Role of diet in fecal incontinence: a systematic review of the literature.

Introduction And Hypothesis: The objective was to perform a systematic review of the literature to examine original research on the role of diet in fecal incontinence (FI) with a dual focus on dietary differences in FI and dietary treatments for FI.

Methods: We searched the PubMed and Embase databases for any peer-reviewed original research in English on the role of diet in FI.

Results: We identified 172 unique citations.

Arginylation regulates purine nucleotide biosynthesis by enhancing the activity of phosphoribosyl pyrophosphate synthase.

Protein arginylation is an emerging post-translational modification that targets a number of metabolic enzymes; however, the mechanisms and downstream effects of this modification are unknown. Here we show that lack of arginylation renders cells vulnerable to purine nucleotide synthesis inhibitors and affects the related glycine and serine biosynthesis pathways. We show that the purine nucleotide biosynthesis enzyme PRPS2 is selectively arginylated, unlike its close homologue PRPS1, and that arginylation of PRPS2 directly facilitates its biological activity.

Is self-reported adherence associated with clinical outcomes in women treated with anticholinergic medication for overactive bladder?

Aim: To determine the association between self-reported adherence to anticholinergic medication and clinical outcomes in women with overactive bladder (OAB).

Methods: A prospective study of women with OAB treated with fesoterodine for 8 weeks. Adherence to medication was measured using the Medication Adherence Self-report Inventory (MASRI).

Structural evidence for perinuclear calcium microdomains in cardiac myocytes.

At each heartbeat, cardiac myocytes are activated by a cytoplasmic Ca(2+) transient in great part due to Ca(2+) release from the sarcoplasmic reticulum via ryanodine receptors (RyRs) clustered within calcium release units (peripheral couplings/dyads). A Ca(2+) transient also occurs in the nucleoplasm, following the cytoplasmic transient with some delay. Under conditions where the InsP3 production is stimulated, these Ca(2+) transients are regulated actively, presumably by an additional release of Ca(2+) via InsP3 receptors (InsP3Rs).