A Study of Biology Teaching in the State of Washington – 1959 versus 1965

It was the purpose of this study to (1) determine the scope and teaching methods used in biology courses in the State of Washington in 1965; (2) to determine the factors which influenced the scope and methods; (3) to compare the scope and methods with similar data collected in 1959; and (4) to determine if changes that occurred gave evidence of trends

The Effect of Energy Patches on Substrate Utilization in Collegiate Cross-Country Runners

It is well established that an increased capacity of skeletal muscle to oxidize fatty acids can spare glycogen and delay the onset of fatigue in mild- to moderate-intensity exercise. The purpose of the following study was to examine the effect of LifeWave® energy patches on non-protein substrate utilization in Division-1 cross-country runners. To determine the effect of the patches subjects were pretested to establish baselines and randomly assigned to an experimental (EX) or placebo (PL) group. Twenty-two trained male (n = 11; mean ± SD, age = 21.1 ± 2.6years, height = 179.6 ± 4.2cm, body mass = 71.4 ± 7.4kg, VO2max = 72.6 ± 7.1mL•kg-1•min-1) and female (n = 11; mean ± SD, age = 21.5 ± 2.4years, height = 166.7 ± 5.7cm, body mass = 53.7 ± 3.2kg, VO2max = 63.6 ± 6.9mL•kg-1•min-1) cross-country runners volunteered to participate in the study. Dependent variables included maximal oxygen consumption (VO2max), rating of perceived exertion (RPE), respiratory exchange ratio (RER), maximum heart rate (HRmax), and time to exhaustion (TTE). Results indicated there were no significant differences between the EX and PL groups at posttesting for RPE, TTE, HRmax, or VO2max. RER was found to be significantly higher for the EX group compared to the PL group during stage 1 of the Bruce-protocol graded exercise test (p = 0.02). Based on the limited available research regarding LifeWave® energy patches effect on non-protein substrate utilization during aerobic exercise there appears to be no performance enhancing benefits

Temperature and magnetic-field dependence of the conductivity of YBaCuO films in the vicinity of superconducting transition: Effect of Tc-inhomogeneity

Temperature and magnetic field dependences of the conductivity of YBaCuO films in the transition region are analyzed taking into account spatial inhomogeneity in transition temperature, Tc. (i) An expression for the superconducting contribution to conductivity, \sigma_s(T,H,Tc), of a homogeneous superconductor for H<<Hc2(T=0) is obtained using the solution of the Ginzburg-Landau equation in form of perturbation expansions [S.Ullah, A.T.Dorsey, PRB 44, 262 (1991)]. (ii) The error in \sigma_s(T,H,Tc) occurring due to the presence of Tc-inhomogeneity is calculated and plotted on an H-T plane diagram. These calculations use an effective medium approximation and a Gaussian distribution of Tc. (iii) Measuring the temperature dependences of a voltage, induced by a focused electron beam, we determine spatial distributions of the critical temperature for YBaCuO microbridges with a 2 micron resolution. A typical Tc-distribution dispersion is found to be approximately 1K. For such dispersion, error in \sigma_s(T,H,Tc) due to Tc-inhomogeneity exceeds 30% for magnetic fields H < 1 T and temperatures |T-Tc| < 0.5 K. (iv) Experimental R(T,H) dependences of resistance are well described by a numerical solution of a set of Kirchoff equations for the resistor network based on the measured spatial distributions of Tc and the expression for \sigma_s(T,H,Tc).Comment: REVTeX, 12 pages including 7 figures, resubmitted to Phys. Rev.

Structural basis of nSH2 regulation and lipid binding in PI3Kα

We report two crystal structures of the wild-type phosphatidylinositol 3-kinase α (PI3Kα) heterodimer refined to 2.9 Å and 3.4 Å resolution: the first as the free enzyme, the second in complex with the lipid substrate, diC4-PIP2, respectively. The first structure shows key interactions of the N-terminal SH2 domain (nSH2) and iSH2 with the activation loop that suggest a mechanism by which the enzyme is inhibited in its basal state. In the second structure, the lipid substrate binds in a positively charged pocket adjacent to the ATP-binding site, bordered by the P-loop, the activation loop and the iSH2 domain. An additional lipid-binding site was identified at the interface of the ABD, iSH2 and kinase domains. The ability of PI3Kα to bind an additional PIP2 molecule was confirmed in vitro by fluorescence quenching experiments. The crystal structures reveal key differences in the way the nSH2 domain interacts with wild-type p110α and with the oncogenic mutant p110αH1047R. Increased buried surface area and two unique salt-bridges observed only in the wild-type structure suggest tighter inhibition in the wild-type PI3Kα than in the oncogenic mutant. These differences may be partially responsible for the increased basal lipid kinase activity and increased membrane binding of the oncogenic mutant

De novo variants predicting haploinsufficiency for DIP2C are associated with expressive speech delay.

The disconnected (disco)-interacting protein 2 (DIP2) gene was first identified in D. melanogaster and contains a DNA methyltransferase-associated protein 1 (DMAP1) binding domain, Acyl-CoA synthetase domain and AMP-binding sites. DIP2 regulates axonal bifurcation of the mushroom body neurons in D. melanogaster and is required for axonal regeneration in the neurons of C. elegans. The DIP2 homologues in vertebrates, Disco-interacting protein 2 homolog A (DIP2A), Disco-interacting protein 2 homolog B (DIP2B), and Disco-interacting protein 2 homolog C (DIP2C), are highly conserved and expressed widely in the central nervous system. Although there is evidence that DIP2C plays a role in cognition, reports of pathogenic variants in these genes are rare and their significance is uncertain. We present 23 individuals with heterozygous DIP2C variants, all manifesting developmental delays that primarily affect expressive language and speech articulation. Eight patients had de novo variants predicting loss-of-function in the DIP2C gene, two patients had de novo missense variants, three had paternally inherited loss of function variants and six had maternally inherited loss-of-function variants, while inheritance was unknown for four variants. Four patients had cardiac defects (hypertrophic cardiomyopathy, atrial septal defects, and bicuspid aortic valve). Minor facial anomalies were inconsistent but included a high anterior hairline with a long forehead, broad nasal tip, and ear anomalies. Brainspan analysis showed elevated DIP2C expression in the human neocortex at 10-24 weeks after conception. With the cases presented herein, we provide phenotypic and genotypic data supporting the association between loss-of-function variants in DIP2C with a neurocognitive phenotype

Inherited variants in CHD3 show variable expressivity in Snijders Blok-Campeau syndrome

Purpose: Common diagnostic next-generation sequencing strategies are not optimized to identify inherited variants in genes associated with dominant neurodevelopmental disorders as causal when the transmitting parent is clinically unaffected, leaving a significant number of cases with neurodevelopmental disorders undiagnosed. Methods: We characterized 21 families with inherited heterozygous missense or protein-truncating variants in CHD3, a gene in which de novo variants cause Snijders Blok-Campeau syndrome. Results: Computational facial and Human Phenotype Ontology–based comparisons showed that the phenotype of probands with inherited CHD3 variants overlaps with the phenotype previously associated with de novo CHD3 variants, whereas heterozygote parents are mildly or not affected, suggesting variable expressivity. In addition, similarly reduced expression levels of CHD3 protein in cells of an affected proband and of healthy family members with a CHD3 protein-truncating variant suggested that compensation of expression from the wild-type allele is unlikely to be an underlying mechanism. Notably, most inherited CHD3 variants were maternally transmitted. Conclusion: Our results point to a significant role of inherited variation in Snijders Blok-Campeau syndrome, a finding that is critical for correct variant interpretation and genetic counseling and warrants further investigation toward understanding the broader contributions of such variation to the landscape of human disease