Characterization of the Protein Corona of Three Chairside Hemoderivatives on Melt Electrowritten Polycaprolactone Scaffolds

In tissue engineering, the relationship between a biomaterial surface and the host’s immune response during wound healing is crucial for tissue regeneration. Despite hemoderivative functionalization of biomaterials becoming a common tissue-engineering strategy for enhanced regeneration, the characteristics of the protein–biomaterial interface have not been fully elucidated. This study characterized the interface formed by the adsorbed proteins from various hemoderivatives with pristine and calcium phosphate (CaP)-coated polycaprolactone (PCL) melt electrowritten scaffolds. PCL scaffolds were fabricated by using melt electrospinning writing (MEW). Three hemoderivatives (pure platelet-rich plasma (P-PRP), leucocyte platelet-rich plasma (L-PRP) and injectable platelet-rich fibrin (i-PRF)) and total blood PLASMA (control) were prepared from ovine blood. Hemoderivatives were characterized via SEM/EDX, cross-linking assay, weight loss, pH and protein quantification. The interface between PCL/CaP and hemoderivative was examined via FTIR, XPS and electrophoresis. i-PRF/PCL-CaP (1653 cm−1), PLASMA/PCL-CaP (1652 cm−1) and i-PRF/PCL (1651 cm−1) demonstrated a strong signal at the Amide I region. PLASMA and i-PRF presented similar N1s spectra, with most of the nitrogen involved in N-C=O bonds (≈400 eV). i-PRF resulted in higher adsorption of low molecular weight (LMW) proteins at 60 min, while PLASMA exhibited the lowest adsorption. L-PRP and P-PRP had a similar pattern of protein adsorption. The characteristics of biomaterial interfaces can be customized, thus creating a specific hemoderivative-defined layer on the PCL surface. i-PRF demonstrated a predominant adsorption of LMW proteins. Further investigation of hemoderivative functionalized biomaterials is required to identify the differential protein corona composition, and the resultant immune response and regenerative capacity

Strength, jumping, and change of direction speed asymmetries are not associated with athletic performance in elite academy soccer players

The aims of the present study were twofold: 1) to measure inter-limb asymmetries from a battery of fitness tests in youth soccer players and, 2) determine the association between asymmetry and measures of athletic performance. Sixteen elite youth soccer players (14.7 ± 0.2 years) performed a single leg Abalakov test (ABK), change of direction (COD) test over 10 m (5 + 5) and 20 m (10 + 10), and an iso-inertial power test. Subjects also performed 10 m, 20 m and 30 m sprints and a bilateral countermovement jump (CMJ), which were correlated with all ABK, COD and iso-inertial asymmetry scores. A one-way repeated measures ANOVA showed significant differences between inter-limb asymmetry scores across multiple tests (p 0.05) between the different inter-limb asymmetry scores, and between asymmetry scores and athletic performance. These findings show the test-specific nature of asymmetries in youth soccer players, with the iso-inertial power test being the most sensitive in detecting asymmetry. Moreover, the results obtained suggest that inherent asymmetry in young soccer players did not negatively impact their performance

Iodine chemistry in the troposphere and its effect on ozone

Despite the potential influence of iodine chemistry on the oxidizing capacity of the troposphere, reactive iodine distributions and their impact on tropospheric ozone remain almost unexplored aspects of the global atmosphere. Here we present a comprehensive global modelling experiment aimed at estimating lower and upper limits of the inorganic iodine burden and its impact on tropospheric ozone. Two sets of simulations without and with the photolysis of IxOy oxides (i.e. I2O2, I2O3 and I2O4) were conducted to define the range of inorganic iodine loading, partitioning and impact in the troposphere. Our results show that the most abundant daytime iodine species throughout the middle to upper troposphere is atomic iodine, with an annual average tropical abundance of (0.15-0.55) pptv. We propose the existence of a "tropical ring of atomic iodine" that peaks in the tropical upper troposphere (∼11-14 km) at the equator and extends to the sub-tropics (30°N-30°S). Annual average daytime I = IO ratios larger than 3 are modelled within the tropics, reaching ratios up to ∼20 during vigorous uplift events within strong convective regions. We calculate that the integrated contribution of catalytic iodine reactions to the total rate of tropospheric ozone loss (IOx Loss) is 2-5 times larger than the combined bromine and chlorine cycles. When IxOy photolysis is included, IOx Loss represents an upper limit of approximately 27, 14 and 27% of the tropical annual ozone loss for the marine boundary layer (MBL), free troposphere (FT) and upper troposphere (UT), respectively, while the lower limit throughout the tropical troposphere is ∼9 %. Our results indicate that iodine is the second strongest ozone-depleting family throughout the global marine UT and in the tropical MBL. We suggest that (i) iodine sources and its chemistry need to be included in global tropospheric chemistry models, (ii) experimental programs designed to quantify the iodine budget in the troposphere should include a strategy for the measurement of atomic I, and (iii) laboratory programs are needed to characterize the photochemistry of higher iodine oxides to determine their atmospheric fate since they can potentially dominate halogen-catalysed ozone destruction in the troposphere

Paper-based chromatic toxicity bioassay by analysis of bacterial ferricyanide reduction

Water quality assessment requires a continuous and strict analysis of samples to guarantee compliance with established standards. Nowadays, the increasing number of pollutants and their synergistic effects lead to the development general toxicity bioassays capable to analyse water pollution as a whole. Current general toxicity methods, e.g. Microtox®, rely on long operation protocols, the use of complex and expensive instrumentation and sample pre-treatment, which should be transported to the laboratory for analysis. These requirements delay sample analysis and hence, the response to avoid an environmental catastrophe. In an attempt to solve it, a fast (15 min) and low-cost toxicity bioassay based on the chromatic changes associated to bacterial ferricyanide reduction is here presented. E. coli cells (used as model bacteria) were stably trapped on low-cost paper matrices (cellulose-based paper discs, PDs) and remained viable for long times (1 month at -20 °C). Apart from bacterial carrier, paper matrices also acted as a fluidic element, allowing fluid management without the need of external pumps. Bioassay evaluation was performed using copper as model toxic agent. Chromatic changes associated to bacterial ferricyanide reduction were determined by three different transduction methods, i.e. (i) optical reflectometry (as reference method), (ii) image analysis and (iii) visual inspection. In all cases, bioassay results (in terms of half maximal effective concentrations, EC50) were in agreement with already reported data, confirming the good performance of the bioassay. The validation of the bioassay was performed by analysis of real samples from natural sources, which were analysed and compared with a reference method (i.e. Microtox). Obtained results showed agreement for about 70% of toxic samples and 80% of non-toxic samples, which may validate the use of this simple and quick protocol in the determination of general toxicity. The minimum instrumentation requirements and the simplicity of the bioassay open the possibility of in-situ water toxicity assessment with a fast and low-cost protocolPostprint (author's final draft

Iron overload causes endolysosomal deficits modulated by NAADP-regulated 2-pore channels and RAB7A

Various neurodegenerative disorders are associated with increased brain iron content. Iron is known to cause oxidative stress, which concomitantly promotes cell death. Whereas endolysosomes are known to serve as intracellular iron storage organelles, the consequences of increased iron on endolysosomal functioning, and effects on cell viability upon modulation of endolysosomal iron release remain largely unknown. Here, we show that increasing intracellular iron causes endolysosomal alterations associated with impaired autophagic clearance of intracellular protein aggregates, increased cytosolic oxidative stress and increased cell death. These effects are subject to regulation by NAADP, a potent second messenger reported to target endolysosomal TPCNs (2-pore channels). Consistent with endolysosomal iron storage, cytosolic iron levels are modulated by NAADP, and increased cytosolic iron is detected when overexpressing active, but not inactive TPCNs, indicating that these channels can modulate endolysosomal iron release. Cell death triggered by altered intralysosomal iron handling is abrogated in the presence of an NAADP antagonist or when inhibiting RAB7A activity. Taken together, our results suggest that increased endolysosomal iron causes cell death associated with increased cytosolic oxidative stress as well as autophagic impairments, and these effects are subject to modulation by endolysosomal ion channel activity in a RAB7A-dependent manner. These data highlight alternative therapeutic strategies for neurodegenerative disorders associated with increased intracellular iron load

New emerging role of protein-tyrosine phosphatase 1B in the regulation of glycogen metabolism in basal and TNF-α-induced insulin-resistant conditions in an immortalised muscle cell line isolated from mice.

Aims/hypothesis Protein-tyrosine phosphatase 1B (PTP1B) negatively regulates insulin action, promoting attenuation of the insulin signalling pathway. The production of this phosphatase is enhanced in insulin-resistant states, such as obesity and type 2 diabetes, where high levels of proinflammatory cytokines (TNF-α, IL-6) are found. In these metabolic conditions, insulin action on glycogen metabolism in skeletal muscle is greatly impaired. We addressed the role of PTP1B on glycogen metabolism in basal and insulin-resistant conditions promoted by TNF-α. Methods We studied the effect of TNF-α in the presence and absence of insulin on glycogen content and synthesis, glycogen synthase (GS) and glycogen phosphorylase (GP) activities and on glycogen synthesis and degradation signalling pathways. For this purpose we used immortalised cell lines isolated from skeletal muscle from mice lacking PTP1B. Results Absence of PTP1B caused activation of GS and GP with a net glycogenolytic effect, reflected in lower amounts of glycogen and activation of the glycogenolytic signalling pathway, with higher rates of phosphorylation of cyclic adenosine monophosphate-dependent kinase (PKA), phosphorylase kinase (PhK) and GP phosphorylation. Nevertheless, insulin action was strongly enhanced in Ptp1b (also known as Ptpn1)−/− cells in terms of glycogen content, synthesis, GS activation rates and GS Ser641 dephosphorylation. Treatment with TNF-α augmented the activity ratios of both GS and GP, and impaired insulin stimulation of glycogen synthesis in wild-type myocytes, whereas Ptp1b −/− myocytes restored this inhibitory effect. We report a glycogenolytic effect of TNF-α, as demonstrated by greater activation of the degradation signalling cascade PKA/PhK/GP. In our model, this effect is mediated by the activation of PKA. Conclusions/interpretation We provide new data about the role of PTP1B in glycogen metabolism and confirm the beneficial effect that absence of the phosphatase confers against an insulin-resistant condition.post-print586 K

Observation of a New Excited Ds+ Meson in B0 →d-D+K+π-Decays

Using pp collision data corresponding to an integrated luminosity of 5.4 fb−1 collected with the LHCb detector at a center-of-mass energy of 13 TeV, the B0 → D−DþKþπ− decay is studied. A new excited Dþ s meson is observed decaying into the DþKþπ− final state with large statistical significance. The pole mass and width, and the spin parity of the new state are measured with an amplitude analysis to be mR ¼ 2591 6 7 MeV, ΓR ¼ 89 16 12 MeV, and JP ¼ 0−, where the first uncertainty is statistical and the second systematic. Fit fractions for all components in the amplitude analysis are also reported. The new resonance, denoted as Ds0ð2590Þþ, is a strong candidate to be the Dsð21 S0Þþ state, the radial excitation of the pseudoscalar ground-state Dþ s meson

Characterization of a Subsurface Biosphere in a Massive Sulfide Deposit At Rio Tinto, Spain: Implications For Extant Life On Mars

The recent discovery of abundant sulfate minerals, particularly Jarosite by the Opportunity Rover at Sinus Merdiani on Mars has been interpreted as evidence for an acidic lake or sea on ancient Mars [1,2], since the mineral Jarosite is soluble in liquid water at pH above 4. The most likely mechanism to produce sufficient protons to acidify a large body of liquid water is near surface oxidation of pyrite rich deposits [3]. The acidic waters of the Rio Tinto, and the associated deposits of Hematite, Goethite, and Jarosite have been recognized as an important chemical analog to the Sinus Merdiani site on Mars [4]. The Rio Tinto is a river in southern Spain that flows 100 km from its source in the Iberian pyrite belt, one of the Earth's largest Volcanically Hosted Massive Sulfide (VHMS) provinces, into the Atlantic ocean. The river originates in artesian springs emanating from ground water that is acidified by the interaction with subsurface pyrite ore deposits. The Mars Analog Rio Tinto Experiment (MARTE) has been investigating the hypothesis that a subsurface biosphere exists at Rio Tinto living within the VHMS deposit living on chemical energy derived from sulfur and iron minerals. Reduced iron and sulfur might provide electron donors for microbial metabolism while in situ oxidized iron or oxidants entrained in recharge water might provide electron acceptors

Association of single nucleotide polymorphisms in Pre-miR-27a, Pre-miR-196a2, Pre-miR-423, miR-608 and Pre-miR-618 with breast cancer susceptibility in a South American population

Indexación: Web of ScienceBackground MicroRNAs (miRNAs) are a novel class of endogenous, non-coding, single-stranded RNAs capable of regulating gene expression by suppressing translation or degrading mRNAs. Single nucleotide polymorphisms (SNP) can alter miRNA expression, resulting in diverse functional consequences. Previous studies have examined the association of miRNA SNPs with breast cancer (BC) susceptibility. The contribution of miRNA gene variants to BC susceptibility in South American women had been unexplored. Our study evaluated the association of the SNPs rs895819 in pre-miR27a, rs11614913 in pre-miR-196a2, rs6505162 in pre-miR-423, rs4919510 in miR-608, and rs2682818 in pre-mir-618 with familial BC and early-onset non-familial BC in non-carriers of BRCA1/2 mutations from a South American population. Results We evaluated the association of five SNPs with BC risk in 440 cases and 807 controls. Our data do not support an association of rs11614913:C > T and rs4919510:C > G with BC risk. The rs6505162:C > A was significantly associated with increased risk of familial BC in persons with a strong family history of BC (OR = 1.7 [95 % CI 1.0–2.0] p = 0.05). The rs2682818:C > A genotype C/A is associated with an increased BC risk in non-familial early-onset BC. For the rs895819:A > G polymorphism, the genotype G/G is significantly associated with reduced BC risk in families with a moderate history of BC (OR = 0.3 [95 % CI 0.1–0.8] p = 0.01). Conclusions The contribution of variant miRNA genes to BC in South American women had been unexplored. Our findings support the following conclusions: a) rs6505162:C > A in pre-miR-423 increases risk of familial BC in families with a strong history of BC; b) the C/A genotype at rs2682818:C > A (pre-miR-618) increases BC risk in non-familial early-onset BC; and c) the G/G genotype at rs895819:A > G (miR-27a) reduces BC risk in families with a moderate history of BC.http://bmcgenet.biomedcentral.com/articles/10.1186/s12863-016-0415-