BIOL 335 Pathophysiology: Bracketology: Disease Edition

This project was designed for use in BIOL 335 Pathophysiology, an elective course for which Anatomy & Physiology I and II are prerequisites. The project is based on a single-elimination bracket where progression to the next round is decided by vote of the class, but the votes are independent of student grades. As individual students are “eliminated” by the voting process, they are assigned to work with another student who is still “in,” so the groups gradually become larger as the project progresses. There are two graded assignments for each round: one is a presentation, and one is a written assignment. The project requires sufficient class time for weekly presentations and for the students to coordinate their research and presentations, especially in the later rounds. “Steps” in the timeline below can be a full class period, a partial class period, or a posted deadline as appropriate.https://digitalcommons.gardner-webb.edu/natural-sciences-oer/1001/thumbnail.jp

BIOL 352 Cell Biology: Journey from the Center of the Cell

This project is intended to be a long-term, scaffolded project across an entire semester course. Due dates are spread throughout the semester, and points are distributed as the professor deems appropriate across the sections of the project.https://digitalcommons.gardner-webb.edu/natural-sciences-oer/1000/thumbnail.jp

Does linguistic input play the same role in language learning for children with and without early brain injury?

Children with unilateral pre- or perinatal brain injury (BI) show remarkable plasticity for language learning. Previous work highlights the important role that lesion characteristics play in explaining individual variation in plasticity in the language development of children with BI. The current study examines whether the linguistic input that children with BI receive from their caregivers also contributes to this early plasticity, and whether linguistic input plays a similar role in children with BI as it does in typically developing (TD) children. Growth in vocabulary and syntactic production is modeled for 80 children (53 TD, 27 BI) between 14 and 46 months. Findings indicate that caregiver input is an equally potent predictor of vocabulary growth in children with BI and in TD children. In contrast, input is a more potent predictor of syntactic growth for children with BI than for TD children. Controlling for input, lesion characteristics (lesion size, type, seizure history) also affect the language trajectories of children with BI. Thus, findings illustrate how both variability in the environment (linguistic input) and variability in the organism (lesion characteristics) work together to contribute to plasticity in language learning

What counts in the development of young children's number knowledge?

Prior studies indicate that children vary widely in their mathematical knowledge by the time they enter preschool and that this variation predicts levels of achievement in elementary school. In a longitudinal study of a diverse sample of 44 preschool children, we examined the extent to which their understanding of the cardinal meanings of the number words (e.g., knowing that the word “four” refers to sets with 4 items) is predicted by the “number talk” they hear from their primary caregiver in the early home environment. Results from 5 visits showed substantial variation in parents’ number talk to children between the ages of 14 and 30 months. Moreover, this variation predicted children’s knowledge of the cardinal meanings of number words at 46 months, even when socioeconomic status and other measures of parent and child talk were controlled. These findings suggest that encouraging parents to talk about number with their toddlers, and providing them with effective ways to do so, may positively impact children’s school achievement

The effect of ageing on fMRI: Correction for the confounding effects of vascular reactivity evaluated by joint fMRI and MEG in 335 adults.

In functional magnetic resonance imaging (fMRI) research one is typically interested in neural activity. However, the blood-oxygenation level-dependent (BOLD) signal is a composite of both neural and vascular activity. As factors such as age or medication may alter vascular function, it is essential to account for changes in neurovascular coupling when investigating neurocognitive functioning with fMRI. The resting-state fluctuation amplitude (RSFA) in the fMRI signal (rsfMRI) has been proposed as an index of vascular reactivity. The RSFA compares favourably with other techniques such as breath-hold and hypercapnia, but the latter are more difficult to perform in some populations, such as older adults. The RSFA is therefore a candidate for use in adjusting for age-related changes in vascular reactivity in fMRI studies. The use of RSFA is predicated on its sensitivity to vascular rather than neural factors; however, the extent to which each of these factors contributes to RSFA remains to be characterized. The present work addressed these issues by comparing RSFA (i.e., rsfMRI variability) to proxy measures of (i) cardiovascular function in terms of heart rate (HR) and heart rate variability (HRV) and (ii) neural activity in terms of resting state magnetoencephalography (rsMEG). We derived summary scores of RSFA, a sensorimotor task BOLD activation, cardiovascular function and rsMEG variability for 335 healthy older adults in the population-based Cambridge Centre for Ageing and Neuroscience cohort (Cam-CAN; www.cam-can.com). Mediation analysis revealed that the effects of ageing on RSFA were significantly mediated by vascular factors, but importantly not by the variability in neuronal activity. Furthermore, the converse effects of ageing on the rsMEG variability were not mediated by vascular factors. We then examined the effect of RSFA scaling of task-based BOLD in the sensorimotor task. The scaling analysis revealed that much of the effects of age on task-based activation studies with fMRI do not survive correction for changes in vascular reactivity, and are likely to have been overestimated in previous fMRI studies of ageing. The results from the mediation analysis demonstrate that RSFA is modulated by measures of vascular function and is not driven solely by changes in the variance of neural activity. Based on these findings we propose that the RSFA scaling method is articularly useful in large scale and longitudinal neuroimaging studies of ageing, or with frail participants, where alternative measures of vascular reactivity are impractical.The Cambridge Centre for Ageing and Neuroscience (Cam-CAN) research was supported by the Biotechnology and Biological Sciences Research Council (grant number BB/H008217/1). We are grateful to the Cam-CAN respondents and their primary care teams in Cambridge for their participation in this study. We also thank col- leagues at the MRC Cognition and Brain Sciences Unit MEG and MRI facilities for their assistance.This is the final version of the article. It first appeared at http://onlinelibrary.wiley.com/doi/10.1002/hbm.22768/ful

Oxidative Stress Promotes Peroxiredoxin Hyperoxidation and Attenuates Pro-survival Signaling in Aging Chondrocytes

Oxidative stress-mediated post-translational modifications of redox-sensitive proteins are postulated as a key mechanism underlying age-related cellular dysfunction and disease progression. Peroxiredoxins (PRX) are critical intracellular antioxidants that also regulate redox signaling events. Age-related osteoarthritis is a common form of arthritis that has been associated with mitochondrial dysfunction and oxidative stress. The objective of this study was to determine the effect of aging and oxidative stress on chondrocyte intracellular signaling, with a specific focus on oxidation of cytosolic PRX2 and mitochondrial PRX3. Menadione was used as a model to induce cellular oxidative stress. Compared with chondrocytes isolated from young adult humans, chondrocytes from older adults exhibited higher levels of PRX1–3 hyperoxidation basally and under conditions of oxidative stress. Peroxiredoxin hyperoxidation was associated with inhibition of pro-survival Akt signaling and stimulation of pro-death p38 signaling. These changes were prevented in cultured human chondrocytes by adenoviral expression of catalase targeted to the mitochondria (MCAT) and in cartilage explants from MCAT transgenic mice. Peroxiredoxin hyperoxidation was observed in situ in human cartilage sections from older adults and in osteoarthritic cartilage. MCAT transgenic mice exhibited less age-related osteoarthritis. These findings demonstrate that age-related oxidative stress can disrupt normal physiological signaling and contribute to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism

Community-Based Participatory Research: Lessons Learned from the Centers for Children’s Environmental Health and Disease Prevention Research

Over the past several decades there has been growing evidence of the increase in incidence rates, morbidity, and mortality for a number of health problems experienced by children. The causation and aggravation of these problems are complex and multifactorial. The burden of these health problems and environmental exposures is borne disproportionately by children from low-income communities and communities of color. Researchers and funding institutions have called for increased attention to the complex issues that affect the health of children living in marginalized communities—and communities more broadly—and have suggested greater community involvement in processes that shape research and intervention approaches, for example, through community-based participatory research (CBPR) partnerships among academic, health services, public health, and community-based organizations. Centers for Children’s Environmental Health and Disease Prevention Research (Children’s Centers) funded by the National Institute of Environmental Health Sciences and U.S. Environmental Protection Agency were required to include a CBPR project. The purpose of this article is to provide a definition and set of CBPR principles, to describe the rationale for and major benefits of using this approach, to draw on the experiences of six of the Children’s Centers in using CBPR, and to provide lessons learned and recommendations for how to successfully establish and maintain CBPR partnerships aimed at enhancing our understanding and addressing the multiple determinants of children’s health

The Cambridge Centre for Ageing and Neuroscience (Cam-CAN) study protocol: a cross-sectional, lifespan, multidisciplinary examination of healthy cognitive ageing.

BACKGROUND: As greater numbers of us are living longer, it is increasingly important to understand how we can age healthily. Although old age is often stereotyped as a time of declining mental abilities and inflexibility, cognitive neuroscience reveals that older adults use neural and cognitive resources flexibly, recruiting novel neural regions and cognitive processes when necessary. Our aim in this project is to understand how age-related changes to neural structure and function interact to support cognitive abilities across the lifespan. METHODS/DESIGN: We are recruiting a population-based cohort of 3000 adults aged 18 and over into Stage 1 of the project, where they complete an interview including health and lifestyle questions, a core cognitive assessment, and a self-completed questionnaire of lifetime experiences and physical activity. Of those interviewed, 700 participants aged 18-87 (100 per age decile) continue to Stage 2 where they undergo cognitive testing and provide measures of brain structure and function. Cognition is assessed across multiple domains including attention and executive control, language, memory, emotion, action control and learning. A subset of 280 adults return for in-depth neurocognitive assessment in Stage 3, using functional neuroimaging experiments across our key cognitive domains.Formal statistical models will be used to examine the changes that occur with healthy ageing, and to evaluate age-related reorganisation in terms of cognitive and neural functions invoked to compensate for overall age-related brain structural decline. Taken together the three stages provide deep phenotyping that will allow us to measure neural activity and flexibility during performance across a number of core cognitive functions. This approach offers hypothesis-driven insights into the relationship between brain and behaviour in healthy ageing that are relevant to the general population. DISCUSSION: Our study is a unique resource of neuroimaging and cognitive measures relevant to change across the adult lifespan. Because we focus on normal age-related changes, our results may contribute to changing views about the ageing process, lead to targeted interventions, and reveal how normal ageing relates to frail ageing in clinicopathological conditions such as Alzheimer's disease.The Cambridge Centre for Ageing and Neuroscience (Cam-CAN) research was supported by the Biotechnology and Biological Sciences Research Council (grant number BB/H008217/1).This is the final published version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s12883-014-0204-

Cognitive Diversity in a Healthy Aging Cohort: Cross-Domain Cognition in the Cam-CAN Project.

Objective: Studies of "healthy" cognitive aging often focus on a limited set of measures that decline with age. The current study argues that defining and supporting healthy cognition requires understanding diverse cognitive performance across the lifespan. Method: Data from the Cambridge Centre for Aging and Neuroscience (Cam-CAN) cohort was examined across a range of cognitive domains. Performance was related to lifestyle including education, social engagement, and enrichment activities. Results: Results indicate variable relationships between cognition and age (positive, negative, or no relationship). Principal components analysis indicated maintained cognitive diversity across the adult lifespan, and that cognition-lifestyle relationships differed by age and domain. Discussion: Our findings support a view of normal cognitive aging as a lifelong developmental process with diverse relationships between cognition, lifestyle, and age. This reinforces the need for large-scale studies of cognitive aging to include a wider range of both ages and cognitive tasks.The Cambridge Centre for Aging and Neuroscience (Cam-CAN) research was supported by the Biotechnology and Biological Sciences Research Council (grant number BB/H008217/1)