Relationship of Cellular Adhesion Molecules and Stress Hormones in Obese Males Following Exercise

The development of atherosclerosis is associated with a steady accumulation of inflammatory molecules. Exercise-induced hormones such as cortisol and catecholamines (epinephrine and norepinephrine) may play a role in endothelial inflammation. Methods: Fifteen obese (BMI \u3e 30 kg/m2) sedentary (less than 2 days per week of physical activity) male volunteers, the ages between 18 and30, participated in the study. The participants performed a single bout of cycling exercise (average energy expenditure ~ 300 kcal) at two different intensities in random order [low-intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate]. Overnight fasting blood samples were collected at baseline, immediate post-exercise (IPE), 1-hr PE, and 24-hr PE for each intensity of exercise to determine the responses of soluble cell adhesion molecules [intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and E-selectin (sE-selectin)] and exercise-induced stress hormones. Data were analyzed by an analysis of variance with repeated measures along with the Bonferroni multiple comparisons. The linear regression analysis was used to examine the interaction between exercise-induced hormones and vascular inflammation markers (p \u3c .05). RESULTS: There exhibited no significant change in sICAM-1, sVCAM-1, E or NE, while sE-selectin at 1-hr PE (10.25±1.07 ng/mL) significantly decreased (p = .045) from baseline (12.22±1.39 ng/mL). COR at IPE (262.12±31.09 ng/ml) was significantly higher (p = .001) than 1-hr PE (189.35±31.11 ng/ml) during high-intensity exercise. In contrast, COR at IPE (187.52±31.09 ng/ml, p = .009) and 1-hr PE (156.24±31.11 ng/ml, p = .001) were significantly lower than baseline (259.75±23.07 ng/ml) during low-intensity exercise. COR and sICAM-1 had a negative relationship at 1-hr PE during low-intensity exercise (r2 = .34, p = .02), whereas COR and sVCAM-1 had a positive relationship at IPE during high-intensity exercise (r2 = .36, p = .02). CONCLUSION: sE-selectin was favorably reduced following exercise, and changes in cortisol were exercise-intensity dependent. Although sICAM-1 and sVCAM-1 did not significantly change following exercise, a significant interaction between cortisol and these cell adhesion molecules suggests that cortisol is one of the responsible exercise-induced hormones that may be associated with cell adhesion molecule metabolism

Mycelial effects on phage retention during transport in a microfluidic platform

Phages (i.e., viruses that infect bacteria) have been considered as good tracers for the hydrological transport of colloids and (pathogenic) viruses. However, little is known about interactions of phages with (fungal) mycelia as the prevalent soil microbial biomass. Forming extensive and dense networks, mycelia provide significant surfaces for phage–hyphal interactions. Here, for the first time, we quantified the mycelial retention of phages in a microfluidic platform that allowed for defined fluid exchange around hyphae. Two common lytic tracer phages (Escherichia coli phage T4 and marine phage PSA-HS2) and two mycelia of differing surface properties (Coprinopsis cinerea and Pythium ultimum) were employed. Phage–hyphal interaction energies were approximated by the extended Derjaguin–Landau–Verwey–Overbeek (XDLVO) approach of colloidal interaction. Our data show initial hyphal retention of phages of up to ≈4 × 107 plaque-forming unit (PFU) mm–2 (≈2550 PFU mm–2 s–1) with a retention efficiency depending on the hyphal and, to a lesser extent, the phage surface properties. Experimental data were supported by XDLVO calculations, which revealed the highest attractive forces for the interaction between hydrophobic T4 phages and hydrophobic C. cinerea surfaces. Our data suggest that mycelia may be relevant for the retention of phages in the subsurface and need to be considered in subsurface phage tracer studies. Mycelia–phage interactions may further be exploited for the development of novel strategies to reduce or hinder the transport of undesirable (bio) colloidal entities in environmental filter systems

Responses of Matrix Metalloproteinases in Obese Men after Undergoing Low and High Intensity Exercise

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that degrade extracellular matrix proteins and play a role in various pathological conditions such as inflammation and endothelial dysfunction. PURPOSE: The current study investigated the responses of MMP-1, -2, and -9 in obese men over a 24-hour period after undergoing different intensities (low vs. high) of cycling exercise. METHODS: Fifteen sedentary (physical activity \u3c 2 days/week) obese [body mass index (BMI) \u3e 30kg/m2] men between the ages of 18 and 30 years participated in the study. Each participant completed a similar volume (average energy expenditure ~ 300 kcal) of cycling exercise at 2 different intensities in random order [low intensity: 50% of maximal heart rate and high-intensity: 80% of maximal heart rate] on a separate occasion. Fasting overnight blood samples were collected at baseline, immediate post exercise (IPE), 1-hour post exercise (1-PE), and 24-hours post exercise (24-PE) for each exercise intensity trial to examine the responses of MMP-1, -2, and -9. An analysis of variance (ANOVA) with repeated measures was used to determine the mean differences in intensity and time on MMP-1, -2, and -9. If necessary, the Sidak’s multiple pairwise comparisons and a follow-up Simple effects test were employed as a post-hot test (p \u3c 0.05). RESULTS: No change was found in MMP-1 following either low- or high-intensity exercise over the 24-hr period. During the low-intensity exercise trial, MMP-2 at 24-hr PE (72.68±6.43 ng/mL) was significantly lower than IPE (87.23±8.02 ng/mL, p=0.008) and 1-hr PE (92.01±7.99 ng/mL, p=0.011). During the high-intensity exercise trial, MMP-9 at IPE (54.19±9.16 ng/mL) was significantly higher than PRE (30.48±5.86 ng/mL, p =0.008), 1-hr PE (34.82±5.08 ng/mL, p=0.040), and 24-hr PE (31.03±4.82 ng/mL, p=0.006). Additionally, MMP-9 at 24-hr PE (31.32±4.82 ng/mL) was significantly lower than PRE (41.43±5.86 ng/mL, p=0.009) during the low-intensity exercise trial. CONCLUSION: Both MMP-2 and -9, but not MMP-1, significantly increased immediately following exercise, which then returned to its baseline values post exercise. This exercise-induced acute change in MMP-2 and MMP-9 was dependent upon exercise intensity since MMP-2 changed with low-intensity exercise, whereas MMP-9 was altered following high-intensity exercise. Additionally, MMP-9 at 24 hours decreased after 24 hours following low intensity exercise. Thus, the current study suggests that the responses of MMP-2 and MMP-9 to exercise are dependent on exercise-intensity, and low-intensity exercise may favorably influence cardiovascular health by lowering both MMP-2 and MMP-9 in obese men

SensorWeb 3G: Extending On-Orbit Sensor Capabilities to Enable Near Realtime User Configurability

This research effort prototypes an implementation of a standard interface, Web Coverage Processing Service (WCPS), which is an Open Geospatial Consortium(OGC) standard, to enable users to define, test, upload and execute algorithms for on-orbit sensor systems. The user is able to customize on-orbit data products that result from raw data streaming from an instrument. This extends the SensorWeb 2.0 concept that was developed under a previous Advanced Information System Technology (AIST) effort in which web services wrap sensors and a standardized Extensible Markup Language (XML) based scripting workflow language orchestrates processing steps across multiple domains. SensorWeb 3G extends the concept by providing the user controls into the flight software modules associated with on-orbit sensor and thus provides a degree of flexibility which does not presently exist. The successful demonstrations to date will be presented, which includes a realistic HyspIRI decadal mission testbed. Furthermore, benchmarks that were run will also be presented along with future demonstration and benchmark tests planned. Finally, we conclude with implications for the future and how this concept dovetails into efforts to develop "cloud computing" methods and standards

Solar UV Doses of Young Americans and Vitamin D3 Production

Background: Sunlight contains ultraviolet B (UVB) radiation (290–315 nm) that affects human health in both detrimental (skin cancers) and beneficial (vitamin D3) ways. Serum 25-hydroxyvitamin D concentrations from young Americans (≤ 19 years) show that many have deficient (< 50 nmol/L, 20 ng/mL) or insufficient (< 75 nmol/L, 30 ng/mL) vitamin D levels, indicating that they are not getting enough sun exposure. Those findings are in conflict with some calculated, published values that suggest people make “ample” vitamin D3 (~ 1,000 IU/day) from their “casual,” or everyday, outdoor exposures even if they diligently use sunscreens with sun protection factor (SPF) 15

Dynamic modelling of electrooptically modulated vertical compound cavity surface emitting semiconductor lasers

A generalized rate equation model is used to simulate the interrelated amplitude and frequency modulation properties of Electrooptically Modulated Vertical Compound Cavity Surface Emitting Semiconductor Lasers in both large and small signal modulation regimes. It is shown that the photon lifetime in the modulator subcavity provides the ultimate limit for the 3 dB modulation cutoff frequency. It is shown that there is an optimum design (number of periods) of both the intermediate and top multistack reflectors to maximise the large-signal modulation quality

The association of circulating amylin with β-amyloid in familial Alzheimer's disease.

INTRODUCTION: This study assessed the hypothesis that circulating human amylin (amyloid-forming) cross-seeds with amyloid beta (Aβ) in early Alzheimer's disease (AD). METHODS: Evidence of amylin-AD pathology interaction was tested in brains of 31 familial AD mutation carriers and 20 cognitively unaffected individuals, in cerebrospinal fluid (CSF) (98 diseased and 117 control samples) and in genetic databases. For functional testing, we genetically manipulated amylin secretion in APP/PS1 and non-APP/PS1 rats. RESULTS: Amylin-Aβ cross-seeding was identified in AD brains. High CSF amylin levels were associated with decreased CSF Aβ42 concentrations. AD risk and amylin gene are not correlated. Suppressed amylin secretion protected APP/PS1 rats against AD-associated effects. In contrast, hypersecretion or intravenous injection of human amylin in APP/PS1 rats exacerbated AD-like pathology through disruption of CSF-brain Aβ exchange and amylin-Aβ cross-seeding. DISCUSSION: These findings strengthened the hypothesis of circulating amylin-AD interaction and suggest that modulation of blood amylin levels may alter Aβ-related pathology/symptoms

Turing learning: : A metric-free approach to inferring behavior and its application to swarms

We propose Turing Learning, a novel system identification method for inferring the behavior of natural or artificial systems. Turing Learning simultaneously optimizes two populations of computer programs, one representing models of the behavior of the system under investigation, and the other representing classifiers. By observing the behavior of the system as well as the behaviors produced by the models, two sets of data samples are obtained. The classifiers are rewarded for discriminating between these two sets, that is, for correctly categorizing data samples as either genuine or counterfeit. Conversely, the models are rewarded for 'tricking' the classifiers into categorizing their data samples as genuine. Unlike other methods for system identification, Turing Learning does not require predefined metrics to quantify the difference between the system and its models. We present two case studies with swarms of simulated robots and prove that the underlying behaviors cannot be inferred by a metric-based system identification method. By contrast, Turing Learning infers the behaviors with high accuracy. It also produces a useful by-product - the classifiers - that can be used to detect abnormal behavior in the swarm. Moreover, we show that Turing Learning also successfully infers the behavior of physical robot swarms. The results show that collective behaviors can be directly inferred from motion trajectories of individuals in the swarm, which may have significant implications for the study of animal collectives. Furthermore, Turing Learning could prove useful whenever a behavior is not easily characterizable using metrics, making it suitable for a wide range of applications.Comment: camera-ready versio

Host-Detrimental Role of Esx-1-Mediated Inflammasome Activation in Mycobacterial Infection

The Esx-1 (type VII) secretion system is a major virulence determinant of pathogenic mycobacteria, including Mycobacterium marinum. However, the molecular events and host-pathogen interactions underlying Esx-1-mediated virulence in vivo remain unclear. Here we address this problem in a non-lethal mouse model of M. marinum infection that allows detailed quantitative analysis of disease progression. M. marinum established local infection in mouse tails, with Esx-1-dependent formation of caseating granulomas similar to those formed in human tuberculosis, and bone deterioration reminiscent of skeletal tuberculosis. Analysis of tails infected with wild type or Esx-1-deficient bacteria showed that Esx-1 enhanced generation of proinflammatory cytokines, including the secreted form of IL-1β, suggesting that Esx-1 promotes inflammasome activation in vivo. In vitro experiments indicated that Esx-1-dependent inflammasome activation required the host NLRP3 and ASC proteins. Infection of wild type and ASC-deficient mice demonstrated that Esx-1-dependent inflammasome activation exacerbated disease without restricting bacterial growth, indicating a host-detrimental role of this inflammatory pathway in mycobacterial infection. These findings define an immunoregulatory role for Esx-1 in a specific host-pathogen interaction in vivo, and indicate that the Esx-1 secretion system promotes disease and inflammation through its ability to activate the inflammasome

Phagosomal Rupture by Mycobacterium tuberculosis Results in Toxicity and Host Cell Death

Survival within macrophages is a central feature of Mycobacterium tuberculosis pathogenesis. Despite significant advances in identifying new immunological parameters associated with mycobacterial disease, some basic questions on the intracellular fate of the causative agent of human tuberculosis in antigen-presenting cells are still under debate. To get novel insights into this matter, we used a single-cell fluorescence resonance energy transfer (FRET)-based method to investigate the potential cytosolic access of M. tuberculosis and the resulting cellular consequences in an unbiased, quantitative way. Analysis of thousands of THP-1 macrophages infected with selected wild-type or mutant strains of the M. tuberculosis complex unambiguously showed that M. tuberculosis induced a change in the FRET signal after 3 to 4 days of infection, indicating phagolysosomal rupture and cytosolic access. These effects were not seen for the strains M. tuberculosisΔRD1 or BCG, both lacking the ESX-1 secreted protein ESAT-6, which reportedly shows membrane-lysing properties. Complementation of these strains with the ESX-1 secretion system of M. tuberculosis restored the ability to cause phagolysosomal rupture. In addition, control experiments with the fish pathogen Mycobacterium marinum showed phagolysosomal translocation only for ESX-1 intact strains, further validating our experimental approach. Most importantly, for M. tuberculosis as well as for M. marinum we observed that phagolysosomal rupture was followed by necrotic cell death of the infected macrophages, whereas ESX-1 deletion- or truncation-mutants that remained enclosed within phagolysosomal compartments did not induce such cytotoxicity. Hence, we provide a novel mechanism how ESX-1 competent, virulent M. tuberculosis and M. marinum strains induce host cell death and thereby escape innate host defenses and favor their spread to new cells. In this respect, our results also open new research directions in relation with the extracellular localization of M. tuberculosis inside necrotic lesions that can now be tackled from a completely new perspective