Patient safety after implementation of a coproduced family centered communication programme: multicenter before and after intervention study.

Objective: To determine whether medical errors, family experience, and communication processes improved after implementation of an intervention to standardize the structure of healthcare provider-family communication on family centered rounds.

Design: Prospective, multicenter before and after intervention study.

Setting: Pediatric inpatient units in seven North American hospitals, 17 December 2014 to 3 January 2017.

Families as Partners in Hospital Error and Adverse Event Surveillance.

Importance: Medical errors and adverse events (AEs) are common among hospitalized children. While clinician reports are the foundation of operational hospital safety surveillance and a key component of multifaceted research surveillance, patient and family reports are not routinely gathered. We hypothesized that a novel family-reporting mechanism would improve incident detection.

Remodeling of protein and mRNA expression in Leishmania mexicana induced by deletion of glucose transporter genes.

Glucose is a major nutrient in the insect vector stage of Leishmania parasites. Glucose transporter null mutants of Leishmania mexicana exhibit profound phenotypic changes in both insect stage promastigotes and mammalian host stage amastigotes that reside within phagolysosomes of host macrophages. Some of these phenotypic changes could be either mediated or attenuated by changes in gene expression that accompany deletion of the glucose transporter genes.

Amplification of an alternate transporter gene suppresses the avirulent phenotype of glucose transporter null mutants in Leishmania mexicana.

A glucose transporter null mutant of the parasitic protozoan Leishmania mexicana, in which three linked glucose transporter genes have been deleted by targeted gene replacement, is unable to replicate as amastigote forms within phagolysomes of mammalian host macrophages and is avirulent. Spontaneous suppressors of the null mutant have been isolated that partially restore replication of parasites within macrophages. These suppressor mutants have amplified the gene for an alternative hexose transporter, the LmGT4 permease (previously called the D2 permease), on a circular extrachromosomal element, and they overexpress LmGT4 mRNA and protein.