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Introduction Academic teaching of ICNP® could contribute to spread it, enhancing nursing process teaching, and promoting students’ clinical reasoning skills. Furthermore, using ICNP® in nursing education offers the opportunity to combine a nursing standardized terminology with any theoretical model to guide teaching of nursing science. This can bring relevant advantages both in nursing education and in clinical practice. However, standards to introduce ICNP® in nursing education oriented by a nursing theoretical model are not available. Some minor didactic guidance is present in the literature. Aim To introduce ICNP® with a theoretical model guiding nursing science teaching in an Italian Nursing School starting from a first year class. Method An action research study was conducted following the stages of a curriculum development process. Results Findings from this action research study were the identification of conditions to implement change and a growing consciousness of the inadequacy of the actual theoretical model with subsequent reformulation of the study aim. Patterns for theoretical and practice lessons according to ICNP® main elements (diagnosis, interventions, axial structure), a guide for students’ data collection, teaching material, and outlines for second year planning were also produced. Conclusion. Introduction of ICNP® in nursing education allowed the start of a changing process thanks to new hints from available literature. Teaching materials analysis allowed a critical review of lessons’ contents and a reflection on the nature of nursing phenomena. Other two cycles of action research have started to complete the introduction of ICNP® within the whole nursing program.

Human T-cell leukemia virus-1 (HTLV-1) is the first pathogenic human retrovirus discovered in 1980.1 HTLV-1 causes 2 devastating diseases: adult T-cell leukemia/lymphoma (ATL) and a neurological disorder, HTLV-1–associated myelopathy/tropical spastic paraparesis (HAM/TSP or, more briefly, HAM). ATL becomes apparent in 2% to 5% of those infected with HTLV-1; another 1% to 2% will develop HAM.2 There are usually 2 to 3 decades of latency after the infection before the onset of symptoms. A second HTLV (HTLV-2) isolated in 1982 has been causally linked to HAM, but not ATL.3 In other cases, HTLV-1 and HTLV-2 infection may remain asymptomatic for years while being transmitted from person-to-person through host cells in body fluids and breast milk, blood cell transfusions, and solid organ transplantation. There are no licensed vaccines to prevent HTLV-1 or HTLV-2 infections.

An assay, specifically optimized to evaluate the anti-HIV activity of antiretrovirals by flow cytometry analysis, is described. As widely used anti-HIV agents, zidovudine (AZT), abaca- vir (ABC), 20,30-dideoxyinosine (DDI), lamivu-dine (3TC), nevirapine (NVP), and efavirenz (EFV), and as drugs of recent approval raltegra- vir (RAL), etravirine (ETR), and rilpivirine (RPV), were utilized as reference drugs. HIV-1 NL4-3 virus was prepared by transfection of HEK293T cells with purified plasmid DNA and quantified by p24 antigen-capture assay. For infection, CEM-GFP cells were exposed to vehicle or to several concentrations of the drugs for 2 hr at 37°C before HIV-1 NL4-3 was added to each sample. The adsorption was prolonged for 3 hr at 37°C. After 72 hr of incubation, HIV-induced GFP expression in infected CEM-GFP cells was assessed by flow cytometry analysis and expressed as % positive cells. For comparison, p24 production in supernatants was assessed by a commercial ELISA kit. On the basis of IC50 values, the anti-HIV activity, as assayed by this method, was EFV>3TC>AZT>NVP>DDI> ABC and ETR>RPV>RAL. The comparison between the IC50 values calculated through flow cytometry and p24 production revealed overlapping results, showing that the opti- mized protocol of CEM-GFP infection with HIV NL4-3 is a suitable method to perform quanti-tative, rapid and low-expensive screening tests to evaluate the in vitro effect of new candidate anti-HIV drugs.

Background: Thymosin a-1 (Ta1) exploits a specific action on lymphoid cells and is able to induce in peripheral blood mononuclear cells (PBMCs) a strong transcriptional response. CD8 antiviral factor activity plays a role in the control or prevention of HIV-1 infection by a non-cytolytic mechanism. The ability of Ta1 to modulate the release of antiretroviral soluble factors by CD8+ cellswas investigated. Methods: Supernatants from lipopolysaccharide (LPS) stimulated CD8+- isolated cells were treated with Ta1 and screened on in vitro infection of human monocyte-derived macrophages (MDMs) and PBMCs with HIV-1, and of PBMCs with human T lymphotropic virus 1 (HTLV-1). In CD8+ cells, as well as in PBMCs of healthy donors as from HIV+ individuals, a microarray analysis to assess the transcriptional response after treatment was performed. Results: Ta1 potentiates the release, in LPS-stimulated CD8+ cells, of soluble factors able to inhibit both in vitro HIV-1 infection of MDMs and PBMCs and in vitro HTLV-1 infection of PBMCs. A distinctive transcriptional profile was induced by Ta1 in PBMCs from HIV+ donors. Conclusions: These findings suggest that Ta1 would represent a re-evaluated approach to antiretroviral therapy in combination with innovative treatments and with vaccine administration.

Although the central nervous system (CNS) has been defined as a privileged site in Alzheimer's disease (AD), periphery can be more than simply witness of events leading to neurodegeneration. The CNS and peripheral blood can mutually communicate through cells and factors trafficking from the circulation into the brain and vice versa. A number of articles have reviewed inflammatory profiles and programmed cell death (PCD) in AD, separately in the CNS and at the peripheral level. This review does not provide an exhaustive account of what has been published on inflammation and PCD in AD. Rather, the aim of this review is to focus on possible linkages between the central and the peripheral compartments during AD progression, by critically analyzing, in a comparative manner, phenomena occurring in the CNS as well as the peripheral blood. In fact, growing evidence suggests that CNS and peripheral inflammation might present common features in the disease. Microarrays and metabolomics revealed that dysfunction of the glycolytic and oxidative pathways is similar in the brain and in the periphery. Moreover, dysregulated autophagosome/lysosomal molecular machinery, both at the CNS and the peripheral level, in AD-related cell damage, has been observed. Possible implications of these observations have been discussed.

This study describes a novel, PCR-based assay that evaluates the ability of compounds to inhibit cDNA generation by HIV reverse transcriptase (RT), of both commercial and viral lysate origin, from a known RNA template. The template consisted of RNA from stable transfectants ectopically expressing the US6 gene of herpes simplex virus-1, coding for glycoprotein D. Controls were carried out to demonstrate that no residual DNA polymerase activity or DNA contamination was responsible for the amplified DNA in the tested, control samples. In this assay, 0.1 μM nevirapine totally inhibited the RT activity of 0.5 U commercial HIV RT, while 10 nM inhibited it by only 10%. Conversely, 10 pM efavirenz completely inhibited 0.5 U HIV RT. Similar results were obtained when a self-prepared viral lysate was used as a source of HIV RT. A reference commercial kit directly measuring HIV RT activity, without amplification, was less sensitive than the new assay. As a consequence, the HIV RT 50% inhibitory concentration of nevirapine and efavirenz in the newly described assay was 8 and 5 × 10(3) times lower, respectively, than in the commercial assay. In conclusion, this novel method was sensitive, reproducible, and sufficiently rapid for screening in vitro the functional activity of known or potential antiretroviral compounds against HIV RT.