p53 target genes, we have found different expression profiles when comparing stable versus transient knockdown of p53. As expected, several genes with profound changes after transient p53 loss were related to apoptosis and cell cycle regulation. In contrast, stable p53 loss produced a greater change in MyoD and other transcription factors with tissue specific roles, suggesting that long term loss of p53 affects tissue homeostasis to a greater degree than changes resulting from acute loss of p53. These differences in gene expression were validated by measuring promoter activity of different pathway specific genes involved in differentiation. These studies suggest that an important role for p53 is context dependent, with a stable reduction in p53 expression affecting normal tissue physiology more than acute loss of p53.

Objective: To determine the impact of performing critical-thinking and reflection assignments within interdisciplinary learning teams in a biochemistry course on pharmacy students' and prospective health professions students' collaboration scores., Design: Pharmacy students and prospective medical, dental, and other health professions students enrolled in a sequence of 2 required biochemistry courses. They were randomly assigned to interdisciplinary learning teams in which they were required to complete case assignments, thinking and reflection exercises, and a team service-learning project., Assessment: Students were asked to complete the Scale of Attitudes Toward Physician-Pharmacist Collaboration prior to the first course, following the first course, and following the second course. The physician-pharmacist collaboration scores of prospective health professions students increased significantly (p<0.001)., Conclusions: Having prospective health professions students work in teams with pharmacy students to think and reflect in and outside the classroom improves their attitudes toward physician-pharmacist collaboration.

Objective: To measure changes in pharmacy and medical students' physician-pharmacist collaboration scores resulting from a workshop designed to promote understanding of the others' roles in health care., Methods: More than 88% of first-year pharmacy (n = 215) and medical (n = 205) students completed the Scale of Attitudes Toward Physician-Pharmacist Collaboration on 3 occasions in order to establish a baseline of median scores and to determine whether the scores were influenced by an interprofessional workshop., Results: Participation in the interprofessional workshop increased pharmacy students' collaboration scores above baseline (p=0.02) and raised the scores of medical students on the education component of the collaboration survey instrument (p=0.015). The collaboration scores of pharmacy students greatly exceeded those of medical students (p<0.0001)., Conclusion: A workshop designed to foster interprofessional understanding between pharmacy and medical students raised the physician-pharmacist collaboration scores of both. Crucial practical goals for the future include raising the collaboration scores of medical students to those of pharmacy students.

Selective knockdown of phosphatase and tensin homolog (PTEN) has been recently shown to increase life long accumulation of bone and its ability to increase osteoblast lifespan. In order to determine how loss of PTEN function affects osteoblast differentiation, we created cell lines with stable knockdown of PTEN expression using short hairpin RNA vectors and characterized several clones. The effect of deregulated PTEN in osteoblasts was studied in relationship to cell proliferation and differentiation. Downregulation of PTEN initially affected the cell's attachment and spreading on plastic but cells recovered after a brief period of time. When cell proliferation was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, we noticed a small but significant increase in growth rates with PTEN reduction. The size of individual cells appeared larger when compared to control cells. Differentiation properties of these osteoblasts were increased as evidenced by higher expression of several of the bone markers tested (alkaline phosphatase, osteocalcin, osterix, bone morphogenetic protein 2, Cbfa1, osteoprotegerin, and receptor activator of NF-kappaB ligand) and their mineralization capacity in culture. As stabilization of beta-catenin is known to be responsible for growth deregulation with PTEN loss in other cell types, we investigated the activation of the canonical Wnt pathway in our cell lines. Immunofluorescence staining, protein expression in subcellular fractions for beta-catenin, and assays for activation of the canonical Wnt/beta-catenin signaling were studied in the PTEN downregulated cells. There was an overall decrease in beta-catenin expression in cells with PTEN knockdown. The distribution of beta-catenin was more diffuse within the cell in the PTEN-reduced clones when compared to controls where they were mostly present in cell borders. Signaling through the canonical pathway was also reduced in the PTEN knockdown cells when compared to control. The results of this study suggest that while decreased PTEN augments cell proliferation and positively affects differentiation, there is a decrease in beta-catenin levels and activity in osteoblasts. Therefore, at least in osteoblasts, beta-catenin is not responsible for mediating the activation of osteoblast differentiation with reduction in PTEN function.

Groups of male Fischer 344 rats were chronically fed semipurified choline-devoid or choline-supplemented diets, high in fat (15%), and containing or not containing 0.06% phenobarbital. Atypical acinar cell nodules were observed in the pancreas of the rats, irrespective of the diet fed, with incidences varying from 38% to 100% in the various groups. No consistent differential effects of the dietary treatments on the incidence and growth of the nodules were evident, even though the diameter of the nodules tended to be greater in some of the groups fed the basal choline-devoid diet. The vast majority of the nodules were of the acidophilic type. More advanced pancreatic acinar cell lesions were observed in a few of the rats. Since the rats were not exposed to a chemical carcinogen(s), development of the nodules and of the more advanced lesions, even in rats fed the control diets, was most likely due to evolution of endogenous (spontaneous) initiated pancreatic cells, promoted primarily by the feeding of semipurified diets with a high fat content.

Reduced levels of putative indigenous DNA modifications (I-compounds) in liver DNA of male Fischer 344 rats fed a hepatocarcinogenic choline-devoid (CD) diet for up to 7 mo have been previously reported. To investigate the persistence of this effect and possible relationships between I-compounds and hepatocarcinogenesis, liver DNA modifications of tumor-free male rats fed a CD diet for 3, 6, 9, or 12 mo, followed by a choline-supplemented (CS) diet to 16 mo, were compared with those in rats fed exclusively the CD or CS diet for 16 mo by a 32P-postlabeling assay. In addition, DNA from nontumorous and tumorous tissues of rats fed the CD diet similarly for 12 or 16 mo was analyzed. It was found that total I-compound levels in male rats consecutively fed CD and CS diets for various lengths of time were similar to those in rats fed the CD diet only and significantly lower than those in rats fed the CS diet only. I-compound levels of nontumorous regions from tumor-bearing livers were 73% of those in tumor-free livers from the same treatment group. I-compound levels were further reduced, some to undetectable levels, in tumor tissues and exhibited an inverse relationship with tumor incidence. The patterns and levels of I-compounds in liver DNA of CD diet-fed female rats, which were not susceptible to CD diet-induced hepatocarcinogenesis, on the other hand, were not significantly different from those of controls. Thus, reduction of I-compound levels by feeding a CD diet lasted for many months after changing from the CD to the CS diet. Whether this persistent DNA alteration contributes to carcinogenesis remains to be determined.

After long-term feeding of a choline-devoid diet to rats, the authors analyzed rasK, rasH, and rasN transcripts and gene structure in livers and liver tumors. They controlled their analysis by studying cell lines derived from chemically induced hepatomas. Transcripts from all three genes were elevated in all tumors, but not in the livers from which they arose. The transcript elevations may represent an effect of active cell proliferation in the tumors. Clone HiHi-3, derived from the Kirsten murine sarcoma virus, detected a large number of hybridization bands, most of which were not part of the rasK-p21 gene. Most tumors had an altered band at 2.6 kb; some had other altered bands. No alterations were seen in liver DNA, and none of the cell lines showed the 2.6 kb band. At low stringency, a rasH probe, which contains a short segment of a similar viral sequence, also detected altered bands in tumors and a single treated liver. These changes in endogenous viral sequences of the rat genome appear to be characteristic of carcinogenesis by a choline-devoid diet.