The methanation of CO2 is of great interest in power-to-gas systems and contributes to the mitigation of climate change through carbon dioxide capture and the subsequent production of high value-added products. This study investigated CO2 methanation with three Ni catalysts supported on Al2O3 and ZrO2, which were simulated using a mathematical model of a packed bed reactor designed based on their chemical kinetics reported in the literature. The simulated reactive system was fed with syngas obtained from residual coffee pulp, obtained after solvent phytochemical extraction process, under several gasification conditions. The results reflect a high incidence of catalyst support, preparation method, and syngas composition on CO2 conversion and CH4 selectivity. For all the syngas compositions, Ni/ZrO2 catalysts show the best values for CO2 conversion and CH4 selectivity for Ni/Al2O3 catalyst.

Purpose: To identify factors linked with nutritional risk via the Malnutrition Universal Screening Tool scale assessment among critically ill patients from a hospital in Cali (Colombia). Materials and methods: A retrospective, analytical observational study was conducted with patients admitted to an intensive care unit (ICU). Sociodemographic, clinical, hematological, and biochemical parameters were analyzed, as well as their association with nutritional risk and patient mortality. Binary logistic regression was applied to outline nutritional risk. Results: Overall, 28.4% prevalence of elevated nutritional risk was observed. An association was found between nutritional risk and hemoglobin and hematocrit values, primary diseases accounting for ICU admission, gastrointestinal symptoms, and nutritional support route (p < 0.05). Mortality was 11.6% and it was correlated with nutritional risk, hemoglobin, and blood urea nitrogen. Conclusions: Gastrointestinal symptoms and the type of nutritional support received during hospitalization may increase nutritional risk, whereas polycythemia was a protective factor. We found an associative model to determine nutritional risk with high specificity and an adequate diagnostic validity index.

Nemaline myopathy (NM) is one of the most common forms of congenital myopathy and it is identified by the presence of "nemaline bodies" (rods) in muscle fibers by histopathological exam-ination. The most common forms of NM are caused by mutations in the ACTA1 (Actin Alpha 1) and NEB (Nebulin) genes. Clinical features include hypotonia and muscle weakness. Unfortunate-ly, there is no curative treatment and the pathogenetic mechanisms remains unclear. In this man-uscript, we examined the pathophysiological alterations in NM using dermal fibroblasts derived from patients with mutations in ACTA1 and NEB genes. Patients’ fibroblasts were stained with rhodamine phalloidin to analyze the polymerization of actin filaments by fluorescence microsco-py. We found that patients' fibroblasts showed incorrect actin filament polymerization compared to control fibroblasts. Actin filament polymerization defects was associated with mitochondrial dysfunction. Furthermore, we identified two mitochondrial boosting compounds, linoleic acid (LA) and L-carnitine (LCAR), that improved the formation of actin filaments in mutant fibro-blasts and corrected mitochondrial bioenergetics. Our results indicate that cellular models can be useful to study the pathophysiological mechanisms involved in NM and to find new potential therapies. Furthermore, targeting mitochondrial dysfunction with LA and LCAR can revert the pathological alterations in NM cellular models.

The term neurodegeneration with brain iron accumulation (NBIA) brings together a broad set of progressive and disabling neurological genetic disorders in which iron is deposited preferentially in certain areas of the brain. Among NBIA disorders, the most frequent subtype is pantothenate kinase-associated neurodegeneration (PKAN) caused by pathologic variants in the PANK2 gene codifying the enzyme pantothenate kinase 2 (PANK2). Nowadays, there are no effective treatments to stop the progression of these diseases. This review discusses the utility of patient-derived cell models as a valuable tool for the identification of commercial pharmacological or natural compounds for implementing polytarget precision medicine in PKAN. In the last years, several studies have described that PKAN patient-derived fibroblasts manifest the main pathological changes associated with the disease including intracellular iron overload. Interestingly, treatment of mutant cell cultures with various supplements such as pantothenate, pantethine, thiamine, L-carnitine, vitamin E, omega 3, and -lipoic acid improved all pathophysiological alterations in PKAN fibroblasts with residual expression of the PANK2 enzyme. The information provided by pharmacological screenings in patient-derived cellular models can help to optimize therapeutic strategies in individual PKAN patients.