The pH and ionic composition of the sub-embryonic fluid of the Japanese quail (Coturnix c. japonica)

The current theory of acid-base chemistry regards [H+] as a dependent variable: changes in pH of a fluid can only occur by alteration of strong ion concentrations ([Na+], [K+], [Cl-]). The objective of this study was to determine whether manipulation of sub-embryonic fluid strong ion composition would alter [H+] in the direction predicted by theory. Changes to fluid strong ion concentrations decreased pH in the way predicted and the changes in Cl- suggest a passive distribution. Also, changes in organic anions suggest an essential role for these in acid-base chemistry of this fluid. It was notable that both Na and HCO3- were unaffected by the treatments emphasising the importance of these two ions in fluid production by the quail blastoderm

Characteristics of chaos evolution in one-dimensional disordered nonlinear lattices

We numerically investigate the characteristics of chaos evolution during wave packet spreading in two typical one-dimensional nonlinear disordered lattices: the Klein-Gordon system and the discrete nonlinear Schr\"{o}dinger equation model. Completing previous investigations \cite{SGF13} we verify that chaotic dynamics is slowing down both for the so-called `weak' and `strong chaos' dynamical regimes encountered in these systems, without showing any signs of a crossover to regular dynamics. The value of the finite-time maximum Lyapunov exponent $\Lambda$ decays in time $t$ as $\Lambda \propto t^{\alpha_{\Lambda}}$, with $\alpha_{\Lambda}$ being different from the $\alpha_{\Lambda}=-1$ value observed in cases of regular motion. In particular, $\alpha_{\Lambda}\approx -0.25$ (weak chaos) and $\alpha_{\Lambda}\approx -0.3$ (strong chaos) for both models, indicating the dynamical differences of the two regimes and the generality of the underlying chaotic mechanisms. The spatiotemporal evolution of the deviation vector associated with $\Lambda$ reveals the meandering of chaotic seeds inside the wave packet, which is needed for obtaining the chaotization of the lattice's excited part.Comment: 11 pages, 10 figure

A study protocol of qualitative data sharing practices in clinical trials in the UK and Ireland: towards the production of good practice guidance [version 1; peer review: awaiting peer review]

Background: Data sharing enables researchers to conduct novel research with previously collected data sets, thus maximising scientific findings and cost effectiveness, and reducing research waste. The value of sharing anonymised data from clinical trials is well recognised with a moderated access approach recommended. While substantial challenges to data sharing remain, there are additional challenges for qualitative data. Qualitative data including videos, interviews, and observations are often more readily identifiable than quantitative data. Existing guidance from UK Economic and Social Research Council applies to sharing qualitative data but does not address the additional challenges related to sharing qualitative data collected within trials, including the need to incorporate the necessary information and consent into already complex recruitment processes, with the additional sensitive nature of health-related data. Methods: Work package 1 will involve separate focus group interviews with members of each stakeholder group: trial managers, clinical trialists, qualitative researchers, members of research funding bodies and trial participants who have been involved in qualitative research. Data will be analysed using thematic analysis and managed within QSR NVivo to enhance transparency. Work package 2 will involve a documentary analysis of current consent procedures for qualitative data collected as part of the conduct of clinical trials. We will include documents such as participant information leaflets and consent forms for the qualitative components in trials. We will extract data such as whether specific clauses for data sharing are included in the consent form. Content analysis will be used to analyse whether and how consent is being obtained for qualitative data sharing. Conclusions: This study will provide insight into the existing practice of sharing of qualitative data in clinical trials and the current issues and opportunities, to help shape future research and development of guidance to encourage maximum learning to be gained from this valuable data

Summaries of the Presentations at the EGALS Seminar 2017 at Katowice University, Poland

Summaries of the presentations given at the seminar of the Educational Group of Animal Law Studies

The evolution of primate short-term memory

* Correspondence should be addressed to Manuel Bohn (manyprimates@gmai l.com).Short-term memory is implicated in a range of cognitive abilities and is critical for understanding primate cognitive evolution. To investigate the effects of phylogeny, ecology and sociality on short-term memory, we tested the largest and most diverse primate sample to date (421 non-human primates across 41 species) in an experimental delayed-response task. Our results confirm previous findings that longer delays decrease memory performance across species and taxa. Our analyses demonstrate a considerable contribution of phylogeny over ecological and social factors on the distribution of short-term memory performance in primates; closely related species had more similar short-term memory abilities. Overall, individuals in the branch of Hominoidea performed better compared to Cercopithecoidea, who in turn performed above Platyrrhini and Strepsirrhini. Interdependencies between phylogeny and socioecology of a given species presented an obstacle to disentangling the effects of each of these factors on the evolution of short-term memory capacity. However, this study offers an important step forward in understanding the interspecies and individual variation in short-term memory ability by providing the first phylogenetic reconstruction of this trait’s evolutionary history. The dataset constitutes a unique resource for studying the evolution of primate cognition and the role of short-term memory in other cognitive abilities.Publisher PDFPeer reviewe

Venture Philanthropy in 2009: Developments in the Field Since Virtuous Capital

This study will examine the evolution of the field of venture philanthropy since the late 1990s and will provide an updated guide to the types of organizations utilizing venture philanthropy strategies across the United States and internationally. The purpose of this research is to investigate how the field has changed as it has matured, to identify the key players and learnings of organizations across the field, and to develop a framework for the types of organizations that have been the most successful in implementing the venture philanthropy model

The role of the co-receptor neuropilin-1 in human vascular smooth muscle cells.

Neuropilin-1 (NRP1) is a co-receptor required for neuronal and vascular development, which binds to class 3 semaphorins and VEGFs. NRP1 has been strongly implicated in VEGF-induced endothelial cell migration. VEGF has been shown to regulate vascular smooth muscle cell (VSMC) function in vitro. Evidence from mutant mice also suggests that NRP1 disruption in vivo can affect VSMC as well as endothelial function. I therefore investigated the role of NRPs in VSMC biological functions and more particularly in their migration. Western blotting showed that NRP1 and the related molecule, NRP2, were strongly expressed in human coronary artery SMC (HCASMC), whereas the major VEGF signalling receptor VEGFR2/KDR was not detectable. A high molecular weight NRP1-immunoreactive band (>250 kDa) was also strongly expressed in HCASMC, but was not detected either in cognate Human coronary artery endothelial cells (HCAEC) or in Human umbilical vein EC. The high molecular weight species was decreased significantly by treating the SMCs with chondroitinase, an enzyme that specifically chondroitin sulphate (CS) residues found in CS proteoglycan. Treatment with heparitinase, an enzymethat specifically heparan sulphate (HS) residues also resulted in a decrease of the highmolecular weight band but to a lesser extent than chondroitinase. Finally, treatment of SMC with both enzymes caused the complete disappearance of the high molecular weight species. Hence, in SMCs, in addition to the known NRP1 species at 130 kDa, NRP1 exists as a glycosaminoglycan containing either chondroitin sulphate or heparan sulphate polysaccharide chains. Mutational analysis of candidate O-linked glycosylation sites in the NRP1 extracellular domain showed that glycosylation occurred at serine 612. The importance of this gly-cosaminoglycan (GAG) modification was assessed by generating a construct of NRP1 lacking this GAG modification, called S612A. This was done by generation of an adenovirus NRP1 mutant with an alanine residue instead of the serine found in the wild-type species, however, the over-expression of the S612A NRP1 mutant in VSMC caused no signicant difference in PDGF-induced HCASMC migration. VEGF was able to bind significantly to ECs and SMCs but did not induce a significant migratory response of SMCs in contrast to PDGF-AA and PDGF-BB. PDGF-BB-induced HCASMC migration in transwell assays was inhibited by EG3287, a NRP1-specific antagonist, which blocks the ability of VEGF-A^1^6^5 to bind to NRP1. Furthermore, the migratory response to PDGF-BB was significantly decreased by siRNA-mediated knockdown of NRP1, NRP2 or a neuropilin interacting protein (NIP1 or synectin), and by pre-treatment with soluble NRP1 or NRP1 b1 domain (NRP1 VEGF binding domain). NRP1 knockdown also inhibited the migratory response to PDGF-AA. NRP1 was found to physically interact with PDGFR\alpha, but not with PDGFR\beta, as determined by co-immunoprecipitation. PDGFR\alpha, but not PDGFR\beta, phosphorylation was decreased in response to PDGF-AA and PDGF-BB when NRP1 was knocked down in HCASMC. Intracellular signalling in response to PDGF-BB stimulation was investigated in HCASMCs with NRP1 knockdown. PDGF-BB stimulated tyrosine phosphorylation of the adapter protein p130Cas, which has been stronlgy implicated in cellular and molecular processes involved in cell migration. NRP1 knockdown reduced p130Cas phosphorylation, but had little effect on signalling pathways, such as ERK1/2, Akt, cofilin, Hsp27 and FAK. To investigate the contribution of the NRP1 intracellular domain in PDGF-induced migration and signalling, I generated a NRP1 construct lacking the intracellular domain by introducing a stop codon after the transmembrane domain. Overexpression of NRP1 lacking its C-terminus in HCASMC resulted in a decrease of PDGF-induced migration and activation of phospho-p130Cas. Furthermore, p130Cas knockdown also inhibited PDGF- induced HCASMC migration, thus reinforcing the importance of p130Cas phosphorylation in NRP1-dependent cell migration. The findings that NRP1 is strongly expressed in HCASMC in a CS-GAG and a HS-GAG modified form and plays a role in the chemotactic response to PDGF-BB, highlight the possible involvement of NRPs in neotintima formation in vasculoproliferative diseases

THE EFFECTS OF LOW-VOLUME/MODERATE-INTENSITY AEROBIC TRAINING ON METABOLIC SYNDROME COMPONENTS IN MORBIDLY OBESE MINORITY ADOLESCENTS

Despite the increased prevalence of obesity and associated diseases among pediatric minorities, the intensity-specific effects of aerobic training have not been examined extensively in adolescent minorities. Fifteen morbidly obese, sedentary and insulin-resistant Black and Latino adolescents completed two-months of low-volume/moderate-intensity aerobic exercise training to examine the effects of training on three phenotypes dysregulated in obese and physically inactive states: insulin sensitivity (SI); fibrinolytic potential, as indicated by plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (t-PA) antigen levels; and chronic low-grade systemic inflammation, as indicated by C-reactive protein (CRP). In response to training, SI increased ~37% (1.00 ± 0.15 to 1.37 ± 0.26 mU.L^-1min^-1, p<0.05) and t-PA antigen levels increased ~15% (6.34 ± 0.51 to 7.32 ± 0.85 ng/mL, p<0.05). No significant changes in CRP or PAI-1 antigen were observed. Our findings demonstrate that aerobic training improves insulin sensitivity and fibrinolytic potential in morbidly obese minority adolescents