Activity

3 and 99.7%, respectively), autoaggregation (93.2%), cell surface hydrophobicity (50.0%), and bacterial adherence with Vero cells (75.8% of the control Lactiplantibacillusplantarum FM03-1). This B. siamensis ML122-2 is a promising probiotic to be used in the food industry and seems to have potential antibacterial properties relevant for the treatment of antibiotic-resistant infections.The aim of this study was to investigate the effects of formulation factors, sea salt (SS), dry sourdough (SD) and fermented sugar (FS) as sodium chloride replacers in wheat flour on dough mixing, extension, pasting and fermentation rheological properties, evaluated by Farinograph, Extensograph, Amylograph and Rheofermentometer devices. With regard to mixing and extension properties, SS and FS presented a strengthening effect, whereas SD presented a weakening one. SS and FS presented a positive effect on dough stability, energy and resistance, whereas SD presented a negative one. On the Amylograph, peak viscosity increased by SS and FS addition and decreased when SD was incorporated in the dough recipe. During fermentation, dough development and gas production in the dough system increased after SS and SD addition, whereas they decreased after FS addition. Response surface methodology (RSM) was used to investigate the effect of independent variables on the rheological properties of the dough. Mathematical models between the independent variables, SS, SD and FS, and the dependent variables, represented by the rheological values of the dough, were obtained. The best formulation obtained was of 0.30 g/100 g SS, 0.50 g/100 g SD and 1.02 mL/100 g FS addition with a 0.618 desirability value, following Derringer’s desirability function approach. For this formulation, bread quality characteristics were better appreciated than for those obtained for the control sample, in which 1.5% NaCl was incorporated in wheat flour.A diverse and dynamic microbial community (known as microbiota) resides within the pig gastrointestinal tract (GIT). The microbiota contributes to host health and performance by mediating nutrient metabolism, stimulating the immune system, and providing colonization resistance against pathogens. Manipulation of gut microbiota to enhance growth performance and disease resilience in pigs has recently become an active area of research in an era defined by increasing scrutiny of antimicrobial use in swine production. In order to develop microbiota-targeted strategies, or to identify potential next-generation probiotic strains originating from the endogenous members of GIT microbiota in pigs, it is necessary to understand the role of key commensal members in host health. Many, though not all, correlative studies have associated members of the genus Prevotella with positive outcomes in pig production, including growth performance and immune response; therefore, a comprehensive review of the genus in the context of pig production is needed. In the present review, we summarize the current state of knowledge about the genus Prevotella in the intestinal microbial community of pigs, including relevant information from other animal species that provide mechanistic insights, and identify gaps in knowledge that must be addressed before development of Prevotella species as next-generation probiotics can be supported.Atopic dermatitis (AD) is a common chronic inflammatory skin disease that exhibits a complex interplay of skin barrier disruption and immune dysregulation. Patients with AD are susceptible to cutaneous infections that may progress to complications, including staphylococcal septicemia. Although most studies have focused on filaggrin mutations, the physical barrier and antimicrobial barrier also play critical roles in the pathogenesis of AD. Within the physical barrier, the stratum corneum and tight junctions play the most important roles. selleck inhibitor The tight junction barrier is involved in the pathogenesis of AD, as structural and functional defects in tight junctions not only disrupt the physical barrier but also contribute to immunological impairments. Furthermore, antimicrobial peptides, such as LL-37, human b-defensins, and S100A7, improve tight junction barrier function. Recent studies elucidating the pathogenesis of AD have led to the development of barrier repair therapy for skin barrier defects in patients with this disease. This review analyzes the association between skin barrier disruption in patients with AD and antimicrobial peptides to determine the effect of these peptides on skin barrier repair and to consider employing antimicrobial peptides in barrier repair strategies as an additional approach for AD management.The ATP-binding cassette transporter A1 (ABCA1) is a membrane-bound exporter protein involved in regulating serum HDL level by exporting cholesterol and phospholipids to load up in lipid-poor ApoA-I and ApoE, which allows the formation of nascent HDL. Mutations in the ABCA1 gene, when presents in both alleles, disrupt the canonical function of ABCA1, which associates with many disorders related to lipid transport. Although many studies have reported the phenotypic effects of a large number of ABCA1 variants, the pathological effect of non-synonymous polymorphisms (nsSNPs) in ABCA1 remains elusive. Therefore, aiming at exploring the structural and functional consequences of nsSNPs in ABCA1, in this study, we employed an integrated computational approach consisting of nine well-known in silico tools to identify damaging SNPs and molecular dynamics (MD) simulation to get insights into the magnitudes of the damaging effects. In silico tools revealed four nsSNPs as being most deleterious, where the two SNPs (G1050V and S1067C) are identified as the highly conserved and functional disrupting mutations located in the NBD1 domain. MD simulation suggested that both SNPs, G1050V and S1067C, changed the overall structural flexibility and dynamics of NBD1, and induced substantial alteration in the structural organization of ATP binding site. Taken together, these findings direct future studies to get more insights into the role of these variants in the loss of the ABCA1 function.