Two Weeks Versus One Week of Maximal Patient-Intensivist Continuity for Adult Medical Intensive Care Patients: A Two-Center Target Trial Emulation.

Objectives: To compare outcomes for 2 weeks vs. 1 week of maximal patient-intensivist continuity in the ICU.

Design: Retrospective cohort study.

Comparative HPLC-DAD-ESI-QTOF/MS/MS Analysis of Bioactive Phenolic Compounds Content in the Methanolic Extracts from Flowering Herbs of Species and Their Free Radical Scavenging and Antimicrobial Activities.

Comparative analysis of flavonoids and phenolic acids composition, in plants of six species of from family Lamiaceae was carried out. The 70% () methanolic extracts of flowering herbs of Cerv. ex Lag.

Delivery of Nucleotide Sugars to the Mammalian Golgi: A Very Well (un)Explained Story.

Nucleotide sugars (NSs) serve as substrates for glycosylation reactions. The majority of these compounds are synthesized in the cytoplasm, whereas glycosylation occurs in the endoplasmic reticulum (ER) and Golgi lumens, where catalytic domains of glycosyltransferases (GTs) are located. Therefore, translocation of NS across the organelle membranes is a prerequisite.

SLC35A2 Deficiency Promotes an Epithelial-to-Mesenchymal Transition-like Phenotype in Madin-Darby Canine Kidney Cells.

In mammalian cells, SLC35A2 delivers UDP-galactose for galactosylation reactions that take place predominantly in the Golgi lumen. Mutations in the corresponding gene cause a subtype of a congenital disorder of glycosylation (SLC35A2-CDG). Although more and more patients are diagnosed with SLC35A2-CDG, the link between defective galactosylation and disease symptoms is not fully understood.

Incorporation of fucose into glycans independent of the GDP-fucose transporter SLC35C1 preferentially utilizes salvaged over de novo GDP-fucose.

Mutations in the SLC35C1 gene encoding the Golgi GDP-fucose transporter are known to cause leukocyte adhesion deficiency II. However, improvement of fucosylation in leukocyte adhesion deficiency II patients treated with exogenous fucose suggests the existence of an SLC35C1-independent route of GDP-fucose transport, which remains a mystery. To investigate this phenomenon, we developed and characterized a human cell-based model deficient in SLC35C1 activity.