Experiential Learning and its Impact on Critical Thinking

Background: In occupational therapy education, it is unclear what educational methods best facilitate the development of critical thinking. Therefore, this pilot study explored whether Level I fieldwork coupled with reflective learning opportunities impacts the development of critical thinking skills. Methods: The researchers employed a pre and post-test design which measured both self-perception of critical thinking and actual performance of critical thinking. Specifically, the Health Science Reasoning Test (HSRT) and a reflective writing assignment graded with a rubric were utilized to measure actual performance. The Self-Assessment of Critical Reflection and Reasoning (SACRR) was used to measure self-perceived performance of critical thinking. Results: In this study, participants demonstrated improvements in critical thinking following a Level I fieldwork. Specific improvements were found in the areas of evaluation and induction skills, which are subscales of the HRST. There was also an increase in participants’ self-perceived confidence in utilizing critical thinking skills. The use of reflective writing assignment was found to increase the participants’ ability to use evaluation, inference, and deduction skills. Conclusion: Experiential learning experiences coupled with a reflective writing assignment is an effective means of developing critical thinking skills. Future research should utilize a bigger sample size to confirm the findings and increase the generalizability of the results

Zinc deficiency and neurodevelopment: the case of neurons

Zinc is essential for normal brain development. Gestational severe zinc deficiency can lead to overt fetal brain malformations. Although not teratogenic, suboptimal zinc nutrition during gestation can have long-term effects on the offspring's nervous system. This article will review current knowledge on the role of zinc in modulating neurogenesis and neuronal apoptosis as well as the proposed underlying mechanisms. A decrease in neuronal zinc causes cell cycle arrest, which in part involves a deregulation of select signals (ERK1/2, p53, and NF-κB). Zinc deficiency also induces apoptotic neuronal death through the intrinsic (mitochondrial) pathway, which can be triggered by the activation of the zinc-regulated enzyme caspase-3, and as a consequence of abnormal regulation of prosurvival signals (ERK1/2 and NF-κB). Alterations in the finely tuned processes of neurogenesis, neuronal migration, differentiation, and apoptosis, which involve the developmental shaping of the nervous system, could have a long-term impact on brain health. Zinc deficiency during gestation, even at the marginal levels observed in human populations, could increase the risk for behavioral/neurological disorders in infancy, adolescence, and adulthood.Fil: Adamo, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Oteiza, Patricia Isabel. University of California at Davis; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Premature Cell Senescence and T Cell Receptor‐Independent Activation of CD8+ T Cells in Juvenile Idiopathic Arthritis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/99044/1/art38015.pd

A Weighted Gene Co-expression Network Analysis for Streptococcus sanguinis Microarray Experiments

Streptococcus sanguinis is a gram-positive, non-motile bacterium native to human mouths. It is the primary cause of endocarditis and is also responsible for tooth decay. Two-component systems (TCSs) are commonly found in bacteria. In response to environmental signals, TCSs may regulate the expression of virulence factor genes. Gene co-expression networks are exploratory tools used to analyze system-level gene functionality. A gene co-expression network consists of gene expression profiles represented as nodes and gene connections, which occur if two genes are significantly co-expressed. An adjacency function transforms the similarity matrix containing co-expression similarities into the adjacency matrix containing connection strengths. Gene modules were determined from the connection strengths, and various network connectivity measures were calculated. S. sanguinis gene expression profile data was loaded for 2272 genes and 14 samples with 3 replicates each. The soft thresholding power β=6 was chosen to maximize R2 while maintaining a high mean number of connections. Nine modules were found. Possible meta-modules were found to be: Module 1: Blue & Green, Module 2: Pink, Module 3: Yellow, Brown & Red, Module 4: Black, Module 5: Magenta & Turquoise. The absolute value of module membership was found to be highly positively correlated with intramodular connectivity. Each of the nine modules were examined. Two methods (intramodular connectivity and TOM-based connectivity followed by network mapping) for identifying candidate hub genes were performed. Most modules provided similar results between the two methods. Similar rankings between the two methods can be considered equivalent and both can be used to detect candidate hub genes. Gene ontology information was unavailable to help select a module of interest. This network analysis would help researchers create new research hypotheses and design experiments for validation of candidate hub genes in biologically important modules

Zinc intake, status and indices of cognitive function in adults and children: a systematic review and meta-analysis

In developing countries, deficiencies of micronutrients are thought to have a major impact on child development; however, a consensus on the specific relationship between dietary zinc intake and cognitive function remains elusive. The aim of this systematic review was to examine the relationship between zinc intake, status and indices of cognitive function in children and adults. A systematic literature search was conducted using EMBASE, MEDLINE and Cochrane Library databases from inception to March 2014. Included studies were those that supplied zinc as supplements or measured dietary zinc intake. A meta-analysis of the extracted data was performed where sufficient data were available. Of all of the potentially relevant papers, 18 studies met the inclusion criteria, 12 of which were randomised controlled trials (RCTs; 11 in children and 1 in adults) and 6 were observational studies (2 in children and 4 in adults). Nine of the 18 studies reported a positive association between zinc intake or status with one or more measure of cognitive function. Meta-analysis of data from the adult’s studies was not possible because of limited number of studies. A meta-analysis of data from the six RCTs conducted in children revealed that there was no significant overall effect of zinc intake on any indices of cognitive function: intelligence, standard mean difference of <0.001 (95% confidence interval (CI) –0.12, 0.13) P=0.95; executive function, standard mean difference of 0.08 (95% CI, –0.06, 022) P=0.26; and motor skills standard mean difference of 0.11 (95% CI –0.17, 0.39) P=0.43. Heterogeneity in the study designs was a major limitation, hence only a small number (n=6) of studies could be included in the meta-analyses. Meta-analysis failed to show a significant effect of zinc supplementation on cognitive functioning in children though, taken as a whole, there were some small indicators of improvement on aspects of executive function and motor development following supplementation but high-quality RCTs are necessary to investigate this further

Calcinosis in juvenile dermatomyositis: Updates on pathogenesis and treatment

Calcinosis, or the deposition of insoluble calcium salts in the skin, subcutaneous tissue, fascia, tendons, and muscles, is a feared complication of juvenile dermatomyositis. Calcinosis is estimated to affect up to 40% of patients with juvenile dermatomyositis and contributes to significant disease morbidity. Calcinosis can be challenging to treat, and the most effective treatment remains unknown because of a lack of comparative studies. We aim to review the literature published in the last 5 years to summarize updates on the pathogenesis and treatment of calcinosis in juvenile dermatomyositis and describe future areas for research

A Path to Prediction of Outcomes in Juvenile Idiopathic Inflammatory Myopathy

Humans have an innate desire to observe and subsequently dissect an event into component pieces in an effort to better characterize the event. We then examine these pieces individually and in combinations using this information to determine the outcome of future similar events and the likelihood of their recurrence. Practically, this attempt to foretell an occurrence and predict its outcomes is evident in multiple disciplines ranging from meteorology to sociologic studies. In this manuscript we share the historical and present-day tools to predict course and outcome in juvenile idiopathic inflammatory myopathy including clinical features, testing, and biomarkers. Further we discuss considerations for building more complex predictive models of outcome especially in diseases such as juvenile idiopathic inflammatory myopathy where patients numbers are low. Many of the barriers to developing risk prediction models for juvenile idiopathic inflammatory myopathy outcomes have improved with many remaining challenges being addressed

The simplicit1 study: A randomized, double-blind, placebo-controlled phase 1b/2 adaptive study of ttp399, a hepatoselective glucokinase activator, for adjunctive treatment of type 1 diabetes

OBJECTIVE Despite advances in exogenous insulin therapy, many patients with type 1 diabetes do not achieve acceptable glycemic control and remain at risk for ketosis and insulin-induced hypoglycemia. We conducted a randomized controlled trial to determine whether TTP399, a novel hepatoselective glucokinase activator, improved glycemic control in people with type 1 diabetes without increasing hypoglycemia or ketosis. RESEARCH DESIGN AND METHODS SimpliciT1 was a phase 1b/2 adaptive study. Phase 2 activities were conducted in two parts. Part 1 randomly assigned 20 participants using continuous glucose monitors and continuous subcutaneous insulin infusion (CSII). Part 2 randomly assigned 85 participants receiving multiple daily injections of insulin or CSII. In both parts 1 and 2, participants were randomly assigned to 800 mg TTP399 or matched placebo (fully blinded) and treated for 12 weeks. The primary end point was change in HbA1c from baseline to week 12. RESULTS The difference in change in HbA1c from baseline to week 12 between TTP399 and placebo was-0.7% (95% CI-1.3,-0.07) in part 1 and-0.21% (95% CI-0.39,-0.04) in part 2. Despite a greater decrease in HbA1c with TTP399, the frequency of severe or symptomatic hypoglycemia decreased by 40% relative to placebo in part 2. In both parts 1 and 2, plasma β-hydroxybutyrate and urinary ketones were lower during treatment with TTP399 than placebo. CONCLUSIONS TTP399 lowers HbA1c and reduces hypoglycemia without increasing the risk of ketosis and should be further evaluated as an adjunctive therapy for the treatment of type 1 diabetes

The Role of Zinc in the Modulation of Neuronal Proliferation and Apoptosis

Although a requirement of zinc (Zn) for normal brain development is well documented, the extent to which Zn can modulate neuronal proliferation and apoptosis is not clear. Thus, we investigated the role of Zn in the regulation of these two critical events. A low Zn availability leads to decreased cell viability in human neuroblastoma IMR-32 cells and primary cultures of rat cortical neurons. This occurs in part as a consequence of decreased cell proliferation and increased apoptotic cell death. In IMR-32 cells, Zn deficiency led to the inhibition of cell proliferation through the arrest of the cell cycle at the G0/G1 phase. Zn deficiency induced apoptosis in both proliferating and quiescent neuronal cells via the intrinsic apoptotic pathway. Reductions in cellular Zn triggered a translocation of the pro-apoptotic protein Bad to the mitochondria, cytochrome c release, and caspase-3 activation. Apoptosis is the resultant of the inhibition of the prosurvival extracellular-signal-regulated kinase, the inhibition of nuclear factor-kappa B, and associated decreased expression of antiapoptotic proteins, and to a direct activation of caspase-3. A deficit of Zn during critical developmental periods can have persistent effects on brain function secondary to a deregulation of neuronal proliferation and apoptosis