A four-factor model of executive functioning: The relationship between personality, intelligence, and executive functioning

Executive functioning is commonly assessed in neuropsychological evaluations, however, the construct of executive functioning is widely defined and understood within the literature. Additionally, researchers have begun to examine the relationship between personality and executive functioning. The present study conducted an exploratory factor analysis using common measures of executive functioning. Results yielded a four-factor model. The Big Five personality traits were used to predict performance on executive functioning factors and intelligence was used as a moderator for this relationship. The present study adds to the literature by expanding upon previous studies examining the factor structure of executive functioning. Further, to our knowledge, this is the first study to investigate how intelligence may influence the relationship between personality and executive functioning

Did Food Increase Fertility? Evaluation of !Kung and Herero History

Low fertility among nomadic !Kung foragers of the northern Kalahari Desert of Botswana has been hypothesized to be an adaptation to scarcity of food. However, a comparison of !Kung fertility before and after a transition to a more sedentary lifestyle indicates that more food did not increase fertility. An examination of the fertility of neighboring sedentary Bantu-speaking Herero pastoralists during the same period also indicates that low female reproductive rates in this region are not unique to the !Kung. Herero fertility has increased dramatically in recent decades, probably in response to the control of sexually transmitted diseases in northwestern Botswana. More food appears to have substantially increased !Kung reproductive success by reducing infant and child mortality rates to levels observed among the Herero. These findings suggest that low !Kung fertility and mortality reflect contact with the Herero, who began expanding in large numbers into !Kung territory in the 1950s. This study emphasizes the need for a more rigorous comparative perspective in anthropology to understand better the significance of findings from restricted populations, and I suggest that evolutionary ecology would benefit from shifting some of its current focus on fertility to mortality

Effects of G-CSF on Monocytes and Neurons: in vitro and in vivo studies in a Mouse Model of Alzheimer\u27s Disease

G-CSF is routinely used to treat neutropenia/leukopenia or to increase hematopoietic stem cell generation in bone marrow donors. G-CSF and its receptor, G-CSFR, are produced by various cell types both in the peripheral circulation and within brain. As a consequence, exogenous administration of G-CSF results in a broad spectrum of effects involving hematopoietic, immune and central nervous systems. G-CSF administration in a mouse model of Alzheimer\u27s disease (AD) has revealed both cognitive benefits and disease modifying effects: a) decreased Aβ plaque burden, b) increased microgliosis, c) increased neurogenesis and d) improved performance in radial arm water maze (RAWM). In clinical studies, G-CSF plasma levels were found to be lower in patients with early AD in comparison to healthy age matched controls. A course of G-CSF administration in humans is known to increase levels of circulating hematopoietic stem cells (CD34 cells), monocytes and neutrophils in patients with neutropenia and when administered to patients with AD, there is also a similar increase in absolute monocyte count, CD34 cells and total neutrophils. The extent to which the beneficial effects of G-CSF in AD depend on monocyte infiltration into CNS, compared to direct neurotrophic actions of G-CSF on the CNS, is not known. The overall goal of this study was to investigate and understand the effects of G-CSF in an AD mouse model, but more specifically to distinguish the actions of G-CSF that affect the peripheral monocyte population from the direct actions on CNS. The first approach was to examine in vitro effects of G-CSF within a monocytic cell line (THP-1) and a neuronal cell line (SH-SY5Y). The second approach was to study effects of G-CSF on infiltration of bone marrow-derived cells into the brain by utilizing a chimeric GFP+ APP/PS1 AD mouse model. The third approach was to assess the effects of G-CSF on hippocampal neurogenesis in both a wild-type and AD mouse model. Comparison of the monocytic and neuronal cell lines showed a) G-CSF interacts with its cognate receptor with different binding kinetics and with a greater affinity for the monocyte G-CSFR, b) the number of G-CSF receptors in neurons is greater than in monocytes, and c) the anti-apoptotic response in neurons occurs at lower concentrations of G-CSF than in monocytes. Various concentrations of G-CSF increased proliferation of both the monocytic and neuronal cell line in vitro. G-CSF did not improve migratory properties of the monocytic cell line, either adhesiveness or migration through a membrane. In vivo G-CSF treatment (250μg/kg s.c. qod for 2 ½ weeks) in both the AD chimeric and non-chimeric AD mice resulted in increased microgliosis and decreased amyloid plaque burden in the hippocampus. In the chimeric AD mice, G-CSF treatment did not increase infiltration of GFP+ bone marrow derived cells (BMDC) into brain parenchyma and did not increase adhesion to microvasculature. In the non-chimeric AD mice there was improvement of neurogenesis to non-transgenic levels after G-CSF treatment and an increase in synaptogenesis in the CA1 region of the hippocampus. The effects of G-CSF on the endogeneous microglial population are most likely responsible for the increase in microgliosis, as no significant increase of BMDC infiltration into the brain parenchyma was found in vivo. The enhanced proliferation and improved viability of the neuronal cell line after G-CSF treatment may explain the improvement in neurogenesis and significant increase in synaptogenesis seen in the AD mouse model. The actions of G-CSF on neural stem/progenitor cells to stimulate hippocampal neurogenesis and to enhance resident microglial capacity to decrease amyloid burden are the most likely mechanisms responsible for the behavioral improvement seen in the AD mouse model

Clinical nurse specialist collaboration with a community-based palliative care program: An evidence-based practice project

PURPOSE/OBJECTIVES: The purpose of the project was to evaluate the impact of a clinical nurse specialist (CNS) collaborating with an established Midwestern community-based palliative care program on the following quality outcomes: care coordination, 30-day readmissions, and emergency department (ED) utilization. DESCRIPTION OF PROJECT: Palliative care services are evolving from the inpatient setting to community-based models to meet the needs of patients in their homes. As community-based programs develop, healthcare systems are examining the various models of care. The evidence-based practice project evaluated a collaborative practice model between a CNS and a community-based palliative care team. Quantitative analysis included 30-day readmissions and ED utilization in a preimplementation and postimplementation design. Qualitative data were obtained from a focus group of the community-based palliative care team to discuss the role of the CNS on the team. OUTCOMES: The addition of a CNS did not significantly impact 30-day readmissions or ED visits. An unexpected outcome was that the CNS intervention was associated with an increase in social work visits. Results of the focus groups suggested that the CNS improved care coordination, nursing support, education, and medical management. CONCLUSION: Both quantitative and qualitative analyses suggest that the CNS enhanced coordination of care and quality outcomes. Examining the CNS contribution over a longer period will further clarify the CNS\u27s impact to the team

Are fertility estimates from retrospective data biased by maternal mortality?: an assessment based on parametric models of family size distribution

Includes bibliographyEl análisis de los efectos de la mortalidad materna en los modelos paramétricos de distribución del tamaño de las familias indica que dicha mortalidad probablemente no es una fuente importante del sesgo en las historias retrospectivas de fecundidad. Las distribuciones de nacimientos que siguen los modelos de la distribución negativa binomial y de Poisson subestiman el tamaño completado de la familia por una tasa constante que es igual a la tasa de mortalidad materna