Training for impact: the socio-economic impact of a fit for purpose health workforce on communities.

Across the globe, a "fit for purpose" health professional workforce is needed to meet health needs and challenges while capitalizing on existing resources and strengths of communities. However, the socio-economic impact of educating and deploying a fit for purpose health workforce can be challenging to evaluate. In this paper, we provide a brief overview of six promising strategies and interventions that provide context-relevant health professional education within the health system. The strategies focused on in the paper are:1. Distributed community-engaged learning: Education occurs in or near underserved communities using a variety of educational modalities including distance learning. Communities served provide input into and actively participate in the education process.2. Curriculum aligned with health needs: The health and social needs of targeted communities guide education, research and service programmes.3. Fit for purpose workers: Education and career tracks are designed to meet the needs of the communities served. This includes cadres such as community health workers, accelerated medically trained clinicians and extended generalists.4. Gender and social empowerment: Ensuring a diverse workforce that includes women having equal opportunity in education and are supported in their delivery of health services.5. Interprofessional training: Teaching the knowledge, skills and attitudes for working in effective teams across professions.6. South-south and north-south partnerships: Sharing of best practices and resources within and between countries.In sum, the sharing of resources, the development of a diverse and interprofessional workforce, the advancement of primary care and a strong community focus all contribute to a world where transformational education improves community health and maximizes the social and economic return on investment.

The global summit on nurse faculty migration.

As global demand for health care workers burgeons, information is scant regarding the migration of faculty who will train new nurses. With dual roles as clinicians and educators, and corresponding dual sets of professional and legal obligations, nurse faculty may confront unique circumstances in migration that can impact nations' ability to secure an adequate, stable nursing workforce. In a seminal effort to address these concerns, the Honor Society of Nursing, Sigma Theta Tau International, and the International Council of Nurses invited a diverse group of international experts to a summit designed to elucidate forces that drive nurse faculty migration. The primary areas of consideration were the impact on nurse faculty migration of rapid health care workforce scale-up, international trade agreements, and workforce aging. Long-term summit goals included initiating action affecting national, regional, and global supplies of nurse educators and helping to avert catastrophic failure of health care delivery systems caused by an inadequate ability to educate next-generation nurses.

Fake medicines: a global threat.

COUNTERFEIT MEDICINES are a growing problem in developing and developed countries. In May, the Medicines and Healthcare products Regulatory Agency (MHRA) announced that £8.6 million of counterfeit and unlicensed medicines, including huge hauls of potentially harmful slimming pills, and controlled drugs such as diazepam and anabolic steroids, had been seized in the UK ( MHRA 2014 ).

Advancing nursing practice through social media: a global perspective.

Social media has been used globally as a key vehicle for communication. As members of an innovative profession, many nurses have embraced social media and are actively utilizing its potential to enhance practice and improve health. The ubiquity of the Internet provides social media with the potential to improve both access to health information and services and equity in health care. Thus there are a number of successful nurse-led initiatives. However, the open and democratising nature of social media creates a number of potential risks, both individual and organisational. This article considers the use of social media within nursing from a global perspective, including discussion of policy and guidance documents. The impact of social media on both healthcare consumers and nurses is reviewed, followed by discussion of selected risks associated with social media. To help nurses make the most of social media tools and avoid potential pitfalls, the article conclusion suggests implications appropriate for global level practice based on available published guidance.

Alteration of protein kinase C conformation in red blood cells: a potential marker for Alzheimer's disease but not for Parkinson's disease.

There is a growing evidence of early changes of blood cells in Alzheimer's disease (AD). We have developed an original novel method for quantifying the alteration of protein kinase C (PKC) by its fluorescence spectrum: by using Fim-1, a specific fluorescent probe made for protein kinase C that detects the conformational changes of this. We show that the PKC conformation is altered in red blood cells (RBC) from AD patients as compared to RBC from healthy controls. This alteration is independent of the patient's age and of the stage of the disease. It is not observed in the RBC of non-demented patients suffering from Parkinson's disease (PD). If PKC alteration is proven to be specific to AD as compared with other dementia, this method could be for a simple, low cost screening test among patients suspected of having AD and may have a strong predictive value.

Delirium detection and improved delirium management in older patients hospitalized for hip fracture.

Delirium is a common and potentially devastating problem for older patients following hip fracture. Although early detection is recommended, description and evaluation of standardized approaches are scarce. The aims of this quality improvement project were to: (1) implement a clinical algorithm for improving delirium detection and management and (2) assess the impact of the clinical algorithm on length of stay, discharge disposition and patient satisfaction. The pilot study was implemented on an orthopedic unit to evaluate the effectiveness of a clinical protocol for delirium detection and management to improve outcomes. Outcomes of 33 elderly post-operative hip fracture patients were compared to historical controls from the same unit. Delirium was detected in 18% of patients. Length of stay was reduced by 22% (P < .001), discharge disposition showed a 13% improvement (P = .17) and patient satisfaction scores showed a 15% (P = .15) improvement post-intervention. Implementation of a clinical algorithm to promote early detection and treatment of delirium in post-operative hip fracture patients is feasible and associated with improved outcomes.

Effects of Low Amyloid-ß (Aß) Concentration on Aß1-42 Oligomers Binding and GluN2B Membrane Expression.

Numerous studies have shown that amyloid-ß (Aß) modulate intracellular metabolic cascades and an intracellular Ca2+ homeostasis and a cell surface NMDA receptor expression alteration in Alzheimer's disease (AD). However most of these findings have been obtained by using non-physiological Aß concentrations. The present study deals with the effect of low Aß concentrations on cellular homeostasis. We used nerve growth factor-differentiated PC12 cells and murine cortical neurons sequentially treated with low chronic monomeric or small oligomeric Aß concentrations and high acute oligomeric Aß concentrations to bring out a priming effect of chronic treatment on subsequently high Aß concentrations-elicited cellular response. Both cell types indeed displayed an enhanced capacity to bind oligomeric Aß after monomeric or small oligomeric Aß application. Furthermore, the results show that monomeric Aß1-42 application to the cells induces an increase of the Ca2+-response and of the membrane expression of the extrasynaptic subunit of the NMDA receptor GluN2B in PC12 cells, while the opposite effects were observed in cultured neurons. This suggests a sequential interaction of Aß with the cellular plasma membrane involving monomers or small Aß oligomers which would facilitate the binding of the deleterious high molecular Aß oligomers. This mechanism would explain the slow progression of AD in the human nervous system and the deep gradient of neuronal death observed around the amyloid plaques in the nervous tissue.

Ca2+ Mobilization in Cultured Rat Cerebellar Cells: Astrocytes are Activated by t-ACPD.

Using primary rat cerebellar cell cultures we observed that trans-1-amino-cyclopentyl-1,3-dicarboxylic acid (t-ACPD) was able to induce an increase in intracellular [Ca2+] in different cell types. This response was not abolished by external Ca2+ withdrawal, indicating that t-ACPD triggered the release of intracellularly stored Ca2+. In neurons the t-ACPD response was monophasic and inhibited by l-2-amino-4-phosphonobutyrate (APB). In astrocytes, characterized by their immunoreactivity to antisera to glial fibrillary acidic protein and S-100 protein, the response was oscillatory and resistant to APB application. These results suggest the presence of glutamate metabotropic receptor subtypes in the mammalian brain.

Economic evaluation of orthoptic screening: results of a field study in 121 German kindergartens.

PURPOSE: The purpose of this study was to analyze the cost-effectiveness of an orthoptic screening program in kindergarten children. METHODS: An empiric cost-effectiveness analysis was conducted as part of a field study of orthoptic screening. Three-year-old children (n = 1180) in 121 German kindergartens were screened by orthoptists. The number of newly diagnosed cases of amblyopia and amblyogenic factors (target conditions) was used as the measure of effectiveness. The direct costs of orthoptic screening were calculated from a third-party-payer perspective based on comprehensive measurement of working hours and material costs. RESULTS: The average cost of a single orthoptic screening examination was 12.58 Euro. This amount consisted of labor costs (10.99 Euro) and costs of materials and traveling (1.60 Euro). With 9.9 children screened on average per kindergarten, average labor time was 279 minutes per kindergarten, or 28 minutes per child. It consisted of time for organization (46%), traveling (16%), preparing the examination site (10%), and the orthoptic examination itself (28%). The total cost of the screening program in all 121 kindergartens (including ophthalmic examination, if required) was 21,253 Euro. Twenty-three new cases of the target conditions were detected. The cost-effectiveness ratio was 924 Euro per detected case. Sensitivity analysis showed that the prevalence and the specificity of orthoptic screening had substantial influence on the cost-effectiveness ratio. CONCLUSIONS: The data on the cost-effectiveness of orthoptic screening in kindergarten may be used by such third-party payers as health insurance or public health services when deciding about organizing and financing preschool vision-screening programs.

Deficits of psychomotor and mnesic functions across aging in mouse lemur primates.

Owing to a similar cerebral neuro-anatomy, non-human primates are viewed as the most valid models for understanding cognitive deficits. This study evaluated psychomotor and mnesic functions of 41 young to old mouse lemurs (Microcebus murinus). Psychomotor capacities and anxiety-related behaviors decreased abruptly from middle to late adulthood. However, mnesic functions were not affected in the same way with increasing age. While results of the spontaneous alternation task point to a progressive and widespread age-related decline of spatial working memory, both spatial reference and novel object recognition (NOR) memory tasks did not reveal any tendency due to large inter-individual variability in the middle-aged and old animals. Indeed, some of the aged animals performed as well as younger ones, whereas some others had bad performances in the Barnes maze and in the object recognition test. Hierarchical cluster analysis revealed that declarative-like memory was strongly impaired only in 7 out of 25 middle-aged/old animals. These results suggest that this analysis allows to distinguish elder populations of good and bad performers in this non-human primate model and to closely compare this to human aging.

Protein kinase C as a peripheral biomarker for Alzheimer's disease.

Numerous studies have been performed, which assess an important role of protein kinase C (PKC) in the physiopathology of Alzheimer disease (AD). The alteration of PKC activity stimulates amyloid-beta peptides production and protein tau hyperphosphorylation. This recently led to consider PKC as a potential therapeutic target for disease modifying drugs. Moreover PKC alterations were also observed in peripheral cells including blood cells. This short review recalls the main findings on the role of PKC in the disease process and focuses on its use as an AD biomarker in blood cells. Using fluorescent probes specific for PKC, it is possible to detect the conformational changes of the enzyme in living cells. Such probes can be used to detect PKC alterations in red blood cells and thus to distinguish AD patients from healthy controls with unmatched specificity and sensitivity.

Clostridium perfringens epsilon toxin targets granule cells in the mouse cerebellum and stimulates glutamate release.

Epsilon toxin (ET) produced by C. perfringens types B and D is a highly potent pore-forming toxin. ET-intoxicated animals express severe neurological disorders that are thought to result from the formation of vasogenic brain edemas and indirect neuronal excitotoxicity. The cerebellum is a predilection site for ET damage. ET has been proposed to bind to glial cells such as astrocytes and oligodendrocytes. However, the possibility that ET binds and attacks the neurons remains an open question. Using specific anti-ET mouse polyclonal antibodies and mouse brain slices preincubated with ET, we found that several brain structures were labeled, the cerebellum being a prominent one. In cerebellar slices, we analyzed the co-staining of ET with specific cell markers, and found that ET binds to the cell body of granule cells, oligodendrocytes, but not astrocytes or nerve endings. Identification of granule cells as neuronal ET targets was confirmed by the observation that ET induced intracellular Ca(2+) rises and glutamate release in primary cultures of granule cells. In cultured cerebellar slices, whole cell patch-clamp recordings of synaptic currents in Purkinje cells revealed that ET greatly stimulates both spontaneous excitatory and inhibitory activities. However, pharmacological dissection of these effects indicated that they were only a result of an increased granule cell firing activity and did not involve a direct action of the toxin on glutamatergic nerve terminals or inhibitory interneurons. Patch-clamp recordings of granule cell somata showed that ET causes a decrease in neuronal membrane resistance associated with pore-opening and depolarization of the neuronal membrane, which subsequently lead to the firing of the neuronal network and stimulation of glutamate release. This work demonstrates that a subset of neurons can be directly targeted by ET, suggesting that part of ET-induced neuronal damage observed in neuronal tissue is due to a direct effect of ET on neurons.