The Predictability of Demographic Academic Factors on the Career Decision Making and Self-efficacy of African American Freshmen College

The purpose of this study was to examine the predictability of selected demographic and academic variables on the career decision making process and self-efficacy of African American freshman college students. Specifically, this study was concerned with the relationship between the demographic and academic variables of gender, age, social economic status, grade point average, academic adjustment and vocational identity, and the career decision-making and self-efficacy scores of African American college students. A correlational research design was used in the study. One hundred forty-nine (149) African American freshman college students were selected to participate in the study. The Career Decision Self-Efficacy Scale and the Jackson’s Demographic and Academic Profile Sheet were used to collect the data. A linear relationship did not exist between the demographic factors of gender, age, socioeconomic status, and the total career decision-making self-efficacy scores among African American freshman college students. A statistically significant relationship did not exist between the demographic factors of gender, age, socio economic status and the career self-efficacy scores among American freshman college students. A significant linear relationship was found to exist between the academic factors of grade point average, academic adjustment, vocational identity, and the total career decision-making self-efficacy scores among African American freshman college students. The variable vocational identity was found to be independently related to the total career decision-making self-efficacy scores of African American freshman college students. A significant relationship did exist between the academic factors of grade point average, academic adjustment, vocational identity, and the career self-efficacy scores of African American freshman college students. Finally, the academic variable of vocational identity was found to contribute significantly to the career self-efficacy scores among African American freshman college students

Interprofessional Working in Practice – Avoiding a Theory-Practice Gap

This paper aims to encourage and promote further discussion around the theme of the theory and practice gap in the teaching and practice of interprofessional education (IPE) in pre-registration health and social care. Following a brief history of IPE, we consider the importance of providing students with supported opportunities to observe, learn and put into practice IPE. We also highlight the necessity of involving practitioners in creating health professionals who are ‘fit for purpose’ at qualification

International Perspectives of Nurses, Midwives and Allied Health Professionals Clinical Academic Roles: Are We at Tipping Point?

Healthcare research activity improves patient outcomes. Nurses, Midwives and Allied Health Professions (NMAHPs) make an important contribution to clinical research. Within the United Kingdom (UK), there is a 25-year history of increasing healthcare research capacity and capability through clinical academic roles. Medical colleagues were the first to introduce the role in 2005. In 2007, a national policy identified inequalities in access to and success of research training fellowships between medical and nursing healthcare professionals. This was followed by a number of national initiatives, which continue to evolve to the present day. There is evidence that the UK has reached the ‘tipping point’ to increase NMAHP research capacity and capability through clinical academic roles. Despite these initiatives substantial gaps remain. Outside, the UK, the term ‘clinical academic’ is not well understood. There is evidence of the presence of senior clinical academic roles, a clinical professor within Australia and the United States, for example, but there is a lack of opportunities and of a formulised research training pathway at a junior level. There is interest and appreciation of the NMAHP research-active clinical academic within the clinical setting in the Nordic countries and China, but the pace of change is slow due to co-existing priorities involving change and innovation. There is a need to develop and agree both national and international definitions that describes the NMAHP research-focused clinical academic role activity

Palliative care needs in patients hospitalized with heart failure (PCHF) study: rationale and design

Abstract Aims The primary aim of this study is to provide data to inform the design of a randomized controlled clinical trial (RCT) of a palliative care (PC) intervention in heart failure (HF). We will identify an appropriate study population with a high prevalence of PC needs defined using quantifiable measures. We will also identify which components a specific and targeted PC intervention in HF should include and attempt to define the most relevant trial outcomes. Methods An unselected, prospective, near-consecutive, cohort of patients admitted to hospital with acute decompensated HF will be enrolled over a 2-year period. All potential participants will be screened using B-type natriuretic peptide and echocardiography, and all those enrolled will be extensively characterized in terms of their HF status, comorbidity, and PC needs. Quantitative assessment of PC needs will include evaluation of general and disease-specific quality of life, mood, symptom burden, caregiver burden, and end of life care. Inpatient assessments will be performed and after discharge outpatient assessments will be carried out every 4 months for up to 2.5 years. Participants will be followed up for a minimum of 1 year for hospital admissions, and place and cause of death. Methods for identifying patients with HF with PC needs will be evaluated, and estimates of healthcare utilisation performed. Conclusion By assessing the prevalence of these needs, describing how these needs change over time, and evaluating how best PC needs can be identified, we will provide the foundation for designing an RCT of a PC intervention in HF

VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization via macrophage recruitment

Lymphangiogenesis, an important initial step in tumor metastasis and transplant sensitization, is mediated by the action of VEGF-C and -D on VEGFR3. In contrast, VEGF-A binds VEGFR1 and VEGFR2 and is an essential hemangiogenic factor. We re-evaluated the potential role of VEGF-A in lymphangiogenesis using a novel model in which both lymphangiogenesis and hemangiogenesis are induced in the normally avascular cornea. Administration of VEGF Trap, a receptor-based fusion protein that binds and neutralizes VEGF-A but not VEGF-C or -D, completely inhibited both hemangiogenesis and the outgrowth of LYVE-1+ lymphatic vessels following injury. Furthermore, both lymphangiogenesis and hemangiogenesis were significantly reduced in mice transgenic for VEGF-A164/164 or VEGF-A188/188 (each of which expresses only one of the three principle VEGF-A isoforms). Because VEGF-A is chemotactic for macrophages and we demonstrate here that macrophages in inflamed corneas release lymphangiogenic VEGF-C/VEGF-D, we evaluated the possibility that macrophage recruitment plays a role in VEGF-A–mediated lymphangiogenesis. Either systemic depletion of all bone marrow–derived cells (by irradiation) or local depletion of macrophages in the cornea (using clodronate liposomes) prior to injury significantly inhibited both hemangiogenesis and lymphangiogenesis. We conclude that VEGF-A recruitment of monocytes/macrophages plays a crucial role in inducing inflammatory neovascularization by supplying/amplifying signals essential for pathological hemangiogenesis and lymphangiogenesis

Genomic analyses in Cornelia de Lange Syndrome and related diagnoses: Novel candidate genes, <scp>genotype–phenotype</scp> correlations and common mechanisms

Cornelia de Lange Syndrome (CdLS) is a rare, dominantly inherited multisystem developmental disorder characterized by highly variable manifestations of growth and developmental delays, upper limb involvement, hypertrichosis, cardiac, gastrointestinal, craniofacial, and other systemic features. Pathogenic variants in genes encoding cohesin complex structural subunits and regulatory proteins (NIPBL, SMC1A, SMC3, HDAC8, and RAD21) are the major pathogenic contributors to CdLS. Heterozygous or hemizygous variants in the genes encoding these five proteins have been found to be contributory to CdLS, with variants in NIPBL accounting for the majority (&gt;60%) of cases, and the only gene identified to date that results in the severe or classic form of CdLS when mutated. Pathogenic variants in cohesin genes other than NIPBL tend to result in a less severe phenotype. Causative variants in additional genes, such as ANKRD11, EP300, AFF4, TAF1, and BRD4, can cause a CdLS‐like phenotype. The common role that these genes, and others, play as critical regulators of developmental transcriptional control has led to the conditions they cause being referred to as disorders of transcriptional regulation (or “DTRs”). Here, we report the results of a comprehensive molecular analysis in a cohort of 716 probands with typical and atypical CdLS in order to delineate the genetic contribution of causative variants in cohesin complex genes as well as novel candidate genes, genotype–phenotype correlations, and the utility of genome sequencing in understanding the mutational landscape in this population

Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma

Objective: Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. Methods: GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. Results: Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. Conclusions: These data suggest several plausible genetic links between DLBCL and SLE