11 research outputs found
A new Aura virus isolate in Brazil shows segment duplication in the variable region of the nsP3 gene
Epidermolysis bullosa and the partnership with autoimmunity: what should we assimilate?
Bullous skin diseases are characterized by genetic abnormalities related to structural epidermal proteins or organ-specific autoantibodies against the same proteins and are revealed by blister formation on skin or mucous membranes, with differences in blister depth, morphology, and topography. Both inherited and autoimmune forms of these disorders can be framed in the context of epidermolysis bullosa. Their clinical spectrum varies from early lethal to mild variants with normal life expectancy, and several distinct phenotypes differ for age of onset, extent, location and depth of skin and mucous lesions, or scarring severity. Recently, different inflammatory processes blended with autoimmune phenomena have been demonstrated in both inherited and acquired epidermolysis bullosa, revealing that this overlapping might cause substantial implications in terms of disease course and outcome. Although several associations between epidermolysis bullosa in its different variants and autoimmune diseases have been reported, it is not yet completely clear how it happens and why this association occurs in only some patients. Autoantibodies are the primary cause of the disease in acquired epidermolysis bullosa, whereas they can be produced as a secondary event due to genetically determined skin damage in inherited epidermolysis bullosa, contributing significantly to the worsening of the disease. The awareness of this overlap may help in identifying new therapeutic approaches with immunosuppressive drugs that could have a significant impact in terms of prognosis
Urinary metabolomic profiling to identify biomarkers of a flavonoid-rich and flavonoid-poor fruits and vegetables diet: the FLAVURS trial in adults: the FLAVURS trial
The present study aims to investigate the dose
dependent effects of consuming diets enriched in flavonoid-rich
and flavonoid-poor fruits and vegetables on the urine
metabolome of adults who had a C1.5 fold increased risk of
cardiovascular diseases. A single-blind, dose-dependent,
parallel randomized controlled dietary intervention was conducted
where volunteers (n = 126) were randomly assigned
to one of three diets: high flavonoid diet, low flavonoid diet or
habitual diet as a control for 18 weeks. High resolution LC–
MS untargeted metabolomics with minimal sample cleanup
was performed using an Orbitrap mass spectrometer. Putative
biomarkers which characterize diets with high and low flavonoid
content were selected by state-of-the-art data analysis
strategies and identified by HR-MS and HR-MS/MS assays.
Discrimination between diets was observed by application of
two linear mixedmodels: one including a diet-time interaction
effect and the second containing only a time effect. Valerolactones,
phenolic acids and their derivatives were among
sixteen biomarkers related to the high flavonoid dietary
exposure. Four biomarkers related to the low flavonoid diet
belonged to the family of phenolic acids. For the first time
abscisic acid glucuronide was reported as a biomarker after a
dietary intake, however its origins have to be examined by
future hypothesis driven experiments using a more targeted
approach. This metabolomic analysis has identified a number
of dose dependent urinary biomarkers (i.e. proline betaine or
iberin-N-acetyl cysteine), which can be used in future observation
and intervention studies to assess flavonoids and nonflavonoid
phenolic intakes and compliance to fruit and
vegetable intervention