Purpose Bayesian calibration is generally superior to standard direct-search algorithms in that it estimates the full joint posterior distribution of the calibrated parameters. However, there are many barriers to using Bayesian calibration in health decision sciences stemming from the need to program complex models in probabilistic programming languages and the associated computational burden of applying Bayesian calibration. In this paper, we propose to use artificial neural networks (ANN) as one practical solution to these challenges. Methods Bayesian Calibration using Artificial Neural Networks (BayCANN) involves (1) training an ANN metamodel on a sample of model inputs and outputs, and (2) then calibrating the trained ANN metamodel instead of the full model in a probabilistic programming language to obtain the posterior joint distribution of the calibrated parameters. We illustrate BayCANN using a colorectal cancer natural history model. We conduct a confirmatory simulation analysis by first obtaining par complexity with minor or no change to its structure. In addition, BayCANN’s efficiency can be especially useful in computationally expensive models. To facilitate BayCANN’s wider adoption, we provide BayCANN’s open-source implementation in R and Stan.The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. DX3-213B clinical trial All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.Arachidonic acid (ARA) is an important ω-6 polyunsaturated fatty acid (PUFA), and docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) and n-3 docosapentaenoic acid (n-3 DPA) are three well-known ω-3 PUFAs. These fatty acids can be metabolized into a number of bioactive lipids. Eicosanoids derived from ARA have drawn great attention because of their important and complex biofunctions. Although EPA, DHA and n-3 DPA have also shown powerful biofunctions, we have fewer studies of metabolites derived from them than those from ARA. Recently, growing research has focused on the bioaction of ω-3 PUFA-derived metabolites, which indicates their great potential for treating metabolic disorders. Most of the functional studies of these bioactive lipids focused on their anti-inflammatory effects. However, several studies elucidated their direct effects on pancreatic β cells, hepatocytes, adipocytes, skeletal muscle cells, and endothelial cells. These researches revealed the importance of studying the functions of metabolites derived from ω-3 polyunsaturated fatty acids other than themselves. The current review summarizes research into the effects of ω-3 PUFA-derived oxylipins on metabolic disorders, including diabetes, non-alcoholic fatty liver disease, adipose tissue dysfunction, and atherosclerosis.Plasma levels of protein analytes might be markers to predict and monitor the kinetics of bone and tissue remodeling, including maximization of orthodontic treatment stability. They could help predict/prevent and/or diagnose possible adverse effects such as bone dehiscences, gingival recession, or root resorption. The objective of this study was to measure plasma levels of markers of bone turnover and inflammation during orthodontic force application in a rat model of orthodontic expansion. Two different orthodontic forces for bilateral buccal expansion of the maxillary arches around second and third molars were applied in 10 rats equally distributed in low-force (LF) or conventional force (CF) groups. Four rats served as the control group. Blood samples were collected at days 0, 1, 2, 3, 6, 13, 21, and 58. Longitudinal concentrations of osteoprotegerin (OPG), soluble receptor activator of nuclear factor kappaB ligand (sRANKL), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor α (TNF), and parathyroid hormone (PTH) were determined in blood samples by a multiplex immunoassay. CF and LF resulted in a significantly maxillary skeletal expansion while the CF group demonstrated significantly higher expansion than the LF group in the long term. Bone turnover demonstrated a two-phase response. During the “early phase” (up to 6 days of force application), LF resulted in more sRANKL expression and increased sRANKL/OPG ratio than the CF and control animals. There was a parallel increase in PTH levels in the early phase in response to LF. During the “late phase” (6-58 days), the markers of bone turnover were stable in both groups. IL-4, IL-6, and IL-10 levels did not significantly change the test groups throughout the study. These results suggest that maxillary expansion in response to different orthodontic forces follows different phases of bone turnover that may be force specific.Carotid body feedback and hypoxia may serve to enhance respiratory-sympathetic nerve coupling (respSNA) and act as a driver of increased blood pressure. Using the Lewis polycystic kidney (LPK) rat model of chronic kidney disease, we examined respSNA in adult female rodents with CKD and their response to acute hypoxia or hypercapnia compared to Lewis control animals. Under urethane anesthesia, phrenic nerve activity, splanchnic sympathetic nerve activity (sSNA), and renal sympathetic nerve activity (rSNA) were recorded under baseline conditions and during mild hypoxic or hypercapnic challenges. At baseline, tonic SNA and blood pressure were greater in female LPK rats versus Lewis rats (all P 0.05). These results demonstrate that female rats with CKD exhibit heightened respSNA coupling at baseline that is further augmented by mild hypoxia, and not by hypercapnia. This mechanism may be a contributing driver of hypertension in this animal model of CKD.