What influences our decision to vaccinate? The social amplification of risk framework and vaccination

The current study applies the social amplification risk framework to the anti-vaccination movement, specifically to the social factors that influence the likelihood to vaccinate. A total of 264 participants were recruited using Amazon’s Mechanical Turk engine and students from a large southern university. Participants responded to questions about their personal, friend, and family experiences with vaccines, their discussion about vaccines, and trust in vaccine literature (CDC, Facebook, family, etc.). Lastly, participants responded to a modified Duke’s social support scale. Results indicated that the likelihood to vaccinate is impacted by several social factors and that those factors can be amplified based on the experiences of others. The results support using the social amplification of risk on individual perceptions of risk

Identification and characterization of downstream effector protein(s) regulated by p53 and pRb

A commonality among cancer types is the high frequency of mutations that inhibit or alter signaling of the p53 and pRb (Retinoblastoma) tumor suppressors. These genes regulate processes vital for cancer suppression such as apoptosis, senescence, and cell cycle arrest among others. Loss of both p53 and pRb promotes processes that support cancer progression and is associated with decreased patient survival and increased rates of tumor reoccurrence. Although data points to the ability of p53 and pRb to collaborate and to inhibit tumorigenesis, it remains unclear how p53 and pRb cooperate toward this task. Using RNA expression profiling, 179 p53 and pRb cross-talk candidates were identified in normal lung fibroblasts (WI38) cells exogenously coexpressing p53 and pRb. Regulator of G protein signaling 16 (RGS16) was among the p53 and pRb cross-talk candidates and reports suggest it inhibits the activation of several oncogenic pathways associated with proliferation, migration, and invasion of cancer cells. RGS16 is downregulated in pancreatic cancer patients with metastases compared to patients without metastasized pancreatic cancer. The role of RGS16 in cancer cell metastasis is unknown; therefore I tested the hypothesis that RGS16 inhibits pancreatic cancer cell migration and invasion in vitro. Expression of RGS16 was decreased in the pancreatic cancer cell lines tested compared to control. Expression of RGS16 inhibited fetal bovine serum (FBS) and epidermal growth factor (EGF) induced migration of the BxPC-3 and AsPC-1 but not PANC-1 pancreatic cancer cells. It also inhibited EGF induced invasion of BxPC-3 and AsPC-1 cells with no impact on cell viability. Although RGS16 inhibited cell migration and invasion of BxPC-3 and AsPC-1 cells, there was no change in F-actin polymerization or the amounts of p-AKT, pERK and the epithelial mesenchymal transition (EMT) marker vimentin proteins, but there was a slight increase in E-cadherin protein expression in BxPC-3 cells. Our data suggests the inhibitory effect of RGS16 on EGF induced pancreatic cancer cell migration is independent of the PI3K and MAPK pathways. To our knowledge, for the first time, we performed analyses to identify p53 and pRb cross-talk candidates and demonstrated a role for RGS16 in suppressing EGF and FBS induced pancreatic cancer migration and invasion

Holding Companies, The New Deal, and the Development of the Aircraft Industry: A Historical Retrospective

William B. Carper is an Associate Professor of Management and Head, Department of Management in the School of Business at Georgia Southern College. Carl Swickley is Director of the Experimental Aircraft Association Museum, Wittman Air Field at Oshkosh. Wisconsin

Outsourcing a High Speed Internet Access Project: An Information Technology Class Case Study in Three Parts

In early 2004, the Hilton Hotels Corporation (HHC) required that all of its hotels (both owned and franchised) install highspeed Internet access (HSIA) in all of their rooms by June 2004. This case focuses on how one of its franchise properties located on the northern gulf coast of Florida (the Hilton Sandestin Beach Golf Resort & Spa—hereinafter referred to as the HSB) responded to this mandate. The (A) part of the HSB case includes the industry situation for the HSB in 2004 plus the details surrounding the initial phase of the HSIA project. Also presented in this part are descriptions of how and why the HSB management made the decision to use a wireless (versus wired) solution as well as to outsource both the installation of the HSIA wireless hardware and the customer support aspects of the HSIA project to what turned out to be a less than experienced vendor. The (B) part of this case describes the situation at HSB after the high speed internet system was installed and made operational, as well as the various problems that the system and its lack of customer support created for the hotel. Part (C) details the actions of the new HSB General Manager who arrived in late 2004 after the initial HSIA implementation and how he resolved the issues that had been created by his predecessor

RGS16, a novel p53 and pRb cross-talk candidate inhibits migration and invasion of pancreatic cancer cells

Data collected since the discovery of p53 and pRb/RB1 suggests these tumor suppressors cooperate to inhibit tumor progression. Patients who have mutations in both p53 and RB1 genes have increased tumor reoccurrence and decreased survival compared to patients with only one tumor suppressor gene inactivated. It remains unclear how p53 and pRb cooperate toward inhibiting tumorigenesis. Using RNA expression profiling we identified 179 p53 and pRb cross-talk candidates in normal lung fibroblasts (WI38) cells exogenously coexpressing p53 and pRb. Regulator of G protein signaling 16 (RGS16) was among the p53 and pRb cross-talk candidates and has been implicated in inhibiting activation of several oncogenic pathways associated with proliferation, migration, and invasion of cancer cells. RGS16 has been found to be downregulated in pancreatic cancer patients with metastases compared to patients without metastasis. Expression of RGS16 mRNA was decreased in the pancreatic cancer cell lines tested compared to control. Expression of RGS16 inhibited migration of the BxPC-3 and AsPC-1 but not PANC-1 cells and inhibited invasion of BxPC-3 and AsPC-1 cells with no impact on cell viability. We have identified for the first time p53 and pRb cross-talk candidates and a role for RGS16 to inhibit pancreatic cancer migration and invasion

Barriers to enrollment in a randomized controlled trial of hydrocortisone for cardiovascular insufficiency in term and late preterm newborn infants.

ObjectiveTo analyze reasons for low enrollment in a randomized controlled trial (RCT) of the effect of hydrocortisone for cardiovascular insufficiency on survival without neurodevelopmental impairment (NDI) in term/late preterm newborns.Study designThe original study was a multicenter RCT. Eligibility: ⩾34 weeks' gestation, <72 h old, mechanically ventilated, receiving inotrope. Primary outcome was NDI at 2 years; infants with diagnoses at high risk for NDI were excluded. This paper presents an analysis of reasons for low patient enrollment.ResultsTwo hundred and fifty-seven of the 932 otherwise eligible infants received inotropes; however, 207 (81%) had exclusionary diagnoses. Only 12 infants were randomized over 10 months; therefore, the study was terminated. Contributing factors included few eligible infants after exclusions, open-label steroid therapy and a narrow enrollment window.ConclusionDespite an observational study to estimate the population, very few infants were enrolled. Successful RCTs of emergent therapy may require fewer exclusions, a short-term primary outcome, waiver of consent and/or other alternatives

Activation of STAT signaling pathways and induction of suppressors of cytokine signaling (SOCS) proteins in mammalian lens by growth factors

PURPOSE. This study was conducted to examine whether the effects of growth factors are mediated in the lens by Janus kinase/signal transducers and activators of transcription (JAK/ STAT) pathways and whether they induce expression of suppressors of cytokine signaling (SOCS), a novel family of feedback regulators of cytokine and growth factor activities. METHODS. STAT activation and SOCS expression were analyzed in transgenic or wild-type mouse lens and lens epithelial cells stimulated with growth factors by immunohistochemistry, RT-PCR, Northern, Western, proliferation, or transient reporter assays. RESULTS. STATs were constitutively expressed at low levels and activated by insulin-like growth factor (IGF)-1, platelet-derived growth factor (PDGF)-aa, and FGF-1 or -2 in the lens. The Intensity of STAT signaling increased at high FGF-2 concentration and FGFs act in synergy with IGF-1 or PDGFaa to enhance STAT signaling and SOCS expression. Growth factor-induced proliferation of lens cells is inhibited by AG-490, a specific inhibitor of JAK2/STAT3. CONCLUSIONS. This is the first report that FGFs activate STAT pathways in the lens and that SOCS proteins are constitutively expressed and upregulated by growth factors in this tissue. Physiological relevance of STAT pathways in the lens is underscored by inhibition of lens cell proliferation by inhibitors of JAK/STAT pathways and by the aberrant proliferation of lens epithelium in the posterior pole of transgenic mice with constitutively activated STAT1 in the lens. Common activation of STAT pathways by FGF-1, FGF-2, IGF-1, or PDGFaa and their synergistic activation of STATs and SOCS in lens cells suggest that activities and crosstalk between these factors are sensitive to the steady state levels of activated STATs in the lens and may be under feedback regulation by SOCS family proteins. (Invest Ophthalmol Vis Sci

cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth

The LKB1 tumor suppressor gene is frequently mutated and inactivated in non–small cell lung cancer (NSCLC). Loss of LKB1 promotes cancer progression and influences therapeutic responses in preclinical studies; however, specific targeted therapies for lung cancer with LKB1 inactivation are currently unavailable. Here, we have identified a long noncoding RNA (lncRNA) signature that is associated with the loss of LKB1 function. We discovered that LINC00473 is consistently the most highly induced gene in LKB1-inactivated human primary NSCLC samples and derived cell lines. Elevated LINC00473 expression correlated with poor prognosis, and sustained LINC00473 expression was required for the growth and survival of LKB1-inactivated NSCLC cells. Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP–responsive element–binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription. Collectively, our study demonstrates that LINC00473 expression potentially serves as a robust biomarker for tumor LKB1 functional status that can be integrated into clinical trials for patient selection and treatment evaluation, and implicates LINC00473 as a therapeutic target for LKB1-inactivated NSCLC

Regression, developmental trajectory and associated problems in disorders in the autism spectrum: the SNAP study

We report rates of regression and associated findings in a population derived group of 255 children aged 9-14 years, participating in a prevalence study of autism spectrum disorders (ASD); 53 with narrowly defined autism, 105 with broader ASD and 97 with non-ASD neurodevelopmental problems, drawn from those with special educational needs within a population of 56,946 children. Language regression was reported in 30% with narrowly defined autism, 8% with broader ASD and less than 3% with developmental problems without ASD. A smaller group of children were identified who underwent a less clear setback. Regression was associated with higher rates of autistic symptoms and a deviation in developmental trajectory. Regression was not associated with epilepsy or gastrointestinal problems

Influences on clinical decision-making during a community placement – reflections of a student nurse

The decision-making process in nursing is complex. High quality care is dependent on good clinical judgement and decision-making. Nurses need to be able to justify and defend their clinical decision-making. In this article, the author, a third-year nursing student reflects on an incident from a community placement involving a collaborative, clinical decision. Carper’s (1978) four fundamental patterns of knowing are used to analyse the decision-making process. It is shown that influences on decision-making include prior knowledge and expertise, law and accountability and ethical principles such as respect for autonomy and beneficence. Good communication, interpersonal skills and a person-centred approach have a bearing on decision-making. It is argued that intuitio