Results 61 to 70 of about 3,211,899 (373)
From omics to AI—mapping the pathogenic pathways in type 2 diabetes
FEBS Letters, EarlyView.Integrating multi‐omics data with AI‐based modelling (unsupervised and supervised machine learning) identify optimal patient clusters, informing AI‐driven accurate risk stratification. Digital twins simulate individual trajectories in real time, guiding precision medicine by matching patients to targeted therapies.
Siobhán O'Sullivan +2 more
wiley +1 more source
Urine Complement Proteins and the Risk of Kidney Disease Progression and Mortality in Type 2 Diabetes. [PDF]
, 2018 ObjectiveWe examined the association of urine complement proteins with progression to end-stage renal disease (ESRD) or death in people with type 2 diabetes and proteinuric diabetic kidney disease (DKD).Research design and methodsUsing targeted mass ...
Afkarian, Maryam +6 more
core +1 more source
SUBSTITUTING COMPLEMENTS [PDF]
Journal of Competition Law & Economics, 2006 The presence of multiple sellers in the provision of (nonsubstitutable) complementary goods leads to outcomes that are worse than those generated by a monopoly (with a vertically integrated production of complements), a problem known in the economic literature as complementary oligopoly and recently popularized in the legal literature as the tragedy of
PARISI, FRANCESCO, G. Dari Mattiacci
openaire +5 more sources
ERBIN limits epithelial cell plasticity via suppression of TGF‐β signaling
FEBS Letters, EarlyView.In breast and lung cancer patients, low ERBIN expression correlates with poor clinical outcomes. Here, we show that ERBIN inhibits TGF‐β‐induced epithelial‐to‐mesenchymal transition in NMuMG breast and A549 lung adenocarcinoma cell lines. ERBIN suppresses TGF‐β/SMAD signaling and reduces TGF‐β‐induced ERK phosphorylation.
Chao Li +3 more
wiley +1 more source
WormBook, 2005 Mutations in many genes can result in a similar phenotype. Finding a number of mutants with the same phenotype tells you little about how many genes you are dealing with, and how mutable those genes are until you can assign those mutations to genetic loci. The genetic assay for gene assignment is called the complementation test.
openaire +2 more sources
Current Biology, 1998 Work in the authors' laboratories is supported by grants from the Arthritis and Rheumatism Council and the Wellcome Trust.
Marina Botto +2 more
openaire +3 more sources
FEBS Letters, EarlyView.Knowing how proteases recognise preferred substrates facilitates matching proteases to applications. The S1′ pocket of protease EA1 directs cleavage to the N‐terminal side of hydrophobic residues, particularly leucine. The S1′ pocket of thermolysin differs from EA's at only one position (leucine in place of phenylalanine), which decreases cleavage ...
Grant R. Broomfield +3 more
wiley +1 more source
Correction to: Immunological features of patients affected by Barraquer-Simons syndrome
Orphanet Journal of Rare Diseases, 2020 Following the publication of the original article [1], the authors have requested to amend the Abstract and Discussion section as follows.
Fernando Corvillo +13 more
doaj +1 more source
COMPLEMENT-MEDIATED ADIPOCYTE LYSIS BY NEPHRITIC FACTOR SERA [PDF]
, 1993 Recent data indicate a previously unsuspected link between the complement system and adipocyte biology. Murine adipocytes produce key components of the alternative pathway of complement and are able to activate this pathway.
Lachmann, PJ +4 more
core +1 more source
FEBS Letters, EarlyView.Spinal muscular atrophy (SMA) is a genetic disease affecting motor neurons. Individuals with SMA experience mitochondrial dysfunction and oxidative stress. The aim of the study was to investigate the effect of an antioxidant and neuroprotective substance, ergothioneine (ERGO), on an SMNΔ7 mouse model of SMA.
Francesca Cadile +8 more
wiley +1 more source