Expression of hepatocyte growth factor-like protein in human wound tissue and its biological functionality in human keratinocytes

Hepatocyte growth factor-like protein (HGFl) and its receptor, Recepteur d'Origine Nantais (RON), have been implicated in the development of wound chronicity. HGFl and RON expression was detected in acute wound tissue, chronic wound tissue and in normal skin using quantitative polymerase chain reaction (Q-PCR). HGFl and RON expression was also assessed in chronic healing and chronic non-healing wound tissues using Q-PCR and immunohistochemical staining. Expression was similarly detected in the HaCaT immortalized human keratinocyte cell line using reverse transcription polymerase chain reaction (RT-PCR). rhHGFl was used to assess the impact of this molecule on HaCaT cell functionality using in vitro growth assays and electric cell-substrate impendence sensing (ECIS) migration assays. HGFl and RON transcript expression were significantly increased in acute wound tissue compared to chronic wound tissue and were also elevated, though non-significantly, in comparison to normal skin. Minimal expression was seen in both healing and non-healing chronic wounds. Treatment of HaCaT cells with rhHGFl had no effect on growth rates but did enhance cell migration. This effect was abolished by the addition of a phospholipase C gamma (PLCγ) small molecule inhibitor. The increased expression of HGFl and RON in acute, healing wounds and the pro-migratory effect of HGFl in an in vitro human keratinocyte model, may indicate a role for HGFl in active wound healing

Mechanization of a High Aspect Ratio Wing for Aerodynamic Control

Investigations are conducted to mechanize a controlled spanwise-varying airfoil camber change for a high aspect ratio wing, resulting in optimized aerodynamic performance for a aircraft that changes weight by 50% over its mission. Mechanisms to achieve these shape changes are designed based on two separate design methodologies: a rigid body kinematics approach and a compliant mechanism approach. A framework for optimizing mechanisms based on each approach is presented. Differences between the approaches are illustrated through the design of a mechanism for a specific set of airfoil shapes. Mechanisms are evaluated based on the error in the shapes and on the energy efficiency of the systems

A comparison of commercial light-emitting diode baited suction traps for surveillance of Culicoides in northern Europe

BACKGROUND: The response of Culicoides biting midges (Diptera: Ceratopogonidae) to artificial light sources has led to the use of light-suction traps in surveillance programmes. Recent integration of light emitting diodes (LED) in traps improves flexibility in trapping through reduced power requirements and also allows the wavelength of light used for trapping to be customized. This study investigates the responses of Culicoides to LED light-suction traps emitting different wavelengths of light to make recommendations for use in surveillance. METHODS: The abundance and diversity of Culicoides collected using commercially available traps fitted with Light Emitting Diode (LED) platforms emitting ultraviolet (UV) (390 nm wavelength), blue (430 nm), green (570 nm), yellow (590 nm), red (660 nm) or white light (425 nm – 750 nm with peaks at 450 nm and 580 nm) were compared. A Centre for Disease Control (CDC) UV light-suction trap was also included within the experimental design which was fitted with a 4 watt UV tube (320-420 nm). Generalised linear models with negative binomial error structure and log-link function were used to compare trap abundance according to LED colour, meteorological conditions and seasonality. RESULTS: The experiment was conducted over 49 nights with 42,766 Culicoides caught in 329 collections. Culicoides obsoletus Meigen and Culicoides scoticus Downes and Kettle responded indiscriminately to all wavelengths of LED used with the exception of red which was significantly less attractive. In contrast, Culicoides dewulfi Goetghebuer and Culicoides pulicaris Linnaeus were found in significantly greater numbers in the green LED trap than in the UV LED trap. The LED traps collected significantly fewer Culicoides than the standard CDC UV light-suction trap. CONCLUSIONS: Catches of Culicoides were reduced in LED traps when compared to the standard CDC UV trap, however, their reduced power requirement and small size fulfils a requirement for trapping in logistically challenging areas or where many traps are deployed at a single site. Future work should combine light wavelengths to improve trapping sensitivity and potentially enable direct comparisons with collections from hosts, although this may ultimately require different forms of baits to be developed. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13071-015-0846-x) contains supplementary material, which is available to authorized users

Using digital health technologies to understand the association between movement behaviors and interstitial glucose: Exploratory analysis

© Andrew P Kingsnorth, Maxine E Whelan, James P Sanders, Lauren B Sherar, Dale W Esliger. Background: Acute reductions in postprandial glucose excursions because of movement behaviors have been demonstrated in experimental studies but less so in free-living settings. Objective: The objective of this study was to explore the nature of the acute stimulus-response model between accelerometer-assessed physical activity, sedentary time, and glucose variability over 13 days in nondiabetic adults. Methods: This study measured physical activity, sedentary time, and interstitial glucose continuously over 13 days in 29 participants (mean age in years: 44.9 [SD 9.1]; female: 59%, 17/29; white: 90%, 26/29; mean body mass index: 25.3 [SD 4.1] ) as part of the Sensing Interstitial Glucose to Nudge Active Lifestyles (SIGNAL) research program. Daily minutes spent sedentary, in light activity, and moderate to vigorous physical activity were associated with daily mean glucose, SD of glucose, and mean amplitude of glycemic excursions (MAGE) using generalized estimating equations. Results: After adjustment for covariates, sedentary time in minutes was positively associated with a higher daily mean glucose (mmol/L; beta=0.0007; 95% CI 0.00030-0.00103; P < .001), SD of glucose (mmol/L; beta=0.0006; 95% CI 0.00037-0.00081; P < .001), and MAGE (mmol/L; beta=0.002; 95% CI 0.00131-0.00273; P < .001) for those of a lower fitness. Additionally, light activity was inversely associated with mean glucose (mmol/L; beta=−0.0004; 95% CI −0.00078 to −0.00006; P=.02), SD of glucose (mmol/L; beta=−0.0006; 95% CI −0.00085 to −0.00039; P < .001), and MAGE (mmol/L; beta=−0.002; 95% CI −0.00285 to −0.00146; P < .001) for those of a lower fitness. Moderate to vigorous physical activity was only inversely associated with mean glucose (mmol/L; beta=−0.002; 95% CI −0.00250 to −0.00058; P=.002). Conclusions: Evidence of an acute stimulus-response model was observed between sedentary time, physical activity, and glucose variability in low fitness individuals, with sedentary time and light activity conferring the most consistent changes in glucose variability. Further work is required to investigate the coupling of movement behaviors and glucose responses in larger samples and whether providing these rich data sources as feedback could induce lifestyle behavior change

Effects of Lab Technician Administered vs. Subject Administered Resistance on Wingate Performance

Graduate Applie

Vascular endothelial growth inhibitor in human cancer (Review)

Vascular endothelial growth inhibitor (VEGI), also known as tumour necrosis factor superfamily member 15 (TNFSF15) and TNF ligand related molecule 1 (TL1), is a recently identified anti-angiogenic cytokine that belongs to the TNF superfamily. Three isoforms of VEGI, VEGI 174, 192, and 251 have been documented, all sharing 151 common C-terminal amino acids but differing in their N-terminal regions. The investigations into the biological functions of VEGI have pointed to a potential cancer inhibitory role for the cytokine. The inhibitory effects of VEGI on cancer are manifested in three main areas, the direct effect on cancer cells, the anti-angiogenic effects on endothelial cells, and stimulation of maturation of dendric cells. The clinical aspect of VEGI in cancer is also being explored in recent years. The present article overviews the recent progress on this molecule and discusses the value of VEGI as a potential therapeutic target in cancer therapy

Aberrant expression and function of death receptor-3 and death decoy receptor-3 in human cancer

Death receptor-3 (DR3) and death decoy receptor-3 (DcR3) are both members of the tumour necrosis factor receptor (TNFR) superfamily. The TNFR superfamily contains eight death domain-containing receptors, including TNFR1 (also called DR1), Fas (also called DR2), DR3, DR4, DR5, DR6, NGFR and EDAR. Upon the binding of these receptors with their corresponding ligands, the death domain recruits various proteins that mediate both the death and proliferation of cells. Receptor function is negatively regulated by decoy receptors (DcR1, DcR2, DcR3 and OPG). DR3/DcR3 are a pair of positive and negative players with which vascular endothelial growth inhibitor (VEGI) interacts. VEGI has been suggested to be a potential tumour suppressor. The inhibitory effects of VEGI on cancer are manifested in three main areas: a direct effect on cancer cells, an anti-angiogenic effect on endothelial cells, and the stimulation of dendritic cell maturation. A recent study indicated that DR3 may be a new receptor for E-selectin, which has been reported to be associated with cancer metastasis. DcR3 is a soluble receptor, highly expressed in various tumours, which lacks an apparent transmembrane segment, prevents cytokine response through ligand binding and neutralization, and is an inhibitor of apoptosis. DcR3 serves as a decoy receptor for FasL, LIGHT and VEGI. The cytokine LIGHT activates various anti-tumour functions and is expected to be a promising candidate for cancer therapy. Certain tumours may escape FasL-dependent immune-cytotoxic attack by expressing DcR3, which blocks FasL function. DR3/DcR3 play profound roles in regulating cell death and proliferation in cancer. The present review briefly discusses DR3/DcR3 and attempts to elucidate the role of these negative and positive players in cancer

Lightweight Formal Methods for Improving Software Security

This research examines how software specifications could be used to build more-secure software. For this project, we analyzed known vulnerabilities for open source projects to identify the corrective actions required to patch the vulnerability. For each vulnerability, we then augmented the program with formal assertions in an attempt to allow a static analysis tool to find the vulnerability. Using the information gathered from these assertions, we hope to determine which assertions are most effective at finding vulnerabilities with today\u27s tools and evaluate new assertions that could be added to the static analysis tool to help uncover more vulnerabilities. My work focuses on a common vulnerability type across multiple projects. In particular, I am examining if vulnerabilities caused by missing authentication could be prevented with proper tool usage

Knockdown of human antigen R reduces the growth and invasion of breast cancer cells in vitro and affects expression of cyclin D1 and MMP-9

HuR, a ubiquitously expressed member of the Hu family, selectively binds and stabilizes ARE-containing mRNAs encoding proto-oncogenes, cell cycle regulators, cytokines and growth factors. The role of HuR and its cellular function in breast cancer remains unclear. This study aimed to provide new insights into the implication of HuR in breast cancer. We show that MCF7 and MDA-MB-231 breast cancer cells stably transfected with a hammerhead ribozyme transgene specifically targeted to HuR (MCF7HuRKO and MDA-MB-231HuRKO) have reduced HuR expression both at mRNA and protein levels. This study reveals that HuR knockdown dramatically reduced cell growth in MCF7 cells (P<0.001) and invasive properties in MDA-MB-231 cells (P<0.001). Furthermore, we report that the decreased cell growth rate in MCF7 cells is seen together with a reduction in cyclin D1 transcript and protein levels and that the change in invasiveness in MDA-MB-231 cells seems to be linked with decreased MMP-9 levels. Our study shows that targeting HuR can influence breast cancer cell growth and invasion and suggests a role for HuR in vitro in enhancing breast cancer cell growth and invasion. These changes may be facilitated through changes in the levels of cyclin D1 and MMP-9