Why hospital design matters: A narrative review of built environments research relevant to stroke care.

Healthcare facilities are among the most expensive buildings to construct, maintain, and operate. How building design can best support healthcare services, staff, and patients is important to consider. In this narrative review, we outline why the healthcare environment matters and describe areas of research focus and current built environment evidence that supports healthcare in general and stroke care in particular. Ward configuration, corridor design, and staff station placements can all impact care provision, staff and patient behavior. Contrary to many new ward design approaches, single-bed rooms are neither uniformly favored, nor strongly evidence-based, for people with stroke. Green spaces are important both for staff (helping to reduce stress and errors), patients and relatives, although access to, and awareness of, these and other communal spaces is often poor. Built environment research specific to stroke is limited but increasing, and we highlight emerging collaborative multistakeholder partnerships (Living Labs) contributing to this evidence base. We believe that involving engaged and informed clinicians in design and research will help shape better hospitals of the future.

Observations on spontaneous tumor formation in mice overexpressing mitotic kinesin Kif14.

The KIF14 locus is gained and overexpressed in various malignancies, with prognostic relevance. Its protein product, a mitotic kinesin, accelerates growth of normal mammary epithelial cells in vitro and retinoblastoma tumours in a mouse model, while KIF14 knockdown blocks growth of brain, liver, ovarian, breast, prostate, and other tumour cells and xenografts. However, the tumour-initiating effects of Kif14 overexpression have not been studied. We aged a cohort of Kif14-overexpressing transgenic mice and wild-type littermates and documented survival, cause of death, and tumour burden. The Kif14 transgene was expressed in all tissues examined, and was associated with increased proliferation marker expression. Neither mouse weights nor overall survival differed between genotypes. However, Kif14 transgenic mice showed a higher incidence of fatal lymphomas (73 vs. 50%, p = 0.03, Fisher's exact test), primarily follicular and diffuse B-cell lymphomas. Non-tumour findings included a bilateral ballooning degeneration of lens in 12% of Kif14 transgenic mice but no wild-type mice (p = 0.02). Overall, this work reveals a novel association of Kif14 overexpression with lymphoma but suggests that Kif14 does not have as prominent a role in initiating cancer in other cell types as it does in accelerating tumour development in response to other oncogenic insults.