Microalgae biomass as an additional ingredient of gluten-free bread: Dough rheology, texture quality and nutritional properties

Microalgae have been widely used as a source of functional ingredients such as pigments, antioxidants, vitamins, and omega-3 polyunsaturated fatty acids. They also represent a promising alternative source of protein. The objective of this study was to evaluate the impact of the addition of two green microalgae species (Nannochloropsis gaditana L2 and Chlamydomonas sp. EL5) on the techno-functional and nutritional properties of gluten-free bread. Microalgae biomass was added in the amounts of 1.0 and 3.0 g/100 g of flour. The behavior of the dough during the mixing as well as the physicochemical properties of the prepared breads were investigated. Gluten-free bread with N. gaditana L2 and Chlamydomonas sp. EL5 presented significantly higher protein and higher levels of lipids and ash, compared with the control bread. The incorporation of 3% microalgae biomass revealed a 100% increase in iron and calcium contents. The fatty acid profile of supplemented bread changed in a species-specific manner with a particular increase in linolenic acid (18:3 ω3) and a decrease in ω3/ω6 ratio. Besides, due to its original biochemical composition, mainly the highly protein content, microalgae incorporation was found to bring an overall structuring effect on the gluten-free bread texture. However, the dough mixing properties were not affected significantly by microalgae addition. A significant change in color was recorded in doughs, breads, crusts and crumbs. This was caused by the presence of pigment in microalgae biomass, which turned into more intense green-yellow tonalities. A sensory analysis revealed that the supplemented breads scored highest for nearly all the sensory parameters with the 3% N. gaditana L2 bread as the preferred one in terms of global appreciation. This innovative approach gives new insights of the possibility of improving gluten-free products, structurally and nutritionally, using only microalgae as a natural and a sustainable food ingredientinfo:eu-repo/semantics/publishedVersio

The Causal Cascade to Multiple Sclerosis: A Model for MS Pathogenesis

BACKGROUND: MS pathogenesis seems to involve both genetic susceptibility and environmental risk factors. Three sequential factors are implicated in the environmental risk. The first acts near birth, the second acts during childhood, and the third acts long thereafter. Two candidate factors (vitamin D deficiency and Epstein-Barr viral infection) seem well suited to the first two environmental events. METHODOLOGY/PRINCIPAL FINDINGS: A mathematical Model for MS pathogenesis is developed, incorporating these environmental and genetic factors into a causal scheme that can explain some of the recent changes in MS-epidemiology (e.g., increasing disease prevalence, a changing sex-ratio, and regional variations in monozygotic twin concordance rates). CONCLUSIONS/SIGNIFICANCE: This Model suggests that genetic susceptibility is overwhelmingly the most important determinant of MS pathogenesis. Indeed, over 99% of individuals seem genetically incapable of developing MS, regardless of what environmental exposures they experience. Nevertheless, the contribution of specific genes to MS-susceptibility seems only modest. Thus, despite HLA DRB1*1501 being the most consistently identified genetic marker of MS-susceptibility (being present in over 50% of northern MS patient populations), only about 1% of individuals with this allele are even genetically susceptible to getting MS. Moreover, because genetic susceptibility seems so similar throughout North America and Europe, environmental differences principally determine the regional variations in disease characteristics. Additionally, despite 75% of MS-patients being women, men are 60% more likely to be genetically-susceptible than women. Also, men develop MS at lower levels of environmental exposure than women. Nevertheless, women are more responsive to the recent changes in environmental-exposure (whatever these have been). This explains both the changing sex-ratio and the increasing disease prevalence (which has increased by a minimum of 32% in Canada over the past 35 years). As noted, environmental risk seems to result from three sequential components of environmental exposure. The potential importance of this Model for MS pathogenesis is that, if correct, a therapeutic strategy, designed to interrupt one or more of these sequential factors, has the potential to markedly reduce or eliminate disease prevalence in the future

Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas

Pituitary adenomas are associated with a variety of clinical manifestations resulting from excessive hormone secretion and tumor mass effects, and require a multidisciplinary management approach. This article discusses the treatment modalities for the management of patients with a prolactinoma, Cushing's disease and acromegaly, and summarizes the options for medical therapy in these patients

Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy

Selective inhibition of the BCR-ABL tyrosine kinase by imatinib (STI571, Glivec/Gleevec) is a promising new therapeutic strategy in patients with chronic myelogenous leukemia (CML). Despite significant hematologic and cytogenetic responses, resistance occurs, particularly in patients with advanced disease. We sought to determine the underlying mechanisms. Sixty-six patients with CML in myeloid blast crisis (n = 33), lymphoid blast crisis (n = 2), accelerated phase (n = 16), chronic phase (n = 13), and BCR-ABL-positive acute lymphoblastic leukemia (n = 2) resistant to imatinib were investigated. Median duration of imatinib therapy was 148 days (range 6-882). Patients were evaluated for genomic amplification of BCR-ABL, overexpression of BCR-ABL transcripts, clonal karyotypic evolution, and mutations of the imatinib binding site in the BCR-ABL tyrosine kinase domain. Results were as follows: (1) Median levels of BCR-ABL transcripts, were not significantly changed at the time of resistance but 7/55 patients showed a >10-fold increase in BCR-ABL levels; (2) genomic amplification of BCR-ABL was found in 2/32 patients evaluated by fluorescence in situ hybridization; (3) additional chromosomal aberrations were observed in 19/36 patients; (4) point mutations of the ABL tyrosine kinase domain resulting in reactivation of the BCR-ABL tyrosine kinase were detected in 23/66 patients. In conclusion, although the heterogeneous development of imatinib resistance is challenging, the fact that BCR-ABL is active in many resistant patients suggests that the chimeric oncoprotein remains a good therapeutic target. However, patients with clonal evolution are more likely to have BCR-ABL-independent mechanisms of resistance. The observations warrant trials combining imatinib with other agents