ABSTRACT
School transitions are a regular feature of the educational career. While they are of general interest as instances of academic change, they also represent instances of peer environment and influence change. Previous theoretical and empirical work suggests peer influence is important for students' academic and educational outcomes, especially for the complex decision-making processes leading up to those outcomes. In this manuscript, we study the impact of peers on educational expectation formation at the 8th-to-9th-grade school transition. In doing so, we test a theoretical model that links institutional settings, social influence, and individual decision-making. We find the 9th grade transition likely represents a negative shock for students' college attendance expectations. Independent of this transition, however, stable peer environments further depress expectations. A more equal mixture of new and old peers in the 9th grade likely increases students' educational expectations in contrast. These effects of peer perturbations and the re-organization of social ties they imply mainly apply to female students. But, both male and female students revise their educational expectations in light of changing peer intelligence comparisons, albeit in countervailing ways.
Subject(s)
Academic Success , Decision Making , Educational Status , Peer Influence , Schools , Social Environment , Students , Achievement , Adolescent , Education , Female , Humans , Intelligence , Interpersonal Relations , Male , Models, Biological , Peer Group , Sex FactorsABSTRACT
OBJECTIVES: We examined the relationship between timing of poverty and risk of first-incidence obesity from ages 3 to 15.5 years. METHODS: We used the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development (1991-2007) to study 1150 children with repeated measures of income, weight, and height from birth to 15.5 years in 10 US cities. Our dependent variable was the first incidence of obesity (body mass index ≥ 95th percentile). We measured poverty (income-to-needs ratio < 2) prior to age 2 years and a lagged, time-varying measure of poverty between ages 2 and 12 years. We estimated discrete-time hazard models of the relative risk of first transition to obesity. RESULTS: Poverty prior to age 2 years was associated with risk of obesity by age 15.5 years in fully adjusted models. These associations did not vary by gender. CONCLUSIONS: Our findings suggest that there are enduring associations between early life poverty and adolescent obesity. This stage in the life course may serve as a critical period for both poverty and obesity prevention.
Subject(s)
Pediatric Obesity/epidemiology , Poverty/statistics & numerical data , Adolescent , Body Mass Index , Body Weights and Measures , Child , Child, Preschool , Female , Humans , Longitudinal Studies , Male , Risk Factors , Socioeconomic FactorsABSTRACT
Like the United States as a whole, Virginia faces a significant shortage of health care workers in nursing, primary care, and behavioral health. If current trends persist, these shortages will increase across Virginia. The authors of this study identify interventions that can help the Virginia Health Workforce Development Authority (VHWDA) address these health care workforce shortages. To accomplish this goal, they applied an analytic framework to existing or potential interventions for retaining, recruiting, and improving the structural efficiency of the nursing, primary care, and behavioral health workforces in Virginia. In this study, they highlight which interventions VHWDA should prioritize based on its desired outcomes and policy goals.
ABSTRACT
ABSTRACT: Resistance training-based exercise is commonly prescribed in the clinic for the treatment of chronic pain. Mechanisms of aerobic exercise for analgesia are frequently studied, while little is known regarding resistance training mechanisms. We developed a resistance training model in mice and hypothesized resistance training would protect against development of muscle pain, mediated through the activation of androgen receptors. Activity-induced muscle hyperalgesia was produced by 2 injections of pH 5.0 stimuli with fatiguing muscle contractions. Resistance training was performed by having mice climb a ladder with attached weights, 3 times per week. Resistance training acutely increased blood lactate and prolonged training increased strength measured via forepaw grip strength and 1 repetition maximum, validating the exercise program as a resistance training model. Eight weeks of resistance training prior to induction of the pain model blocked the development of muscle hyperalgesia in both sexes. Resistance training initiated after induction of the pain model reversed muscle hyperalgesia in male mice only. A single resistance training bout acutely increased testosterone in male but not female mice. Administration of the androgen receptor antagonist flutamide (200 mg pellets) throughout the 8-week training program blocked the exercise-induced protection against muscle pain in both sexes. However, single administration of flutamide (1, 3, 10 mg/kg) in resistance-trained animals had no effect on existing exercise-induced protection against muscle pain. Therefore, resistance training acutely increases lactate and testosterone and strength overtime. Eight weeks of resistance training prevents the development of hyperalgesia through the activation of androgen receptors in an animal model of muscle pain.
Subject(s)
Myalgia , Physical Conditioning, Animal , Receptors, Androgen , Androgen Receptor Antagonists , Animals , Female , Flutamide/pharmacology , Humans , Hyperalgesia , Lactates , Male , Mice , Muscle Strength , Muscle, Skeletal , Myalgia/prevention & control , Receptors, Androgen/metabolism , Resistance Training , TestosteroneABSTRACT
PURPOSE: To quantify the reduction of relative displacement between the implanted intracavitary applicator and the patient bony anatomy, due to the use of a hover transport system during the patient transports between the imaging table and the treatment table. MATERIAL AND METHODS: The displacement of the applicator inside the patient was measured by comparing the distance between the tip of the tandem and the pubic bone on X-ray radiography images taken before and after moving a patient to magnetic resonance/computed tomography imaging. Displacements were evaluated for 27 fractions of treatment using hover transport and 185 fractions of treatment using manual transport. RESULTS: The use of hover transport system reduced the percentage of fractions with displacements greater than 5 mm from 22.7% to 7.4%. The reduction of applicator displacement using hover transport is statistically significant, compared to the manual transport method (p-value 0.0086; mean displacement 3.41 mm [95% CI: 2.96-3.97] for manual transport, and 2.27 mm [95% CI: 1.71-2.97] for hover transport fractions). CONCLUSIONS: This study indicates that the hover transport system is effectively reducing displacement between tandem and patient bony anatomy during patient transports. The potential improvement in dosimetric accuracy due to this reduction warrants further study.
ABSTRACT
Although grade retention may be consequential for a number of important educational and socioeconomic outcomes, we know surprisingly little about the actual rate at which students are made to repeat grades. We build on Hauser, Frederick, and Andrew's (2007) measure of grade retention using data from the 1995 through 2010 Current Population Surveys. We make technical improvements to their measure; provide more recent estimates; and validate the measure against external criteria. Our measure describes large disparities in grade retention rates by sex, race/ethnicity, geographic locale, and students' socioeconomic circumstances. However, both absolute retention rates and disparities in retention rates have declined markedly since 2005. We conclude by describing how our measures might be used to model the impact of economic and policy contexts on grade retention rates.
ABSTRACT
PTPRJ/CD148 is a tyrosine phosphatase that has tumour suppressor-like activity. Quantitative PCR of various cells and tissues revealed that it is preferentially expressed in macrophage-enriched tissues. Within lymphoid tissues immunohistochemistry revealed that PTPRJ/CD148 co-localised with F4/80, indicating that macrophages most strongly express the protein. Macrophages express the highest basal level of ptprj, and this is elevated further by treatment with LPS and other Toll-like receptor ligands. In contrast, CSF-1 treatment reduced basal and stimulated Ptprj expression in human and mouse cells, and interferon also repressed Ptprj expression. We identified a 1006 nucleotide long noncoding RNA species, Ptprj-as1 that is transcribed antisense to Ptprj. Ptprj-as1 was highly expressed in macrophage-enriched tissue and was transiently induced by Toll-like receptor ligands with a similar time course to Ptprj. Finally, putative transcription factor binding sites in the promoter region of Ptprj were identified.
Subject(s)
Inflammation/genetics , Macrophages/metabolism , RNA, Untranslated/genetics , Receptor-Like Protein Tyrosine Phosphatases, Class 3/genetics , Receptor-Like Protein Tyrosine Phosphatases, Class 3/metabolism , Animals , Base Sequence , Cell Line , HEK293 Cells , Humans , Inflammation/metabolism , Macrophage Colony-Stimulating Factor/genetics , Macrophage Colony-Stimulating Factor/metabolism , Male , Mice , Mice, Inbred C57BL , Molecular Sequence Data , NIH 3T3 Cells , Phagocytes/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , RNA, Untranslated/metabolism , Toll-Like Receptors/genetics , Toll-Like Receptors/metabolismABSTRACT
The protein tyrosine phosphatase receptor J, PTPRJ, is a tumor suppressor gene that has been implicated in a range of cancers, including breast cancer, yet little is known about its role in normal breast physiology or in mammary gland tumorigenesis. In this paper we show that PTPRJ mRNA is expressed in normal breast tissue and reduced in corresponding tumors. Meta-analysis revealed that the gene encoding PTPRJ is frequently lost in breast tumors and that low expression of the transcript associated with poorer overall survival at 20 years. Immunohistochemistry of PTPRJ protein in normal human breast tissue revealed a distinctive apical localisation in the luminal cells of alveoli and ducts. Qualitative analysis of a cohort of invasive ductal carcinomas revealed retention of normal apical PTPRJ localization where tubule formation was maintained but that tumors mostly exhibited diffuse cytoplasmic staining, indicating that dysregulation of localisation associated with loss of tissue architecture in tumorigenesis. The murine ortholog, Ptprj, exhibited a similar localisation in normal mammary gland, and was differentially regulated throughout lactational development, and in an in vitro model of mammary epithelial differentiation. Furthermore, ectopic expression of human PTPRJ in HC11 murine mammary epithelial cells inhibited dome formation. These data indicate that PTPRJ may regulate differentiation of normal mammary epithelia and that dysregulation of protein localisation may be associated with tumorigenesis.