Food Addiction Screening, Diagnosis and Treatment: A Protocol for Residential Treatment of Eating Disorders, Substance Use Disorders and Trauma-Related Psychiatric Comorbidity.

Food addiction, or ultra-processed food addiction (UPFA), has emerged as a reliable and validated clinical entity that is especially common in individuals seeking treatment for eating disorders (EDs), substance use disorders (SUDs) and co-occurring psychiatric disorders (including mood, anxiety and trauma-related disorders). The clinical science of UPFA has relied on the development and proven reliability of the Yale Food Addiction Scale (YFAS), or subsequent versions, e.g., the modified YFAS 2.0 (mYFAS2.0), as well as neurobiological advances in understanding hedonic eating. Despite its emergence as a valid and reliable clinical entity with important clinical implications, the best treatment approaches remain elusive. To address this gap, we have developed and described a standardized assessment and treatment protocol for patients being treated in a residential program serving patients with psychiatric multi-morbidity. Patients who meet mYFAS2.0 criteria are offered one of three possible approaches: (1) treatment as usual (TAU), using standard ED treatment dietary approaches; (2) harm reduction (HR), offering support in decreasing consumption of all UPFs or particular identified UPFs; and (3) abstinence-based (AB), offering support in abstaining completely from UPFs or particular UPFs. Changes in mYFAS2.0 scores and other clinical measures of common psychiatric comorbidities are compared between admission and discharge.

Modeling kinetics of a large-scale fed-batch CHO cell culture by Markov chain Monte Carlo method.

Markov chain Monte Carlo (MCMC) method was applied to model kinetics of a fed-batch Chinese hamster ovary cell culture process in 5,000-L bioreactors. The kinetic model consists of six differential equations, which describe dynamics of viable cell density and concentrations of glucose, glutamine, ammonia, lactate, and the antibody fusion protein B1 (B1). The kinetic model has 18 parameters, six of which were calculated from the cell culture data, whereas the other 12 were estimated from a training data set that comprised of seven cell culture runs using a MCMC method. The model was confirmed in two validation data sets that represented a perturbation of the cell culture condition. The agreement between the predicted and measured values of both validation data sets may indicate high reliability of the model estimates. The kinetic model uniquely incorporated the ammonia removal and the exponential function of B1 protein concentration. The model indicated that ammonia and lactate play critical roles in cell growth and that low concentrations of glucose (0.17 mM) and glutamine (0.09 mM) in the cell culture medium may help reduce ammonia and lactate production. The model demonstrated that 83% of the glucose consumed was used for cell maintenance during the late phase of the cell cultures, whereas the maintenance coefficient for glutamine was negligible. Finally, the kinetic model suggests that it is critical for B1 production to sustain a high number of viable cells. The MCMC methodology may be a useful tool for modeling kinetics of a fed-batch mammalian cell culture process.

Medium osmolarity and pericellular matrix development improves chondrocyte survival when photoencapsulated in poly(ethylene glycol) hydrogels at low densities.

The ability to encapsulate cells over a range of cell densities is important toward mimicking cell densities of native tissues and rationally designing strategies where cell source and/or cell numbers are clinically limited. Our preliminary findings demonstrate that survival of freshly isolated adult bovine chondrocytes dramatically decreases when photoencapsulated in poly(ethylene glycol) hydrogels at low densities (4 million cells/mL). During enzymatic digestion of cartilage, chondrocytes undergo a harsh change in their microenvironment. We hypothesize that the absence of exogenous antioxidants, the hyposmotic environment, and the loss of a protective pericellular matrix (PCM) increase chondrocytes' susceptibility to free radical damage during photoencapsulation. Incorporation of antioxidants and serum into the encapsulation medium improved cell survival twofold compared to phosphate-buffered saline. Increasing medium osmolarity from 330 to 400 mOsm (physiological) improved cell survival by 40% and resulted in approximately 2-fold increase in adenosine triphosphate (ATP) production 24 h postencapsulation. However, cell survival was only temporary. Allowing cells to reproduce some PCM before photoencapsulation in 400 mOsm medium resulted in superior cell survival during and postencapsulation for up to 15 days. In summary, the combination of antioxidants, physiological osmolarity, and the development of some PCM result in an improved robustness against free radical damage during photoencapsulation.