The purpose of this study was to evaluate the effect of the consumption of seed oils from Vitis vinifera and Arachis hypogaea in platelet aggregation. The initial hypothesis suggested that subjects who have consumed these seed oils undergo modified platelet aggregation. This study was performed using a pre-post test design, with a control group, and double blind. The effects of the consumption of grape seed and peanut oils were measured for platelet aggregation in clinical and laboratory tests in 30 healthy subjects. In addition to this group, a control group of 4 health subjects received no treatment with oils, just 500 mg oral administration acetylsalicylic acid for 7 days. Platelet aggregation was assessed by the Born turbidimetric method, using 3 different concentrations of adenosine diphosphate as agonists (2, 54; 1, 17; and 0, 58 μM). The study subjects had very similar results; both oils were shown to have a significant reduction in platelet aggregation. Grape seed oil showed a decrease of 8.4 ± 1% in aggregation, compared with peanut oil, which decreased aggregation by 10.4 ± 1%. The control group, taking 500 mg OD aspirin for 7 days, showed a significant decrease in platelet aggregation, similar to that of oil ingestion. Each of the oils was analyzed for fatty acids, to determine which particular acids were presents in greater levels, which could explain the reduction in platelet aggregation. The oil found to be most abundant in grape seeds was linoleic acid (omega-6), and in peanuts, it was oleic acid (omega-9). However, in fact, both acids reduced platelet aggregation. Consumption of plant oils from grape seeds and peanuts had a lowering effect on platelet aggregation, in addition to containing a high content of unsaturated fatty acids. However, omega-3, omega-6, and omega-9 fatty acids were not specifically responsible for the reductions mentioned above.
Severe congenital eye malformations, particularly microphthalmia and anophthalmia, are one of the main causes of visual handicap worldwide. They can arise from multifactorial, chromosomal, or monogenic factors and can be associated with extensive clinical variability. Genetic analysis of individuals with these defects has allowed the recognition of dozens of genes whose mutations lead to disruption of normal ocular embryonic development. Recent application of next generation sequencing (NGS) techniques for genetic screening of patients with congenital eye defects has greatly improved the recognition of monogenic cases. In this study, we applied clinical exome NGS to a group of 14 Mexican patients (including 7 familial and 7 sporadic cases) with microphthalmia and/or anophthalmia. Causal or likely causal pathogenic variants were demonstrated in ~60% (8 out of 14 patients) individuals. Seven out of 8 different identified mutations occurred in well-known microphthalmia/anophthalmia genes (OTX2, VSX2, MFRP, VSX1) or in genes associated with syndromes that include ocular defects (CHD7, COL4A1) (including two instances of CHD7 pathogenic variants). A single pathogenic variant was identified in PIEZO2, a gene that was not previously associated with isolated ocular defects. NGS efficiently identified the genetic etiology of microphthalmia/anophthalmia in ~60% of cases included in this cohort, the first from Mexican origin analyzed to date. The molecular defects identified through clinical exome sequencing in this study expands the phenotypic spectra of CHD7-associated disorders and implicate PIEZO2 as a candidate gene for major eye developmental defects.
a reduction in the results for the parameters tested in patients of MS is improved by a greater consumption of dietary fiber, such as oat bran. However, additional studies are required to generate clearer recommendations.
Glycosylation is a post-translational modification that affects the stability, structure, antigenicity and charge of proteins. In the immune system, glycosylation is involved in the regulation of ligand–receptor interactions, such as in B-cell and T-cell activating receptors. Alterations in glycosylation have been described in several autoimmune diseases, such as systemic lupus erythematosus (SLE), in which alterations have been found mainly in the glycosylation of B lymphocytes, T lymphocytes and immunoglobulins. In immunoglobulin G of lupus patients, a decrease in galactosylation, sialylation, and nucleotide fucose, as well as an increase in the N-acetylglucosamine bisector, are observed. These changes in glycoisolation affect the interactions of immunoglobulins with Fc receptors and are associated with pericarditis, proteinuria, nephritis, and the presence of antinuclear antibodies. In T cells, alterations have been described in the glycosylation of receptors involved in activation, such as the T cell receptor; these changes affect the affinity with their ligands and modulate the binding to endogenous lectins such as galectins. In T cells from lupus patients, a decrease in galectin 1 binding is observed, which could favor activation and reduce apoptosis. Furthermore, these alterations in glycosylation correlate with disease activity and clinical manifestations, and thus have potential use as biomarkers. In this review, we summarize findings on glycosylation alterations in SLE and how they relate to immune system defects and their clinical manifestations.
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