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Anaerobic digestion processes can be improved by engineering the addition of other organic wastes of different compositions to the feedstock. This paper presents an integrated model to determine the optimal ratio of such additions once the practical characteristics and hydrolysis kinetics of each feedstock are known. Several model nodes were built in an integrated manner around the International Water Association Anaerobic Digestion Model Number 1, (IWA-ADM1) using the Matlab-Simulink simulation platform. Transformer model nodes were developed to estimate the waste fractions of carbohydrates, proteins and lipids to generate a detailed input for ADM1. Hydrolysis nodes were modeled separately for each feedstock. The fluxes from the hydrolysis nodes were combined and generated a detailed input vector to the 1WAADM 1. The integrated model was applied to a co-digestion case study of diluted dairy manure and kitchen wastes. The integrated model implementation lead to an improved simulation speed that made it feasible to run calibration and optimization of this case study. The integrated model was used to calibrate the hydrolysis kinetics of each waste and particulate fractions using bench scale experiments. An optimization case study based on 100 steady state simulations determined the operational limits for maximum methane production. For the tested waste concentrations, the optimum retention time was 10 days with an optimal kitchen waste to diluted manure ratio of 755%. [ABSTRACT FROM AUTHOR]

The adipocyte-derived hormone adiponectin promotes insulin sensitivity and anti-atherogenic effects. Serum adiponectin levels are low in obese, insulin-resistant individuals but high in lean states such as caloric restriction (CR) or anorexia nervosa. Indeed, despite being produced exclusively by adipose tissue, serum adiponectin inversely correlates with % body fat. The basis for this so-called 'adiponectin paradox' is yet to be resolved. The discovery of adiponectin preceded our current understanding of white adipose tissue (WAT) as a major endocrine organ. In contrast, research has largely neglected another adipose depot: bone marrow adipose tissue (MAT). In humans MAT accounts for ≤ 70% of marrow volume and, in contrast to WAT, MAT increases in states of leanness such as CR or anorexia nervosa. Moreover, pharmacological agents such as thiazolidinediones or fibroblast growth factor-21 increase marrow adiposity. Notably, each of these conditions is also associated with increased serum adiponectin. Based on these observations, we investigated the hypothesis that MAT is a major source of serum adiponectin. To do so, we first isolated WAT and MAT from rabbits, mice and humans. Rabbits were sedated by i.m. injection of ketamine (40 mg/kg) and xylazine (5 mg/kg) before euthanising by i.v. injection of pentobarbital (65 mg/kg); mice were euthanised by CO2 asphyxiation followed by cervical dislocation; and human tissues were obtained with consent from patients undergoing lower-limb amputation. Immunoblotting of tissue lysates revealed that, in rabbits (n = 9) and mice (n = 6), adiponectin expression is markedly higher in MAT than in WAT. Although this was not consistently observed in human tissues (n = 7), human MAT had increased expression of Ero1-Lα, a protein chaperone that promotes adiponectin secretion. Indeed, adiponectin secretion from cultured MAT explants was far higher than that from WAT explants of rabbits (n = 9) or humans (n = 4), as assessed by immunoblotting. We next investigated if blocking MAT formation affects serum adiponectin levels. To do so we used Ocn-Wnt10b mice, in which the antiadipogenic effector Wnt10b is transgenically expressed in bone. Expression of adiponectin mRNA in WAT did not differ between Ocn-Wnt10b (1.00 ± 0.21; n = 10) and control mice (0.91 ± 0.11; n = 10); however, Ocn-Wnt10b mice resisted increases in MAT and serum adiponectin with CR. Moreover, we found that, in mice (n = 24), total serum adiponectin negatively correlates with WAT mass (R² = 0.441; P = 0.031) but positively correlates with MAT volume (R² = 0.524; P = 0.009). In summary, our observations support the hypothesis that MAT expansion is required for increased serum adiponectin with CR, suggesting that MAT may be a major source of serum adiponectin. Thus, adiponectin production from MAT may account, at least in part, for the adiponectin paradox. [ABSTRACT FROM AUTHOR]