Ask about this productRelated genes to: GALE Blocking Peptide
- Gene:
- GALE NIH gene
- Name:
- UDP-galactose-4-epimerase
- Previous symbol:
- -
- Synonyms:
- SDR1E1
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: GALE Blocking Peptide
Related articles to: GALE Blocking Peptide
- Heart failure (HF) is a common sequela of type 2 diabetes (diabetes), and models have been developed for its prediction. We aimed to synthesize the available evidence by performing a systematic review and meta-analysis of models predicting incident HF and HF hospitalization (HFH) in individuals with diabetes. - Source: PubMed
Publication date: 2026/05/10
Mircescu AlexandraAllan WilliamHaris MohammadHurdus BenHelbitz AnnaGinks WilliamWu JianhuaSattar NaveedPetrie Mark CAjjan RamziNadarajah RameshGale Chris P - Good communication is vital to high-quality care for adults with learning disabilities in long-term care settings, influencing their health and well-being. Evidence on how best to support their communication needs is limited. - Source: PubMed
Publication date: 2026/04/27
Bauer AnnetteGaczkowska InezGale-St Ives ElisabethDixon KateHatton ChrisHoekstra RosaKnapp MartinLeadbitter KathyMikulak MagdalenaRatti VictoriaSlonims VickyTuudah ElizabethBusk MaryQuazi PerveenWilliams AlanBradshaw Jill - Artificial intelligence algorithms have been developed to support clinicians in diagnosing fractures, with the intention to improve the diagnostic accuracy of clinicians reviewing X-rays. The purpose of this rapid early value assessment was to identify the existing evidence base for the technology and to assess whether there was a prima facie case for the technology to represent positive outcomes for patients and a value-for-money investment for people in the National Health Service. - Source: PubMed
Farmer CarolineCoelho HelenMuthukumar MadhusubramanianRobinson SophieMeertens RobertUkoumunne Obioha CSanto ValGale NiamhEvans Jonathan TEvans Jonathan PLowe JennyMelendez-Torres G JWilson Edward Cf - differentiation of human pluripotent stem cells into pancreatic islet organoids (SC-islets) is critical for widespread diabetes therapy but remains limited by incomplete control of cell fate specification. Despite significant insights gained from single-cell sequencing technologies, the field lacks a predictive framework to resolve cell fate specification and infer the regulatory determinants of lineage trajectories. Here, we report an integrated digital twin of pancreatic islet differentiation constructed from temporal multi-omic data spanning development. This predictive engine resolves lineage trajectories and defines cell-state-specific regulatory networks across differentiation. Analysis of over 1,000 transcription factor perturbations identifies the key candidate regulators of key developmental branch points, including previously unrecognized drivers of lineage specification. Prospective perturbation experiments validate model-predicted regulators of lineage specification, establishing causal inference of cell fate decisions. We describe a predictive digital twin that enables causal inference of cell fate decisions and provides a foundation for improving SC-islet biomanufacturing and therapeutic development. - Source: PubMed
Publication date: 2026/04/30
Sanchez-Castro Enrique EIshahak MatthewLe TaiMaestas Marlie MHernandez-Rincon Diana CMukherjee NoyonikaBradley KameronLu JamesGale Sarah EMillman Jeffrey R - We evaluated how much cardiorespiratory fitness (CRF)-related genetics contribute to the risk of common noncommunicable diseases (NCDs) and mortality, and whether individuals with different levels of CRF and genetic predispositions differ in health characteristics. We used a validated SBayesR-based genome-wide polygenic score, leveraging information from 905 707 single-nucleotide polymorphisms, to measure CRF genetics (PGS CRF). Associations with register-based incident NCDs and mortality were analyzed using Cox proportional hazards models in the FinnGen cohort (N = 262 137; 53.5-years at baseline, 52.0% women) and replicated in the HUNT3 cohort (N = 26 115; 59.0-years, 52.4% women). In HUNT3, we also compared the health characteristics of individuals having age- and sex-specific high or low CRF (V̇O), and high or low PGS CRF (N = 1316). PGS CRF was negatively associated with any CVD (hazard ratio [HR] 0.99, 95% confidence interval 0.98-1.00), ischemic heart diseases (HR 0.98, 0.97-0.99), hypertensive diseases (HR 0.99, 0.97-1.00), stroke (HR 0.98, 0.97-1.00), lung cancer (HR 0.95, 0.92-0.97), chronic lower respiratory disease (HR 0.98, 0.97-0.99), chronic obstructive pulmonary disease (HR 0.97, 0.95-0.99), type 2 diabetes (T2D) (HR 0.96, 0.95-0.97), and all-cause mortality (HR 0.98, 0.97-0.99), per each standard deviation increase in PGS. Replication analyses supported the association with T2D. No differences in health characteristics were observed by genetic predisposition to CRF, while those with high V̇O had a healthier profile in comparison to those with low V̇O. The genome-wide PGS explains only a fraction of the CRF phenotype, yet some small associations were observed, particularly for T2D incidence. - Source: PubMed
Joensuu LLukander VHerranen PTynkkynen N PKujala ULopéz-Bueno RNordeidet A NKlevjer MØvretveit KWisløff UBye AEkelund UOllikainen M Sillanpää E