The effect of high-intensity aerobic interval training on markers of systemic inflammation in sedentary populations

© 2017, Springer-Verlag Berlin Heidelberg. Purpose: This study examined the effects of high-intensity interval training (HIIT; 30 s sprint, 4–5 min passive recovery) and prolonged intermittent sprint training (PIST; 10 s sprint, 2–3 min moderate exercise) on the systemic inflammatory markers C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α), aerobic capacity, and anthropometry in a middle-aged, sedentary population. Methods: Fifty-five sedentary adults (age 49.2 ± 6.1 years) were randomised into HIIT (n = 20), PIST (n = 21), or a sedentary control group (CTRL n = 14). HIIT and PIST performed three training sessions per week for 9 weeks on a cycle ergometer, matched for total high-intensity time, while CTRL continued normal sedentary behaviours. Pre- and post-intervention testing involved measures of anthropometry, peak oxygen consumption (VO2peak), and venous blood collection for analyses of CRP and TNF-α. Results: HIIT and PIST increased VO2peak compared to CTRL (+3.66 ± 2.23 and 3.74 ± 2.62 mL kg min−1). A group × time interaction (p = 0.042) and main effect of time (p = 0.026) were evident for waist girth, with only HIIT showing a significant reduction compared to CTRL (−2.1 ± 2.8 cm). TNF-α and CRP showed no group × time interaction or time effect (p > 0.05). Conclusions: In sedentary individuals, 9 weeks of HIIT or PIST were effective to improve aerobic capacity; however, only HIIT significantly reduced waist girth and WHR compared to CTRL. Markers of systemic inflammation remained unchanged across all groups. Accordingly, for inflammation and VO2peak, the distribution of sprints and the active or passive recovery periods are inconsequential provided that total duration of high-intensity efforts is similar

Baseline study in environmental risk assessment: Escalating need for computer models to be whole-system approach

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this record.Accepted author version posted online: 12 Dec 2016Despite landfills having the potential to pollute the environment both during their operation and long after they have ceased to receive waste, they remain a dominant waste management option, particularly in the UK. In order to combat the environmental pollution caused by landfills, risk analysis is increasingly being employed through computer models. However, for a risk analysis process to be successful, its foundation has to be well established through a baseline study. This paper aims to identify knowledge gaps in software packages regarding environmental risk assessments in general, and especially those that have been developed specifically for landfills and landfill leachate. The research establishes that there is no holistic computer model for the baseline study of landfills, which risk assessors can use to conduct risk analyses specifically for landfill leachate. This paper also describes a number of factors and features that should be added to the baseline study system in order to render it more integrated—thereby enhancing quantitative risk analysis, and subsequently environmental risk management.The authors acknowledge the financial support of Dundee City Council in this project. We are additionally grateful for the discussion and help received from Mr Peter Goldie of the Environment & Consumer Protection Department, Dundee City Council. The support from Dr I. M. Spence (Consultant Environmental Geologist, Scotland), and colleagues at the University of Abertay Dundee, including Dr Kehinde O. K. Oduyemi and Mr Phillip Jenkins is also highly 39 appreciated. It must be noted that concepts and ideas presented in this article by the authors do not necessarily represent views that of their respective employer organization

Ethyl 1-oxo-1,2,3,4-tetra­hydro-9H-carbazole-3-carboxyl­ate

The title compound, C15H15NO3, contains a carbazole skeleton with an ethoxy­carbonyl group at the 3 position. In the indole ring system, the benzene and pyrrole rings are nearly coplanar, forming a dihedral angle of 1.95 (8)°. The cyclo­hexenone ring has an envelope conformation. In the crystal structure, pairs of strong N—H⋯O hydrogen bonds link the mol­ecules into centrosymmetric dimers with R 2 2(10) ring motifs. π–π contacts between parallel pyrrole rings [centroid–centroid distance = 3.776 (2) Å] may further stabilize the structure. A weak C—H⋯π inter­action is also observed

Polysomnographic and Subjective Sleep Predictors of Alcoholic Relapse

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65219/1/j.1530-0277.1998.tb03995.x.pd

Undescended testis: 513 patients’ characteristics, age at orchidopexy and patterns of referral

10.1136/archdischild-2013-305225Archives of Disease in Childhood995401-40

TGF-beta 1 induces human alveolar epithelial to mesenchymal cell transition (EMT)

Background: Fibroblastic foci are characteristic features in lung parenchyma of patients with idiopathic pulmonary fibrosis (IPF). They comprise aggregates of mesenchymal cells which underlie sites of unresolved epithelial injury and are associated with progression of fibrosis. However, the cellular origins of these mesenchymal phenotypes remain unclear. We examined whether the potent fibrogenic cytokine TGF-β1 could induce epithelial mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and investigated the signaling pathway of TGF-β1-mediated EMT. Methods: A549 cells were examined for evidence of EMT after treatment with TGF-β1. EMT was assessed by: morphology under phase-contrast microscopy; Western analysis of cell lysates for expression of mesenchymal phenotypic markers including fibronectin EDA (Fn-EDA), and expression of epithelial phenotypic markers including E-cadherin (E-cad). Markers of fibrogenesis, including collagens and connective tissue growth factor (CTGF) were also evaluated by measuring mRNA level using RT-PCR, and protein by immunofluorescence or Western blotting. Signaling pathways for EMT were characterized by Western analysis of cell lysates using monoclonal antibodies to detect phosphorylated Erk1/2 and Smad2 after TGF-β1 treatment in the presence or absence of MEK inhibitors. The role of Smad2 in TGF-β1-mediated EMT was investigated using siRNA. Results: The data showed that TGF-β1, but not TNF-α or IL-1β, induced A549 cells with an alveolar epithelial type II cell phenotype to undergo EMT in a time-and concentration-dependent manner. The process of EMT was accompanied by morphological alteration and expression of the fibroblast phenotypic markers Fn-EDA and vimentin, concomitant with a downregulation of the epithelial phenotype marker E-cad. Furthermore, cells that had undergone EMT showed enhanced expression of markers of fibrogenesis including collagens type I and III and CTGF. MMP-2 expression was also evidenced. TGF-β1-induced EMT occurred through phosphorylation of Smad2 and was inhibited by Smad2 gene silencing; MEK inhibitors failed to attenuate either EMT-associated Smad2 phosphorylation or the observed phenotypic changes. Conclusion: Our study shows that TGF-β1 induces A549 alveolar epithelial cells to undergo EMT via Smad2 activation. Our data support the concept of EMT in lung epithelial cells, and suggest the need for further studies to investigate the phenomenon

Self-Consistent Electron-Nucleus Cusp Correction for Molecular Orbitals

We describe a method for imposing the correct electron-nucleus (e-n) cusp in molecular orbitals expanded as a linear combination of (cuspless) Gaussian basis functions. Enforcing the e-n cusp in trial wave functions is an important asset in quantum Monte Carlo calculations as it significantly reduces the variance of the local energy during the Monte Carlo sampling. In the method presented here, the Gaussian basis set is augmented with a small number of Slater basis functions. Note that, unlike other e-n cusp correction schemes, the presence of the Slater function is not limited to the vicinity of the nuclei. Both the coefficients of these cuspless Gaussian and cusp-correcting Slater basis functions may be self-consistently optimized by diagonalization of an orbital-dependent effective Fock operator. Illustrative examples are reported for atoms (\ce{H}, \ce{He} and \ce{Ne}) as well as for a small molecular system (\ce{BeH2}). For the simple case of the \ce{He} atom, we observe that, with respect to the cuspless version, the variance is reduced by one order of magnitude by applying our cusp-corrected scheme.Comment: 23 pages, 5 figure

Barriers and enablers to integrating maternal and child health services to antenatal care in low and middle income countries.

UNLABELLED: Antenatal care (ANC) represents a delivery platform for a broad range of health services; however, these opportunities are insufficiently utilised. This review explores key barriers and enablers for successful integration of health s"ervices with ANC in different contexts. Data from peer-reviewed and grey literature were organised using the SURE checklist. We identified 46 reports focusing on integration of HIV, tuberculosis, malaria, syphilis or nutrition services with ANC from Asia, Africa and the Pacific. Perspectives of service users and providers, social and political factors, and health system characteristics (such as resource availability and organisational structures) affected ease of integration. TWEETABLE ABSTRACT: Health system factors, context and stakeholders must be considered for integrated antenatal care services

Travel to school and housing markets: a case study of Sheffield, England

How children travel to school is at the centre of a complex set of interrelated issues with significant policy implications. This paper reviews the relation of patterns of travel to school to concerns about public health, school choice, urban form, and residential housing markets. The spatial relations between pupils’ homes and the schools that they attend provides the basis of an analytical framework that links local neighbourhood characteristics, school performance, and house prices to the distance and mode of travel to school and the level of ‘excess commuting’ in the urban system. A unique analysis of several integrated micro-datasets from Sheffield, UK, suggests that, while there are high levels of excess commuting, there remains a complex interrelationship between housing and neighbourhood characteristics, school performance, and commuting patterns. There are differences between the pictures for primary schools and secondary schools. Policies aimed at promoting transport efficiency and those promoting school choice are likely to remain in tension

ERK1/2 signaling dominates over RhoA signaling in regulating early changes in RNA expression induced by endothelin-1 in neonatal rat cardiomyocytes

Cardiomyocyte hypertrophy is associated with changes in gene expression. Extracellular signal-regulated kinases 1/2 (ERK1/2) and RhoA [activated by hypertrophic agonists (e.g. endothelin-1)] regulate gene expression and are implicated in the response, but their relative significance in regulating the cardiomyocyte transcriptome is unknown. Our aim was to establish the significance of ERK1/2 and/or RhoA in the early cardiomyocyte transcriptomic response to endothelin-1.Cardiomyocytes were exposed to endothelin-1 (1 h) with/without PD184352 (to inhibit ERK1/2) or C3 transferase (C3T, to inhibit RhoA). RNA expression was analyzed using microarrays and qPCR. ERK1/2 signaling positively regulated approximately 65% of the early gene expression response to ET-1 with a small (approximately 2%) negative effect, whereas RhoA signaling positively regulated approximately 10% of the early gene expression response to ET-1 with a greater (approximately 14%) negative contribution. Of RNAs non-responsive to endothelin-1, 66 or 448 were regulated by PD184352 or C3T, respectively, indicating that RhoA had a more significant effect on baseline RNA expression. mRNAs upregulated by endothelin-1 encoded a number of receptor ligands (e.g. Ereg, Areg, Hbegf) and transcription factors (e.g. Abra/Srf) that potentially propagate the response.ERK1/2 dominates over RhoA in the early transcriptomic response to endothelin-1. RhoA plays a major role in maintaining baseline RNA expression but, with upregulation of Abra/Srf by endothelin-1, RhoA may regulate changes in RNA expression over longer times. Our data identify ERK1/2 as a more significant node than RhoA in regulating the early stages of cardiomyocyte hypertrophy