Ocean Acidification Impairs Foraging Behavior by Interfering With Olfactory Neural Signal Transduction in Black Sea Bream, Acanthopagrus schlegelii

In recent years, ocean acidification (OA) caused by oceanic absorption of anthropogenic carbon dioxide (CO2) has drawn worldwide concern over its physiological and ecological effects on marine organisms. However, the behavioral impacts of OA and especially the underlying physiological mechanisms causing these impacts are still poorly understood in marine species. Therefore, in the present study, the effects of elevated pCO2 on foraging behavior, in vivo contents of two important neurotransmitters, and the expression of genes encoding key modulatory enzymes from the olfactory transduction pathway were investigated in the larval black sea bream. The results showed that larval sea breams (length of 4.71 ± 0.45 cm) reared in pCO2 acidified seawater (pH at 7.8 and 7.4) for 15 days tend to stall longer at their acclimated zone and swim with a significant slower velocity in a more zigzag manner toward food source, thereby taking twice the amount of time than control (pH at 8.1) to reach the food source. These findings indicate that the foraging behavior of the sea bream was significantly impaired by ocean acidification. In addition, compared to a control, significant reductions in the in vivo contents of γ-aminobutyric acid (GABA) and Acetylcholine (ACh) were detected in ocean acidification-treated sea breams. Furthermore, in the acidified experiment groups, the expression of genes encoding positive regulators, the olfaction-specific G protein (Golf) and the G-protein signaling 2 (RGS2) and negative regulators, the G protein-coupled receptor kinase (GRK) and arrestin in the olfactory transduction pathway were found to be significantly suppressed and up-regulated, respectively. Changes in neurotransmitter content and expression of olfactory transduction related genes indicate a significant disruptive effect caused by OA on olfactory neural signal transduction, which might reveal the underlying cause of the hampered foraging behavior

Seawater carbonate chemistry and foraging behavior of Acanthopagrus schlegelii

In recent years, ocean acidification (OA) caused by oceanic absorption of anthropogenic carbon dioxide (CO2) has drawn worldwide concern over its physiological and ecological effects on marine organisms. However, the behavioral impacts of OA and especially the underlying physiological mechanisms causing these impacts are still poorly understood in marine species. Therefore, in the present study, the effects of elevated pCO2 on foraging behavior, in vivo contents of two important neurotransmitters, and the expression of genes encoding key modulatory enzymes from the olfactory transduction pathway were investigated in the larval black sea bream. The results showed that larval sea breams (length of 4.71 +- 0.45 cm) reared in pCO2 acidified seawater (pH at 7.8 and 7.4) for 15 days tend to stall longer at their acclimated zone and swim with a significant slower velocity in a more zigzag manner toward food source, thereby taking twice the amount of time than control (pH at 8.1) to reach the food source. These findings indicate that the foraging behavior of the sea bream was significantly impaired by ocean acidification. In addition, compared to a control, significant reductions in the in vivo contents of gama-aminobutyric acid (GABA) and Acetylcholine (ACh) were detected in ocean acidification-treated sea breams. Furthermore, in the acidified experiment groups, the expression of genes encoding positive regulators, the olfaction-specific G protein (Golf) and the G-protein signaling 2 (RGS2) and negative regulators, the G protein-coupled receptor kinase (GRK) and arrestin in the olfactory transduction pathway were found to be significantly suppressed and up-regulated, respectively. Changes in neurotransmitter content and expression of olfactory transduction related genes indicate a significant disruptive effect caused by OA on olfactory neural signal transduction, which might reveal the underlying cause of the hampered foraging behavior

Simulation of left heart-arterial system using electronic model

Conference Name:2012 International Conference on Advances in Mechanics Engineering, ICAME 2012. Conference Address: Hong kong. Time:August 3, 2012 - August 5, 2012.An analog circuit model of the left heart-arterial coupling system has been designed to study the behavior of the left heart-arterial system. Then the state variable method was used to analyze the circuit model and establish the mathematical model. We use Matlab/Simullink tool to simulate the mathematical model. Some important parameters of the left heart circulation system, such as left ventricular (LV) pressure, left atrium pressure, aortic pressure, aortic flow, LV end-diastolic volume and end-systolic volume, can be obtained. The results are matched the actual physiological, which suggests that the model presented in this paper provides a useful tool to investigate the functional status of left heart-arterial system. 漏 (2012) Trans Tech Publications, Switzerland

CONSTITUTIVE MODELING AND FINITE ELEMENT ANALYSIS OF MYXOMATOUS MITRAL LEAFLET TISSUE

National Natural Science Foundation of China [61102137, 61271336]; Natural Science Foundation of Fujian Province [2011J01366]Although rarely discussed, material modeling of the myxomatous leaflet is considered as the cornerstone of mitral valve finite element analysis. The present study presents an incompressible, hyperelastic constitutive model to characterize myxoid mitral leaflet tissue mechanics. The model incorporates the transversely isotropic response and the layered structure of the tissue. First, an analytical constitutive model for the tissue is developed based on continuum mechanics and layered composites theory. Second, the material constants of the constitutive equation are determined by fitting the model to the experimental data. The analytical material model is then implemented using solid finite element methods by simulating a biaxial tensile test. A numerical simulation of the out-of-plane pressure loading is also conducted. Both the analytical outcomes and the simulated results agree well with experimental data and show good mutual agreement. The calculated strain distribution of the out-of-plane pressure loading simulation indicates myxoid leaflets exhibit enhanced extensibility and decreased stiffness compared to normal valves; the radial direction is more extensible than the circumferential direction. The presented material approximation is able to capture the myxomatous mitral leaflet mechanics. The results of the numerical simulation conform to those of the experimental tests

Noninvasive right ventricular work in patients with atrial septal defects: a proof-of-concept study

Abstract Background Noninvasive right ventricular (RV) myocardial work (RVMW) determined by echocardiography is a novel indicator used to estimate RV systolic function. To date, the feasibility of using RVMW has not been verified in assessing RV function in patients with atrial septal defect (ASD). Methods Noninvasive RVMW was analysed in 29 ASD patients (median age, 49 years; 21% male) and 29 age- and sex-matched individuals without cardiovascular disease. The ASD patients underwent echocardiography and right heart catheterization (RHC) within 24 h. Results The RV global work index (RVGWI), RV global constructive work (RVGCW), and RV global wasted work (RVGWW) were significantly higher in the ASD patients than in the controls, while there was no significant difference in RV global work efficiency (RVGWE). RV global longitudinal strain (RV GLS), RVGWI, RVGCW, and RVGWW demonstrated significant correlations with RHC-derived stroke volume (SV) and SV index. The RVGWI (area under receiver operating characteristic curve [AUC] = 0.895), RVGCW (AUC = 0.922), and RVGWW (AUC = 0.870) could be considered good predictors of ASD and were superior to RV GLS (AUC = 0.656). Conclusion The RVGWI, RVGCW, and RVGWW could be used to assess RV systolic function and are correlated with RHC-derived SV and SV index in patients with ASD. Graphical Abstrac

Effects of SIRT1 activator SRT1720 on the expression and/or release of SIRT1, IL-1β and TNF-α in RAW264.7 cell culture treated with 30 mM high glucose.

<p>(A-D) RAW264.7 cells were pretreated with 1 μM SRT1720 for 6h and then cultured in 30 mM D-glucose-containing medium for additional 8h. Cells were then harvested and used for western blot analysis for SIRT1protein level (A, <i>df</i> = 5, <i>f</i> = 53.307, <i>p</i> < 0.001), and real-time PCR analysis for <i>SIRT1</i> (B, <i>df</i> = 5, <i>f</i> = 16.042, <i>p</i> = 0.002), <i>IL-1β</i> (C, <i>df</i> = 5, <i>f</i> = 328.474, <i>p</i> < 0.001) or <i>TNF-α</i> mRNA level (D, <i>df</i> = 5, <i>f</i> = 43.581, <i>p</i> < 0.001). Each data point is the mean ± SEM of <i>n</i> = 3 and normalized against corresponding β-ACTIN protien level or <i>GAPDH</i> mRNA level with the value in NG without SRT1720 group arbitrarily set as 1. (E-F) The culture medium was also collected and used for ELISA for detecting the release of IL-1β (E, <i>df</i> = 5, <i>f</i> = 5739.982, <i>p</i> < 0.001) and TNF-α (F, <i>df</i> = 5, <i>f</i> = 108.365, <i>p</i> < 0.001). Each data point is the mean ± SEM of <i>n</i> = 3. *<i>p</i> < 0.05; ***<i>p</i> < 0.001. 30 mM of D-mannitol served as an osmotic control. ‘NG’, 5.6 mM normal glucose; ‘HG’, 30 mM high glucose; ‘DM’, 30 mM D-mannitol.</p

Assessment of the mRNA level and the release of IL-1β and TNF-α in RAW264.7 cell culture treated with 30 mM high glucose over time.

<p>(A-B) RAW264.7 cells were exposed to 30 mM D-glucose and cultured for indicated time periods of 0, 4, 8, 24, 36 and 48h. The mRNA levels of two inflammatory cytokines, IL-1β (A, <i>df</i> = 5, <i>f</i> = 62.812, <i>p</i> < 0.001) and TNF-α (B, <i>df</i> = 5, <i>f</i> = 5.492, <i>p</i> = 0.03), were assessed by real-time PCR. Each data point is the mean ± SEM of <i>n</i> = 3 and normalized against corresponding <i>GAPDH</i> mRNA level with the value at 0h arbitrarily set as 1. (C-D) The release of IL-1β (C, <i>df</i> = 5, <i>f</i> = 27.324, <i>p</i> < 0.001) and TNF-α (D, <i>df</i> = 5, <i>f</i> = 48.74, <i>p</i> < 0.001) in culture medium was assessed by ELISA. Each data point is the mean ± SEM of <i>n</i> = 3. *<i>p</i> < 0.05; **<i>p</i> < 0.01; ***<i>p</i> < 0.001.</p