Definitions of Physician Certification Used in the North American Literature: A Scoping Review.

INTRODUCTION: The authors sought to identify how physician specialty certification is defined in the North American literature. METHODS: A rigorous, established six-stage scoping review framework was used to identify the North American certification literature published between January 2006 and May 2016 relating to physician specialty certification. Data were abstracted using a charting form developed by the study team. Quantitative summary data and qualitative thematic analysis of the purpose of certification were derived from the extracted data. RESULTS: A two stage screening process identified 88 articles that met predefined criteria. Only 14 of the 88 articles (16%) contained a referenced purpose of certification. Eighteen definitions were identified from these articles. Definitional concepts included lifelong learning and continuous professional development, assessment of competence and performance, performance improvement, public accountability, and professional standing. DISCUSSION: Most articles identified in this scoping review did not define certification or describe its purpose or intent. Future studies should provide a definition of certification to further scholarly examination of its intent and effects and inform its further evolution.

Nanoformulated SOD1 ameliorates the combined NASH and alcohol-associated liver disease partly via regulating CYP2E1 expression in adipose tissue and liver.

Enhanced free fatty acid (FFA) flux from adipose tissue (AT) to liver plays an important role in the development of nonalcoholic steatohepatitis (NASH) and alcohol-associated liver disease (AALD). We determined the effectiveness of nanoformulated superoxide dismutase 1 (Nano) in attenuating liver injury in a mouse model exhibiting a combination of NASH and AALD. Male C57BL6/J mice were fed a chow diet (CD) or a high-fat diet (HF) for 10 wk followed by pair feeding of the Lieber-DeCarli control (control) or ethanol (ET) diet for 4 wk. Nano was administered once every other day for the last 2 wk of ET feeding. Mice were divided into 1) CD + control diet (CD + Cont), 2) high-fat diet (HF) + control diet (HF + Cont), 3) HF + Cont + Nano, 4) HF + ET diet (HF + ET), and 5) HF + ET + Nano. The total fat mass, visceral AT mass (VAT), and VAT perilipin 1 content were significantly lower only in HF + ET-fed mice but not in HF + ET + Nano-treated mice compared with controls. The HF + ET-fed mice showed an upregulation of VAT CYP2E1 protein, and Nano abrogated this effect. We noted a significant rise in plasma FFAs, ALT, and monocyte chemoattractant protein-1 in HF + ET-fed mice, which was blunted in HF + ET + Nano-treated mice. HF + ET-induced increases in hepatic steatosis and inflammatory markers were attenuated upon Nano treatment. Nano reduced hepatic CYP2E1 and enhanced catalase levels in HF + ET-fed mice with a concomitant increase in SOD1 protein and activity in liver. Nano was effective in attenuating AT and liver injury in mice exhibiting a combination of NASH and AALD, partly via reduced CYP2E1-mediated ET metabolism in these organs.NEW & NOTEWORTHY Increased free fatty acid flux from adipose tissue (AT) to liver accompanied by oxidative stress promotes nonalcoholic steatohepatitis (NASH) and alcohol-associated liver injury (AALD). Obesity increases the severity of AALD. Using a two-hit model involving a high-fat diet and chronic ethanol feeding to mice, and treating them with nanoformulated superoxide dismutase (nanoSOD), we have shown that nanoSOD improves AT lipid storage, reduces CYP2E1 in AT and liver, and attenuates the combined NASH/AALD in mice.

Effect of nanoformulated copper/zinc superoxide dismutase on chronic ethanol-induced alterations in liver and adipose tissue.

BACKGROUND: We previously reported that nanoformulated copper/zinc superoxide dismutase (Nano) attenuates non-alcoholic fatty liver disease and adipose tissue (AT) inflammation in obese animals. Here, we sought to determine whether Nano treatment attenuates alcohol-associated liver disease (AALD) and AT inflammation in alcohol-fed mice. METHODS: We pre-treated E-47 cells (HepG2 cells that over-express CYP2E1) with native- or nano-superoxide dismutase (SOD) for 6 h, followed by treatment with ethanol and/or linoleic acid (LA), a free fatty acid. For in vivo studies, male C57BL/6 mice were fed the Lieber-DeCarli control or ethanol liquid diet for 4 weeks. The mice received Nano once every 2 days during the last 2 weeks of ethanol feeding. RESULTS: Our in vitro studies revealed that Nano pretreatment reduced LA + ethanol-induced oxidative stress in E-47 cells. Our in vivo experiments showed that ethanol-fed Nano-treated mice had 22% lower hepatic triglyceride levels than mice fed ethanol alone. Nano-treated ethanol-fed mice also had 2-fold lower levels of Cd68 and similarly reduced levels of Ccl2 and Mmp12 mRNAs, than in untreated ethanol-fed mice. We also noted that ethanol feeding caused a remarkable increase in hepatic and/or plasma MCP-1 and CCR2 protein, which was blunted in ethanol + Nano-treated animals. The hepatic content of SREBP-1c, a transcription factor that promotes lipogenesis, was higher in ethanol-fed mice than controls but was attenuated in ethanol + Nano-treated animals. Further, livers of ethanol + Nano-treated mice had significantly higher levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) than both control and ethanol-fed mice. In AT, the levels of Il6 mRNA, a hepatoprotective cytokine, and that of Arg1, a marker of anti-inflammatory macrophages, were significantly increased in ethanol + Nano-treated mice compared with control mice. CONCLUSION: Our data indicate that Nano treatment attenuates ethanol-induced steatohepatitis and that this effect is associated with an apparent activation of AMPK signaling. Our data also suggest that Nano induces Arg1 and Il6 expression in AT, suggesting anti-inflammatory effects in this tissue.

Constructing a Sensitizing Definition of Certification in Nursing for Research Purposes: A Hybrid Methodology Using Consensus-Building Approach.

OBJECTIVE: The aim of this study was to construct a sensitizing definition of certification in nursing for research purposes that can provide a foundation from which to further develop a coherent research program building evidence about the impact of certification on healthcare outcomes. BACKGROUND: The lack of a single definition of certification in nursing makes it difficult to draw conclusions about the relationship between specialty certification and patient outcomes. METHODS: This study was guided by the Delphi-Chaffee hybrid methodology proposed by Grant et al. DISCUSSION: Constructing a single, sensitizing definition of certification: 1) provides coherency for direction of certification research; 2) serves as a guide for researchers; and 3) facilitates multimethodological approaches to exploring the relationship among the different components of the definition of certification. CONCLUSION: A sensitizing definition of certification provides an opportunity for researchers to study the relationship between nursing certification and patient outcomes.

Conceptualization and Operationalization of Certification in the US and Canadian Nursing Literature.

OBJECTIVE: To identify how certification is defined, conceptualized, and discussed in the nursing literature. BACKGROUND: Although it is hypothesized that credentialing is associated with better patient outcomes, the evidence is relatively limited. Some authors have suggested that the lack of consistency used to define certification in nursing literature may be one of the dominant obstacles in credentialing research. METHODS: This scoping review was guided by Arksey and O'Malley's framework, and quantitative and qualitative analyses were conducted. RESULTS: The final data set contained a total of 36 articles, of which 14 articles provided a referenced definition of certification. Thematic analysis of the definitions yielded 8 dominant themes. CONCLUSION: The lack of a common definition of certification in nursing must be addressed to advance research into the relationship between certification processes in nursing and healthcare outcomes.

Nanoformulated copper/zinc superoxide dismutase exerts differential effects on glucose vs lipid homeostasis depending on the diet composition possibly via altered AMPK signaling.

Evidence suggests that superoxide dismutase 1 (SOD1) promotes glucose vs lipid metabolism depending on the diet type. We recently reported that nanoformulated SOD1 (Nano) improved lipid metabolism without altering glucose homeostasis in high-fat (HF) diet-fed mice. Here, we sought to determine the effects and potential mechanisms of Nano in modulating glucose and lipid homeostasis in mice fed a normal chow diet (CD) vs HF diet. Mice were fed a CD or a HF diet (45%) for 10 wk and injected with Nano once every 2 days for 15 days. The fasting glucose level was lower (P < 0.05) in CD + Nano-treated mice compared to control. Conversely, blood glucose was not altered but serum triglycerides were lower in HF + Nano-treated mice. Genes involved in fatty acid synthesis were reduced by Nano in the skeletal muscle of CD but not of HF diet-fed mice. Adenosine monophosphate-activated protein kinase (AMPK), which promotes both glucose and lipid metabolism depending on the fuel availability, is activated by Nano in CD-fed mice. Moreover, Nano increased phosphorylation of ACC, a downstream target of AMPK, in both CD and HF diet-fed mice. Nano increased mitochondrial respiration in C2C12 myocytes in the presence of glucose or fatty acid, and this effect is inhibited by Compound C, an AMPK inhibitor. Our data suggest that Nano promotes glucose and lipid metabolism in CD and HF diet-fed mice, respectively, and this effect is mediated partly via AMPK signaling.

Hemostasis and Safety of a Novel Fibrin Dressing Versus Standard Gauze in Bleeding Cancellous Bone in a Caprine Spine Surgery Model.

BACKGROUND: Decorticated bone is a significant source of blood loss in scoliosis surgery. Current hemostatic methods include packed gauze (GS), physical barriers such as bone wax, and xenograft collagen-based materials. We assessed the safety and efficacy of a novel fibrin dressing (dextran-thrombin-fibrinogen [DTF]) compared to GS. This dressing comprises lyophilized thrombin and fibrinogen embedded in an elastic electrospun nanofiber dextran matrix. PURPOSE: The study tests the hypothesis that DTF is more efficacious than GS in control of bleeding from cancellous bone. STUDY DESIGN: A preclinical Good Laboratory Practices (GLP) study. METHODS: We enrolled 10 goats that were followed for 28 ± 1 days. Each animal was randomly assigned to the test or control group. Both test and control animals had 4 cancellous bone injuries. Test animal injuries were treated with DTF, whereas standard GS was used to control bleeding in the control animals. Bleeding at the bone injury site was characterized as either none, oozing, flowing, or pulsatile and was assessed at 4 and 8 minutes after dressing application. Goats were survived 28 ± 1 days and then necropsied. RESULTS: Application of the fibrin dressing to bleeding cancellous bone, both posterior spinal lamina, and iliac crest graft sites, resulted in control of bleeding within 4 minutes at all injury sites. Eighty percent of control injury sites continued to bleed after 8 minutes and required application of bone wax to control bleeding. There were no differences in prothrombin time, partial thromboplastin time, or fibrinogen levels between test and control animals at 1 or 28 days. We observed no adverse histologic reactions at 28 days. CONCLUSION: The fibrin dressing is an efficacious and safe method of controlling blood loss from cancellous bone in a spine surgery model.

A combination of dietary N-3 fatty acids and a cyclooxygenase-1 inhibitor attenuates nonalcoholic fatty liver disease in mice.

We sought to determine whether a combination of purified n-3 fatty acids (n-3) and SC-560 (SC), a cyclooxygenase-1-specific inhibitor, is effective in ameliorating nonalcoholic fatty liver disease in obesity. Female wild-type mice were fed a high-fat and high-cholesterol diet (HF) supplemented with n-3 in the presence or absence of SC. Mice treated with SC alone exhibited no change in liver lipids, whereas n-3-fed mice tended to have lower hepatic lipids. Mice given n-3+SC had significantly lower liver lipids compared with HF controls indicating enhanced lipid clearance. Total and sulfated bile acids were significantly higher only in n-3+SC-treated mice compared with chow diet (CD) controls. Regarding mechanisms, the level of pregnane X receptor (PXR), a nuclear receptor regulating drug/bile detoxification, was significantly higher in mice given n-3 or n-3+SC. Studies in precision-cut liver slices and in cultured hepatoma cells showed that n-3+SC enhanced not only the expression/activation of PXR and its target genes but also the expression of farnesoid X receptor (FXR), another regulator of bile synthesis/clearance, indicating that n-3+SC can induce both PXR and FXR. The mRNA level of FGFR4 which inhibits bile formation showed a significant reduction in Huh 7 cells upon n-3 and n-3+SC treatment. PXR overexpression in hepatoma cells confirmed that n-3 or SC each induced the expression of PXR target genes and in combination had an enhanced effect. Our findings suggest that combining SC with n-3 potentiates its lipid-lowering effect, in part, by enhanced PXR and/or altered FXR/FGFR4 signaling.

Nanoformulated copper/zinc superoxide dismutase reduces adipose inflammation in obesity.

OBJECTIVE: An intimate association exists between oxidative stress and inflammation. Because adipose tissue (AT) inflammation is intricately linked to metabolic disorders, it was hypothesized that reducing oxidative stress would be effective in ameliorating AT inflammation in obesity. METHODS: Wild-type mice were fed a high-fat diet (HF) for 8 weeks followed by a 2-week treatment with nanoformulated copper/zinc superoxide dismutase (NanoSOD). The mice were divided into: 1) chow diet, 2) HF, and 3) HF + NanoSOD. RESULTS: The HF + NanoSOD-treated mice showed a significant decrease in plasma and liver triglycerides when compared with HF-fed mice. Interestingly, NanoSOD reduced the expression of macrophage and inflammatory markers in visceral AT (VAT) and stromal cells derived from VAT. Moreover, the activation of proinflammatory signaling pathways, in particular, the extracellular signal-regulated kinases, was blunted in VAT on NanoSOD treatment. However, markers of oxidative stress were not altered significantly in the HF + NanoSOD group in the experimental conditions. Pretreatment of either macrophages or adipocytes significantly reduced the inflammatory response invoked in an in vitro coculture system, further supporting the role of NanoSOD in inhibiting obesity-linked inflammation. CONCLUSIONS: This data suggest that NanoSOD is effective not only in reducing AT macrophage accumulation and AT inflammation but also in promoting triglyceride metabolism in obesity.

Nanoformulated copper/zinc superoxide dismutase attenuates vascular cell activation and aortic inflammation in obesity.

OBJECTIVE: Endothelial cell (EC) oxidative stress can lead to vascular dysfunction which is an underlying event in the development of cardiovascular disease (CVD). The lack of a potent and bioavailable anti-oxidant enzyme is a major challenge in studies on antioxidant therapy. The objective of this study is to determine whether copper/zinc superoxide dismutase (CuZnSOD or SOD1) after nanoformulation (nanoSOD) can effectively reduce EC oxidative stress and/or vascular inflammation in obesity. METHODS: Human aortic endothelial cells (HAECs) were treated with native- or nanoSOD for 6 h followed by treatment with linoleic acid (LA), a free fatty acid, for 6-24 h. To determine the in vivo relevance, the effectiveness of nanoSOD in reducing vascular cell activation was studied in a mouse model of diet-induced obesity. RESULTS: We noted that nanoSOD was more effectively taken up by ECs than native SOD. Western blot analysis further confirmed that the intracellular accumulation of SOD1 protein was greatly increased upon nanoSOD treatment. Importantly, nanoSOD pretreatment led to a significant decrease in LA-induced oxidative stress in ECs which was associated with a marked increase in SOD enzyme activity in ECs. In vivo studies showed a significant decrease in markers of EC/vascular cell activation and/or inflammation in visceral adipose tissue (VAT), thoracic aorta, and heart collected from nanoSOD-treated mice compared to obese control mice. Interestingly, the expression of metallothionein 2, an antioxidant gene was significantly increased in nanoSOD-treated mice. CONCLUSION: Our data show that nanoSOD is very effective in delivering active SOD to ECs and in reducing EC oxidative stress. Our data also demonstrate that nanoSOD will be a useful tool to reduce vascular cell activation in VAT and aorta in obesity which, in turn, can protect against obesity-associated CVD, in particular, hypertension.