Promoting physical activity via physical therapist following knee replacement: A pilot randomized controlled trial.

BACKGROUND: Outpatient physical therapy may be an opportune time to promote aerobic physical activity after knee replacement; however, it is unknown if it is feasible to integrate a physical activity intervention within standard physical therapy. OBJECTIVE: To examine the feasibility and acceptability of a physical activity intervention delivered within outpatient physical therapy for adults after knee replacement. METHODS: As part of a cluster randomized trial, adults with knee replacement starting outpatient physical therapy were recruited across four physical therapy sites. Sites were randomized and physical therapists delivered either an enhanced physical activity intervention or a control condition. The enhanced physical activity intervention consisted of standard postoperative physical therapy plus goal setting, problem-solving, and use of motivational interviewing techniques to promote 150 minutes/week of aerobic moderate intensity physical activity. The control group received standard postoperative physical therapy only. Feasibility and acceptability were determined based on recruitment and retention rates at 12 weeks after surgery. Outcomes including objectively measured physical activity, pain, and self-reported function were examined at the baseline postoperative visit and 12 weeks later. RESULTS: Thirty-three percent of candidates screened were randomized (n = 45) and retention at 12 weeks after surgery was 91% (no difference by condition). Moderate-intensity activity increased, pain decreased, and self-reported function improved, but there were no statistically significant group differences between baseline and 12 weeks. CONCLUSION: Implementing a physical activity intervention within outpatient physical therapy for adults after knee replacement is feasible; however, in this pilot study, changes were not observed in moderate intensity physical activity as compared to standard postoperative physical therapy. Future studies are needed to explore additional low-cost strategies and the optimal time to promote physical activity after knee replacement.

Transforming the Workforce From Individual to Collective Competence.

Competent individuals can provide incompetent care if they are not able to function as a team. The current column provides highlights from a presentation given by the authors at this year's Association for Nursing Professional Development annual convention, expanding on the concept of collective competence with real-life situations. J Contin Educ Nurs. 2017;48(10):440-441.

Severe hemiparesis as a prehospital tool to triage stroke severity: a pilot study to assess diagnostic accuracy and treatment times.

INTRODUCTION: With the publication of the recent trials showing the tremendous benefits of mechanical thrombectomy, opportunities exist to refine prehospital processes to identify patients with larger stroke syndromes. MATERIALS AND METHODS: We retrospectively reviewed consecutive patients who were brought via scene flight from rural parts of the region to our institution, from December 1, 2014 to June 5, 2015, with severe hemiparesis or hemiplegia. We assessed the accuracy of the diagnosis of stroke and the number of patients requiring endovascular therapy. Moreover, we reviewed the times along the pathway of patients who were treated with endovascular therapy. RESULTS: 45 patients were brought via helicopter from the field to our institution. 27 (60%) patients were diagnosed with an ischemic stroke. Of these, 12 (26.7%) were treated with mechanical thrombectomy and 6 (13.3%) with intravenous tissue plasminogen activator alone. An additional three patients required embolization procedures for either a dural arteriovenous fistula or cerebral aneurysm. Thus a total of 15 (33%) patients received an endovascular procedure and 21/45 (46.7%) received an acute treatment. For patients treated with thrombectomy, the median time from first medical contact to groin puncture was 101 min, with 8 of the 12 patients (66.7%) being discharged to home. CONCLUSIONS: We have presented a pilot study showing that severe hemiparesis or hemiplegia may be a reasonable prehospital tool in recognizing patients requiring endovascular treatment. Patients being identified earlier may be treated faster and potentially improve outcomes. Further prospective controlled studies are required to assess the impact on outcomes and cost effectiveness using this methodology.

Motivators and barriers to returning to school: RN to BSN.

With national emphasis on increasing baccalaureate-prepared nurses, the role of the staff development educator of promoting lifelong learning is ideal for advising and mentoring non-bachelor's-prepared nurses to return to school. However, an understanding of the motivators and barriers for nurses to return to school is essential for success. A descriptive correlational research study was completed to determine the motivators and barriers of returning to school for registered nurses without a bachelor's degree.

Prion protein interacts with BACE1 protein and differentially regulates its activity toward wild type and Swedish mutant amyloid precursor protein.

In Alzheimer disease amyloid-ß (Aß) peptides derived from the amyloid precursor protein (APP) accumulate in the brain. Cleavage of APP by the ß-secretase BACE1 is the rate-limiting step in the production of Aß. We have reported previously that the cellular prion protein (PrP(C)) inhibited the action of BACE1 toward human wild type APP (APP(WT)) in cellular models and that the levels of endogenous murine Aß were significantly increased in PrP(C)-null mouse brain. Here we investigated the molecular and cellular mechanisms underlying this observation. PrP(C) interacted directly with the prodomain of the immature Golgi-localized form of BACE1. This interaction decreased BACE1 at the cell surface and in endosomes where it preferentially cleaves APP(WT) but increased it in the Golgi where it preferentially cleaves APP with the Swedish mutation (APP(Swe)). In transgenic mice expressing human APP with the Swedish and Indiana familial mutations (APP(Swe,Ind)), PrP(C) deletion had no influence on APP proteolytic processing, Aß plaque deposition, or levels of soluble Aß or Aß oligomers. In cells, although PrP(C) inhibited the action of BACE1 on APP(WT), it did not inhibit BACE1 activity toward APP(Swe). The differential subcellular location of the BACE1 cleavage of APP(Swe) relative to APP(WT) provides an explanation for the failure of PrP(C) deletion to affect Aß accumulation in APP(Swe,Ind) mice. Thus, although PrP(C) exerts no control on cleavage of APP(Swe) by BACE1, it has a profound influence on the cleavage of APP(WT), suggesting that PrP(C) may be a key protective player against sporadic Alzheimer disease.

Glycosylation of PrPC determines timing of neuroinvasion and targeting in the brain following transmissible spongiform encephalopathy infection by a peripheral route.

Transmissible spongiform encephalopathy (TSE) infectivity naturally spreads from site of entry in the periphery to the central nervous system where pathological lesions are formed. Several routes and cells within the host have been identified as important for facilitating the infectious process. Expression of the glycoprotein cellular PrP (PrP(C)) is considered a key factor for replication of infectivity in the central nervous system (CNS) and its transport to the brain, and it has been suggested that the infectious agent propagates from cell to cell via a domino-like effect. However, precisely how this is achieved and what involvement the different glycoforms of PrP have in these processes remain to be determined. To address this issue, we have used our unique models of gene-targeted transgenic mice expressing different glycosylated forms of PrP. Two TSE strains were inoculated intraperitoneally into these mice to assess the contribution of diglycosylated, monoglycosylated, and unglycosylated PrP in spreading of infectivity to the brain. This study demonstrates that glycosylation of host PrP has a profound effect in determining the outcome of disease. Lack of diglycosylated PrP slowed or prevented disease onset after peripheral challenge, suggesting an important role for fully glycosylated PrP in either the replication of the infectious agent in the periphery or its transport to the CNS. Moreover, mice expressing unglycosylated PrP did not develop clinical disease, and mice expressing monoglycosylated PrP showed strikingly different neuropathologic features compared to those expressing diglycosylated PrP. This demonstrates that targeting in the brain following peripheral inoculation is profoundly influenced by the glycosylation status of host PrP.

Immunohistochemical comparison of anti-prion protein (PrP) antibodies in the CNS of mice infected with scrapie.

One of the pathological changes characteristic of the transmissible spongiform encephalopathies (TSEs) is the accumulation of disease-specific PrP (PrP(sc)). Immunolabeling of PrP(sc) was compared using a panel of monoclonal and polyclonal antibodies. To determine the effects of tissue fixation on immunostaining, we performed a supplementary investigation reviewing the fixatives formol saline and periodate-lysine-paraformaldehyde (PLP). The main target sites of the antibodies were similar. However the monoclonal antibodies (MAbs) 6H4, 7A12 and 8H4 revealed targeted PrP(sc) labeling with no background labeling. Although 7A12 and 8H4 did not detect early PrP deposition, we propose that during the later stages of disease 7A12 and 8H4 can be used with equal effectiveness in place of 6H4. Tissues taken during the early stages of disease that had been fixed in PLP displayed more PrP immunolabeling than tissues that had undergone formol fixation. PLP fixation on 6H4-immunostained tissue revealed interweaving granular linear PrP deposits in the hippocampus. This labeling was not observed in tissue that had undergone formol fixation, suggesting that PLP fixation might enhance the sensitivity of the immunohistochemical (IHC) detection of PrP. In the two scrapie mouse models studied here, PLP fixation and immunolabeling with the anti-PrP antibody 6H4 gave superior results.

Properties of the cellular prion protein expressed in Xenopus oocytes.

The cellular prion protein (PrPC) from different species can be reproducibly expressed in Xenopus oocytes following injection of in vitro transcribed mRNAs. The level of PrPC accumulation increases with the amount of RNA injected and with the duration of incubation. PrPC expressed in oocytes is similar in size and abundance to PrPC protein in mouse brain and >100 ng of PrPC is expressed per oocyte allowing complete experiments to be carried out in single living cells. The protein is glycosylated, fully protease sensitive and expressed on the cell surface. Xenopus oocytes therefore provide a useful model system for the study of prion proteins and their associated disease processes.