EXPLORING THE EFFECTS OF RECESS ON ACADEMIC PERFORMANCE

This paper seeks to explore the effects of recess on an elementary student’s academic performance based on interviews completed with educational professionals. By answering the interview questions, these responses helped gauge the attitudes and perspectives these professionals have towards the inclusion of recess in their students’ days. Recess is currently being left out of daily routine for sake of more instructional time in a classroom. This study seeks to add to the stance of students needing recess as a time of unstructured play, in which they can learn meaningful interactions that would otherwise be omitted from their learning

Myanmar: Malaria

Myanmar is an underdeveloped country that struggles with the problem of lack of medical access and expensive healthcare. The endemic of Malaria has been going on for several years in this country and many efforts have been made to try and decrease the Public Health issue. However, Myanmar still has the highest number of Malaria-related deaths. The Myanmar government is continuously working at improving the healthcare system to help with the Malaria endemic. However, the poor country still continues to struggle with this issue. The parasite, P. falciparum, has been an ongoing issue since it is resistant to the anti-malarial vaccines making the risk of contracting Malaria much higher. Symptoms of this disease are likely to be fatal if they are not addressed within a certain time period. With this disease affecting two-thirds of the population, a lagging healthcare system, and a lack of insecticide-treated nets, this makes Malaria a major concern in Myanmar

Flawed Phospholipid Formation or Faulty Fatty Acid Oxidation: Determining the Cause of Mitochondrial Dysfunction in Hearts Lacking ACSL1

Cardiovascular disease is the number one cause of death worldwide. In the heart, mitochondria provide up to 95% of energy, with most of this energy coming from metabolism of fatty acids (FA). FA must be converted to acyl-CoAs by acyl-CoA synthetases (ACS) before entry into pathways of β- oxidation or glycerolipid synthesis. ACSL1 contributes more than 90% of total cardiac ACSL activity, and mice with an inducible knockout of ACSL1 (Acsl1T-/-) have impaired cardiac FA oxidation. The effects of loss of ACSL1 on mitochondrial respiratory function, phospholipid formation, or autophagic flux have not yet been studied. Acsl1T-/- hearts contained 3-fold more mitochondria with abnormal structure and displayed lower respiratory function. Because ACSL1 exhibited a strong substrate preference for linoleate (18:2), we investigated the composition of mitochondrial phospholipids. Acsl1T-/- hearts contained 83% less tetralinoleoyl-cardiolipin (CL), the major form present in control hearts. Modulating ACSL1 expression in cell lines confirmed that ACSL1 is necessary for linoleate incorporation into CL. To determine whether increasing content of linoleate in CL would improve mitochondrial respiratory function, control and Acsl1T-/- mice were fed a high linoleate diet, which normalized amount of tetralinoleoyl-CL, but did not improve respiratory function. The metabolic switch from FA use to high glucose use activates mechanistic target of rapamycin complex 1 (mTORC1), which initiates growth by increasing protein and RNA synthesis and FA metabolism while decreasing autophagy. Short-term mTORC1 inhibition normalized mitochondrial structure, number, and maximal respiration rate in Acsl1T-/- hearts but not ADP-stimulated oxygen consumption, which was likely caused by lower ATP synthase activity present in both vehicle- and rapamycin-treated Acsl1T-/- hearts. The autophagic rate was 88% lower in Acsl1T-/- hearts. mTORC1 inhibition increased autophagy to a rate that was 3.1-fold higher than in controls, allowing clearance of damaged mitochondria. ACSL1 deficiency in heart activated mTORC1, thereby inhibiting autophagy and increasing the number of damaged mitochondria with impaired respiratory capacity. ACSL1 is required for the normal composition of phospholipid species and maintenance of FA oxidation to prevent low autophagic rate. Loss of ACSL1 causes impaired mitochondrial respiratory function, which can be partially improved by clearing damaged mitochondria but not by normalizing CL.Doctor of Philosoph

Balancing different types of actin polymerization at distinct sites: roles for Abelson kinase and Enabled

The proto-oncogenic kinase Abelson (Abl) regulates actin in response to cell signaling. Drosophila Abl is required in the nervous system, and also in epithelial cells, where it regulates adherens junction stability and actin organization. Abl acts at least in part via the actin regulator Enabled (Ena), but the mechanism by which Abl regulates Ena is unknown. We describe a novel role for Abl in early Drosophila development, where it regulates the site and type of actin structures produced. In Abl's absence, excess actin is polymerized in apical microvilli, whereas too little actin is assembled into pseudocleavage and cellularization furrows. These effects involve Ena misregulation. In abl mutants, Ena accumulates ectopically at the apical cortex where excess actin is observed, suggesting that Abl regulates Ena's subcellular localization. We also examined other actin regulators. Loss of Abl leads to changes in the localization of the Arp2/3 complex and the formin Diaphanous, and mutations in diaphanous or capping protein β enhance abl phenotypes

Abelson kinase regulates epithelial morphogenesis in Drosophila

Activation of the nonreceptor tyrosine kinase Abelson (Abl) contributes to the development of leukemia, but the complex roles of Abl in normal development are not fully understood. Drosophila Abl links neural axon guidance receptors to the cytoskeleton. Here we report a novel role for Drosophila Abl in epithelial cells, where it is critical for morphogenesis. Embryos completely lacking both maternal and zygotic Abl die with defects in several morphogenetic processes requiring cell shape changes and cell migration. We describe the cellular defects that underlie these problems, focusing on dorsal closure as an example. Further, we show that the Abl target Enabled (Ena), a modulator of actin dynamics, is involved with Abl in morphogenesis. We find that Ena localizes to adherens junctions of most epithelial cells, and that it genetically interacts with the adherens junction protein Armadillo (Arm) during morphogenesis. The defects of abl mutants are strongly enhanced by heterozygosity for shotgun, which encodes DE-cadherin. Finally, loss of Abl reduces Arm and α-catenin accumulation in adherens junctions, while having little or no effect on other components of the cytoskeleton or cell polarity machinery. We discuss possible models for Abl function during epithelial morphogenesis in light of these data

The Assessment of Quad to Quad and Hamstring to Quad Ratios in Patients Twelve to Twenty-Four Months Post Completion of a Supervised Anterior Cruciate Ligament Reconstruction Rehabilitation Program

Context: The assessment of quadriceps to quadriceps (Q-Q) and hamstring to quadriceps (H-Q) ratios following anterior cruciate ligament (ACL) reconstruction is an important factor for returning to sport. Significant differences in these ratios can result in reinjury. Objective: The purpose of this study is to assess Q-Q and H-Q ratios in collegiate athletes who have undergone ACL reconstruction and have successfully completed a supervised physical therapy program in the last 12-24 months and compare the results to established normative return to play guidelines (Q-Q = 90% and H-Q = 60%). Design: Cross-sectional study. Setting: Midwest outpatient physical therapy clinic. Patients or Other Participants: Four collegiate athletes (2 females and 2 males; age range = 19-21). Inclusion criteria included a previous ACL reconstruction using a bone-patellar tendon-bone graft and completion of a supervised physical therapy program in the past 12-24 months. Methods: Isokinetic strength measurement and peak torque values of knee flexion and extension between injured and uninjured legs using the Humac Norm Isokinetic Dynamometer by CSMI. The Q-Q and H-Q ratios were calculated using raw data. Main Outcome Measures: Q-Q and H-Q Ratios Results: Subject 1: Q-Q = 97%, H-Q = 62%; Subject 2: Q-Q = 109%, H-Q = 65%; Subject 3: Q-Q = 110%, H-Q = 61%; Subject 4: Q-Q = 113%, H-Q = 77%. Conclusions: Results indicate that each of the subjects met return to play normative values. Due to the small number of participants, further research is needed to discover any true discrepancies

Drosophila APC2 and APC1 Play Overlapping Roles in Wingless Signaling in the Embryo and Imaginal Discs

The regulation of signal transduction plays a key role in cell fate choices, and its disregulation contributes to oncogenesis. This duality is exemplified by the tumor suppressor APC. Originally identified for its role in colon tumors, APC family members were subsequently shown to negatively regulate Wnt signaling in both development and disease. The analysis of the normal roles of APC proteins is complicated by the presence of two APC family members in flies and mice. Previous work demonstrated that, in some tissues, single mutations in each gene have no effect, raising the question of whether there is functional overlap between the two APCs or whether APC-independent mechanisms of Wnt regulation exist. We addressed this by eliminating the function of both APC genes simultaneously. We find that APC1 and APC2 play overlapping roles in regulating Wingless signaling in the embryonic epidermis and the imaginal discs. Surprisingly, APC1 function in embryos occurs at levels of expression nearly too low to detect. Further, the overlapping functions exist despite striking differences in the intracellular localization of the two APC family members

Modeling the transition from decompensated to pathological hypertrophy

Background--Long-chain acyl-CoA synthetases (ACSL) catalyze the conversion of long-chain fatty acids to fatty acyl-CoAs. Cardiac-specific ACSL1 temporal knockout at 2 months results in a shift from FA oxidation toward glycolysis that promotes mTORC1-mediated ventricular hypertrophy. We used unbiased metabolomics and gene expression analyses to examine the early effects of genetic inactivation of fatty acid oxidation on cardiac metabolism, hypertrophy development, and function. Methods and Results--Global cardiac transcriptional analysis revealed differential expression of genes involved in cardiac metabolism, fibrosis, and hypertrophy development in Acsl1 H-/- hearts 2 weeks after Acsl1 ablation. Comparison of the 2- and 10-week transcriptional responses uncovered 137 genes whose expression was uniquely changed upon knockdown of cardiac ACSL1, including the distinct upregulation of fibrosis genes, a phenomenon not observed after complete ACSL1 knockout. Metabolomic analysis identified metabolites altered in hearts displaying partially reduced ACSL activity, and rapamycin treatment normalized the cardiac metabolomic fingerprint. Conclusions--Short-term cardiac-specific ACSL1 inactivation resulted in metabolic and transcriptional derangements distinct from those observed upon complete ACSL1 knockout, suggesting heart-specific mTOR (mechanistic target of rapamycin) signaling that occurs during the early stages of substrate switching. The hypertrophy observed with partial Acsl1 ablation occurs in the context of normal cardiac function and is reminiscent of a physiological process, making this a useful model to study the transition from physiological to pathological hypertrophy

Glycerol-3-phosphate Acyltransferase Isoform-4 (GPAT4) Limits Oxidation of Exogenous Fatty Acids in Brown Adipocytes

Glycerol-3-phosphate acyltransferase-4 (GPAT4) null pups grew poorly during the suckling period and, as adults, were protected from high fat diet-induced obesity. To determine why Gpat4−/− mice failed to gain weight during these two periods of high fat feeding, we examined energy metabolism. Compared with controls, the metabolic rate of Gpat4−/− mice fed a 45% fat diet was 12% higher. Core body temperature was 1 ºC higher after high fat feeding. Food intake, fat absorption, and activity were similar in both genotypes. Impaired weight gain in Gpat4−/− mice did not result from increased heat loss, because both cold tolerance and response to a β3-adrenergic agonist were similar in both genotypes. Because GPAT4 comprises 65% of the total GPAT activity in brown adipose tissue (BAT), we characterized BAT function. A 45% fat diet increased the Gpat4−/− BAT expression of peroxisome proliferator-activated receptor α (PPAR) target genes, Cpt1α, Pgc1α, and Ucp1, and BAT mitochondria oxidized oleate and pyruvate at higher rates than controls, suggesting that fatty acid signaling and flux through the TCA cycle were enhanced. To assess the role of GPAT4 directly, neonatal BAT preadipocytes were differentiated to adipocytes. Compared with controls, Gpat4−/− brown adipocytes incorporated 33% less fatty acid into triacylglycerol and 46% more into the pathway of β-oxidation. The increased oxidation rate was due solely to an increase in the oxidation of exogenous fatty acids. These data suggest that in the absence of cold exposure, GPAT4 limits excessive fatty acid oxidation and the detrimental induction of a hypermetabolic state