Supported TiO2 on Borosilicate Glass Plates for Efficient Photocatalytic Degradation of Fenamiphos

Supported titanium dioxide (TiO2) was investigated for the photodegradation of the insecticide fenamiphos in water. The photocatalyst was immobilised on borosilicate glass plates and the kinetics of degradation were studied in a stirred tank reactor under UV irradiation. Two types of TiO2, for example, Millennium PC500 (100% anatase) and Degussa P25 (80% anatase, 20% rutile), were used. Their activities have been based on the rates of insecticide disappearance. Experiments were investigated to evaluate the effect of pH and initial concentrations of fenamiphos as well as catalyst doses on the photocatalytic degradation of fenamiphos. Kinetic parameters were experimentally determined and an apparent first-order kinetic was observed. For photolysis process of fenamiphos, two photoproducts were identified and characterized using high performance liquid chromatography/mass spectrometry (HPLC/MS). The plausible mechanism of photolysis involved is the oxidation of sulfonamide group. In presence of photocatalyst TiO2, photodegradation was observed. Under identical conditions, Degussa P25 shows higher photocatalytic activity in regard to PC500 Millennium and complete degradation was observed after 180 min

FORME INHABITUELLE DE LA SARCOÏDOSE : LOCALISATION NASOSINUSIENNE, OSSEUSE ET CUTANEE

La sarcoïdose est une granulomatose systémique d’étiologie inconnue affectant principalement le poumon, les ganglions et la peau. Les atteintes nasosinusiennes et ostéo-articulaires restent rares [1-2], parfois inaugurales et souvent méconnues. Nous en rapportons une nouvelle observation

Ensiling characteristics of prickly pear (opuntia-ficus indica) rejects with and without molasses for animal feed

Purpose The aim of this work was to study the effect of adding sugar beet molasses on the biochemical properties, microbial flora, fermentation quality, and aerobic stability of prickly pear cactus (Opuntia ficus-indica) waste silage.Method Molasses (0%, 2%, 4%, 6%, 8% and 10%, w/w) was mixed with the cactus fruit scraps, straw and wheat bran.Results The dry matter content, pH, total and reducing sugars of the pre-ensiling material increased after adding different percentages of the beet molasses (P < 0.05). During fermentation, we observed substantial protein and sugar degradation. All silage treatments reached stable pH values (pH 4.3-4.6). Among all the concentrations, the 10% beet molasses treatment underwent the highest lactic acid fermentation. Accordingly, the pH drop was higher in the 10% concentration (1.13 units) compared to lower beet molasses concertation  (1.03 units). Also, the 10% concentration has the highest number of lactic acid bacteria. The number of yeast and total aerobic mesophiles decreased continuously during silage. Moreover, during post-fermentation testing, the yeast multiplied little for the 10% concentration of beet molasses.Conclusion The results show that the addition of molasses has a significant effect on silage characteristics of prickly pear cactus

A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration

Myocardial regeneration is restricted to early postnatal life, when mammalian cardiomyocytes still retain the ability to proliferate. The molecular cues that induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated adult heart muscle cells remain obscure. Here we report that the miR-106b~25 cluster is higher expressed in the early postnatal myocardium and decreases in expression towards adulthood, especially under conditions of overload, and orchestrates the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome. In line, gene delivery of miR-106b~25 to the mouse heart provokes cardiomyocyte proliferation by targeting a network of negative cell cycle regulators including E2f5, Cdkn1c, Ccne1 and Wee1. Conversely, gene-targeted miR-106b~25 null mice display spontaneous hypertrophic remodeling and exaggerated remodeling to overload by derepression of the prohypertrophic transcription factors Hand2 and Mef2d. Taking advantage of the regulatory function of miR-106b~25 on cardiomyocyte hyperplasia and hypertrophy, viral gene delivery of miR-106b~25 provokes nearly complete regeneration of the adult myocardium after ischemic injury. Our data demonstrate that exploitation of conserved molecular programs can enhance the regenerative capacity of the injured heart.E.D. is supported by a VENI award 916-150-16 from the Netherlands Organization for Health Research and Development (ZonMW), an EMBO Long-term Fellowship (EMBO ALTF 848-2013) and a FP7 Marie Curie Intra-European Fellowship (Project number 627539). V.S.P. was funded by a fellowship from the FCT/ Ministério da Ciência, Tec-nologia e Inovação SFRH/BD/111799/2015. P.D.C.M. is an Established Investigator of the Dutch Heart Foundation. L.D.W. acknowledges support from the Dutch CardioVascular Alliance (ARENA-PRIME). L.D.W. was further supported by grant 311549 from the European Research Council (ERC), a VICI award 918-156-47 from the Dutch Research Council and Marie Sklodowska-Curie grant agreement no. 813716 (TRAIN-HEART)

The transverse aortic constriction heart failure animal model: a systematic review and meta-analysis

The transverse aortic constriction (TAC) model is frequently used to study adverse cardiac remodeling upon pressure overload. We set out to define the most important characteristics that define the degree of cardiac remodeling in this model. A systematic review and meta-analyses were performed on studies using the TAC mouse/rat model and reporting echocardiographic outcome parameters. We included all animal studies in which a constriction around the transverse aorta and at least one of the predefined echocardiography or MRI outcome parameters were assessed. A total of 502 articles and > 3000 wild-type, untreated animals undergoing TAC were included in this study and referenced to a control group. The duration of aortic constriction correlated to the degree of adverse remodeling. However, the mouse data is strongly biased by the preferential use of male C57Bl/6 mice (66% of studies). Furthermore, mostly ketamine/xylazine anesthetics, 27G needle constriction, and silk sutures are used. Nonetheless, despite the homogeneity in experimental design, the model contained a substantial degree of heterogeneity in the functional outcome measures. When looking at study quality, only 12% reported randomization, 23% mentioned any sort of blinding, 25% adequately addressed the outcomes, and an amazingly low percentage (2%) showed sample size calculation. Meta-analyses did not detect specific study characteristics that explained the heterogeneity in the reported outcome measures, however this might be related to the strong bias towards the use of specific mouse lines, sex as well as age or to poor reporting of characteristics of study quality

MiR-337-3p Promotes Adipocyte Browning by Inhibiting TWIST1

The prevalence of metabolic syndrome (MetS) and obesity is an alarming health issue worldwide. Obesity is characterized by an excessive accumulation of white adipose tissue (WAT), and it is associated with diminished brown adipose tissue (BAT) activity. Twist1 acts as a negative feedback regulator of BAT metabolism. Therefore, targeting Twist1 could become a strategy for obesity and metabolic disease. Here, we have identified miR-337-3p as an upstream regulator of Twist1. Increased miR-337-3p expression paralleled decreased expression of TWIST1 in BAT compared to WAT. Overexpression of miR-337-3p in brown pre-adipocytes provoked a reduction in Twist1 expression that was accompanied by increased expression of brown/mitochondrial markers. Luciferase assays confirmed an interaction between the miR-337 seed sequence and Twist1 3 0UTR. The inverse relationship between the expression of TWIST1 and miR-337 was finally validated in adipose tissue samples from non-MetS and MetS subjects that demonstrated a dysregulation of the miR-337-Twist1 molecular axis in MetS. The present study demonstrates that adipocyte miR-337-3p suppresses Twist1 repression and enhances the browning of adipocytes

MicroRNA-132/212 family enhances arteriogenesis after hindlimb ischaemia through modulation of the Ras-MAPK pathway

Arteriogenesis is a complicated process induced by increased local shear-and radial wall-stress, leading to an increase in arterial diameter. This process is enhanced by growth factors secreted by both inflammatory and endothelial cells in response to physical stress. Although therapeutic promotion of arteriogenesis is of great interest for ischaemic diseases, little is known about the modulation of the signalling cascades via microRNAs. We observed that miR-132/212 expression was significantly upregulated after occlusion of the femoral artery. miR-132/212 knockout (KO) mice display a slower perfusion recovery after hind-limb ischaemia compared to wildtype (WT) mice. Immunohistochemical analysis demonstrates a clear trend towards smaller collateral arteries in KO mice. Although Ex vivo aortic ring assays score similar number of branches in miR-132/212 KO mice compared to WT, it can be stimulated with exogenous miR-132, a dominant member of the miR-132/212 family. Moreover, in in vitro pericyte-endothelial co-culture cell assays, overexpression of miR-132 and mir-212 in endothelial cells results in enhanced vascularization, as shown by an increase in tubular structures and junctions. Our results suggested that miR-132/212 may exert their effects by enhancing the Ras-Mitogen-activated protein kinases MAPK signalling pathway through direct inhibition of Rasa1, and Spred1. The miR-132/212 cluster promotes arteriogenesis by modulating Ras-MAPK signalling via direct targeting of its inhibitors Rasa1 and Spred1

Potential role of p53 on metallothionein induction in human epithelial breast cancer cells

The expression and induction of metallothionein has been associated with protection against oxidative stress and apoptosis. This study examines the effect of tumour suppressor protein p53 on metallothionein expression following CdCl2 treatment in eight human epithelial breast cancer cell lines differing in p53 and oestrogen-receptor status. Cells were treated with 10 μM CdCl2 for 24 h and metallothionein protein levels were measured by cadmium binding assay. MCF7 cells which are p53-positive (p53+) and oestrogen-receptor-positive showed a large induction in metallothionein synthesis by 10.79±1.36-fold. Other breast cancer cell lines which are p53-negative (p53−) and oestrogen-receptor-negative or weakly oestrogen-receptor-positive showed a small induction ranging from 1.40±0.10 to 3.65±0.30-fold. RT–PCR analysis showed an induction of metallothionein mRNA in MCF7 cells by about 1.61±0.08-fold, while in HCC1806 cells (p53−, oestrogen-receptor-negative) by 1.11±0.13-fold, and in MDA-MB-231 (p53−, oestrogen-receptor-negative) by 1.25±0.06-fold. Metallothionein localisation was determined by immunohistochemical staining. Prior to metal treatment, metallothionein was localised mainly in the cytoplasm of MCF7 and MDA-MB-231 cells. After treatment with 10 μM CdCl2 for 24 h, MCF7 cells showed intense nuclear and cytoplasmic staining for metallothionein, while MDA-MB-231 cells showed staining in the cytoplasm with weak nuclear staining. Apoptosis induced by 10–40 μM CdCl2 at time points between 4 and 48 h was examined with TUNEL assay. In MCF7 cells, apoptosis increased with higher concentrations of CdCl2, it peaked at 6–8 h and appeared again at 48 h for all concentrations of CdCl2 tested. In MDA-MB-231 cells, apoptosis remained at low levels for 10–40 μM CdCl2 at all time points. Studies on cadmium uptake showed similar uptake and accumulation of cadmium at 8 and 24 h in all the cell lines. The data demonstrate that treatment of epithelial breast cancer cells with 10 μM CdCl2 for 24 h caused a greater induction of metallothionein protein and mRNA expression in p53+ and oestrogen-receptor-positive cells as compared to p53− and oestrogen-receptor-negative or weakly oestrogen-receptor-positive cells. This effect may be associated with the occurrence of apoptosis and suggests a role for p53 and oestrogen-receptor on the expression and induction of metallothionein in epithelial cells