Perceived Risk of Predation Affects Reproductive Life - History Traits in Gambusia holbrooki, but Not in Heterandria formosa

Key to predicting impacts of predation is understanding the mechanisms through which predators impact prey populations. While consumptive effects are well-known, non-consumptive predator effects (risk effects) are increasingly being recognized as important. Studies of risk effects, however, have focused largely on how trade-offs between food and safety affect fitness. Less documented, and appreciated, is the potential for predator presence to directly suppress prey reproduction and affect life-history characteristics. For the first time, we tested the effects of visual predator cues on reproduction of two prey species with different reproductive modes, lecithotrophy (i.e. embryonic development primarily fueled by yolk) and matrotrophy (i.e. energy for embryonic development directly supplied by the mother to the embryo through a vascular connection). Predation risk suppressed reproduction in the lecithotrophic prey (Gambusia holbrokii) but not the matrotroph (Heterandria formosa). Predator stress caused G. holbrooki to reduce clutch size by 43%, and to produce larger and heavier offspring compared to control females. H. formosa, however, did not show any such difference. In G. holbrooki we also found a significantly high percentage (14%) of stillbirths in predator-exposed treatments compared to controls (2%). To the best of our knowledge, this is the first direct empirical evidence of predation stress affecting stillbirths in prey. Our results suggest that matrotrophy, superfetation (clutch overlap), or both decrease the sensitivity of mothers to environmental fluctuation in resource (food) and stress (predation risk) levels compared to lecithotrophy. These mechanisms should be considered both when modeling consequences of perceived risk of predation on prey-predator population dynamics and when seeking to understand the evolution of reproductive modes

Forming Student Online Teams For Maximum Performance

What is the best way to assign graduate business students to online team-based projects?  Team assignments are frequently made on the basis of alphabet, time zones or previous performance.  This study reviews personality as an indicator of student online team performance.  The personality assessment IDE (Insights Discovery Evaluator) was administered to 450 students in the first six-week course of a proprietary online university MBA program. The IDE was utilized for the study because the university had selected the IDE as a part of its business curriculum. In the second week, students were randomly placed on 138 virtual teams and quantitative data collected from an assignment where students self-reported their IDE type. A qualitative method was used to determine subject IDE type in those cases where subjects did not clearly identify their type. Performance was measured using three instructor- graded assignments completed during the course. Student virtual teams were categorized as random, variable and dominant, contingent upon the composition of team personality types. This study found no statistically significant relationship between IDE’s personality types or the cognitive trait variables of attitude (extroversion and introversion) or trait function (thinking and feeling) on team performance.  Personality trait did not appear to be a variable with the intentional formation of higher performing online student teams. All personality traits performed equally as well. Personality Bias (IDE type homogeneity) was the closest to being statistically significant as a factor in virtual team performance. A model is presented describing the relationship between personality and performance

Structural Color 3D Printing By Shrinking Photonic Crystals

The rings, spots and stripes found on some butterflies, Pachyrhynchus weevils, and many chameleons are notable examples of natural organisms employing photonic crystals to produce colorful patterns. Despite advances in nanotechnology, we still lack the ability to print arbitrary colors and shapes in all three dimensions at this microscopic length scale. Commercial nanoscale 3D printers based on two-photon polymerization are incapable of patterning photonic crystal structures with the requisite ~300 nm lattice constant to achieve photonic stopbands/ bandgaps in the visible spectrum and generate colors. Here, we introduce a means to produce 3D-printed photonic crystals with a 5x reduction in lattice constants (periodicity as small as 280 nm), achieving sub-100-nm features with a full range of colors. The reliability of this process enables us to engineer the bandstructures of woodpile photonic crystals that match experiments, showing that observed colors can be attributed to either slow light modes or stopbands. With these lattice structures as 3D color volumetric elements (voxels), we printed 3D microscopic scale objects, including the first multi-color microscopic model of the Eiffel Tower measuring only 39-microns tall with a color pixel size of 1.45 microns. The technology to print 3D structures in color at the microscopic scale promises the direct patterning and integration of spectrally selective devices, such as photonic crystal-based color filters, onto free-form optical elements and curved surfaces

Evolution of the HIV-1 nef gene in HLA-B*57 Positive Elite Suppressors

Elite controllers or suppressors (ES) are HIV-1 infected patients who maintain viral loads of < 50 copies/ml without antiretroviral therapy. CD8+ T cells are thought to play a key role in the control of viral replication and exert selective pressure on gag and nef in HLA-B*57 positive ES. We previously showed evolution in the gag gene of ES which surprisingly was mostly due to synonymous mutations rather than non-synonymous mutation in targeted CTL epitopes. This finding could be the result of structural constraints on Gag, and we therefore examined the less conserved nef gene. We found slow evolution of nef in plasma virus in some ES. This evolution is mostly due to synonymous mutations and occurs at a rate similar to that seen in the gag gene in the same patients. The results provide further evidence of ongoing viral replication in ES and suggest that the nef and gag genes in these patients respond similarly to selective pressure from the host

Tracheotomy care simulation training program for inpatient providers

Objectives: Tracheotomy complications can be life-threatening. Many of these complications may be avoided with proper education of health care providers. Unfortunately, access to high-quality tracheotomy care curricula is limited. We developed a program to address this gap in tracheotomy care education for inpatient providers. This study aimed to assess the efficacy of this training program in improving trainee knowledge and comfort with tracheotomy care. Methods: The curriculum includes asynchronous online modules coupled with a self-directed hands-on simulation activity using a low-cost tracheotomy care task trainer. The program was offered to inpatient providers including medical students, residents, medical assistants, nurses, and respiratory therapists. Efficacy of the training was assessed using pre-training and post-training surveys of learner comfort, knowledge, and qualitative feedback. Results: Data was collected on 41 participants. After completing the program, participants exhibited significantly improved comfort in performing tracheotomy care activities and 15% improvement in knowledge scores, with large effect sizes respectively and greater gains among those with little prior tracheotomy care experience. Conclusion: This study has demonstrated that completion of this integrated online and hands-on tracheotomy simulation curriculum training increases comfort and knowledge, especially for less-experienced learners. This training addresses an important gap in tracheotomy care education among health care professionals with low levels of tracheotomy care experience and ultimately aims to improve patient safety and quality of care. This curriculum is easily transferrable as it requires only access to the online modules and low-cost simulation materials and could be used in other hospitals, long-term care facilities, outpatient clinics, and home settings

Clumpy Galaxies in CANDELS. I. The Definition of UV Clumps and the Fraction of Clumpy Galaxies at 0.5<z<3

Although giant clumps of stars are crucial to galaxy formation and evolution, the most basic demographics of clumps are still uncertain, mainly because the definition of clumps has not been thoroughly discussed. In this paper, we study the basic demographics of clumps in star-forming galaxies (SFGs) at 0.5<z<3, using our proposed physical definition that UV-bright clumps are discrete star-forming regions that individually contribute more than 8% of the rest-frame UV light of their galaxies. Clumps defined this way are significantly brighter than the HII regions of nearby large spiral galaxies, either individually or blended, when physical spatial resolution and cosmological dimming are considered. Under this definition, we measure the fraction of SFGs that contain at least one off-center clump (Fclumpy) and the contributions of clumps to the rest-frame UV light and star formation rate of SFGs in the CANDELS/GOODS-S and UDS fields, where our mass-complete sample consists of 3239 galaxies with axial ratio q>0.5. The redshift evolution of Fclumpy changes with the stellar mass (M*) of the galaxies. Low-mass (log(M*/Msun)<9.8) galaxies keep an almost constant Fclumpy of about 60% from z~3.0 to z~0.5. Intermediate-mass and massive galaxies drop their Fclumpy from 55% at z~3.0 to 40% and 15%, respectively, at z~0.5. We find that (1) the trend of disk stabilization predicted by violent disk instability matches the Fclumpy trend of massive galaxies; (2) minor mergers are a viable explanation of the Fclumpy trend of intermediate-mass galaxies at z<1.5, given a realistic observability timescale; and (3) major mergers are unlikely responsible for the Fclumpy trend in all masses at z<1.5. The clump contribution to the rest-frame UV light of SFGs shows a broad peak around galaxies with log(M*/Msun)~10.5 at all redshifts, possibly linked to the molecular gas fraction of the galaxies. (Abridged)Comment: 22 pages, 15 figures. Appeared in ApJ (2015, 800, 39). A few typos correcte

Differential effects of RASA3 mutations on hematopoiesis are profoundly influenced by genetic background and molecular variant.

Studies of the severely pancytopenic scat mouse model first demonstrated the crucial role of RASA3, a dual RAS and RAP GTPase activating protein (GAP), in hematopoiesis. RASA3 is required for survival in utero; germline deletion is lethal at E12.5-13.5 due to severe hemorrhage. Here, conditional deletion in hematopoietic stem and progenitor cells (HSPCs) using Vav-iCre recapitulates the null phenotype demonstrating that RASA3 is required at the stem and progenitor level to maintain blood vessel development and integrity and effective blood production. In adults, bone marrow blood cell production and spleen stress erythropoiesis are suppressed significantly upon induction of RASA3 deficiency, leading to pancytopenia and death within two weeks. Notably, RASA3 missense mutations in two mouse models, scat (G125V) and hlb381 (H794L), show dramatically different hematopoietic consequences specific to both genetic background and molecular variant. The mutation effect is mediated at least in part by differential effects on RAS and RAP activation. In addition, we show that the role of RASA3 is conserved during human terminal erythropoiesis, highlighting a potential function for the RASA3-RAS axis in disordered erythropoiesis in humans. Finally, global transcriptomic studies in scat suggest potential targets to ameliorate disease progression

Mutant KLF1 in Adult Anemic Nan Mice Leads to Profound Transcriptome Changes and Disordered Erythropoiesis.

Anemic Nan mice carry a mutation (E339D) in the second zinc finger of erythroid transcription factor KLF1. Nan-KLF1 fails to bind a subset of normal KLF1 targets and ectopically binds a large set of genes not normally engaged by KLF1, resulting in a corrupted fetal liver transcriptome. Here, we performed RNAseq using flow cytometric-sorted spleen erythroid precursors from adult Nan and WT littermates rendered anemic by phlebotomy to identify global transcriptome changes specific to the Nan Klf1 mutation as opposed to anemia generally. Mutant Nan-KLF1 leads to extensive and progressive transcriptome corruption in adult spleen erythroid precursors such that stress erythropoiesis is severely compromised. Terminal erythroid differentiation is defective in the bone marrow as well. Principle component analysis reveals two major patterns of differential gene expression predicting that defects in basic cellular processes including translation, cell cycle, and DNA repair could contribute to disordered erythropoiesis and anemia in Nan. Significant erythroid precursor stage specific changes were identified in some of these processes in Nan. Remarkably, however, despite expression changes in large numbers of associated genes, most basic cellular processes were intact in Nan indicating that developing red cells display significant physiological resiliency and establish new homeostatic set points in vivo

The GLY2019SER Mutation in LRRK2 is Not Fully Penetrant in Familial Parkinson\u27s Disease: the GenePD Study

Background: We report age-dependent penetrance estimates for leucine-rich repeat kinase 2 (LRRK2)-related Parkinson\u27s disease (PD) in a large sample of familial PD. The most frequently seen LRRK2 mutation, Gly2019Ser (G2019S), is associated with approximately 5 to 6% of familial PD cases and 1 to 2% of idiopathic cases, making it the most common known genetic cause of PD. Studies of the penetrance of LRRK2 mutations have produced a wide range of estimates, possibly due to differences in study design and recruitment, including in particular differences between samples of familial PD versus sporadic PD. Methods: A sample, including 903 affected and 58 unaffected members from 509 families ascertained for having two or more PD-affected members, 126 randomly ascertained PD patients and 197 controls, was screened for five different LRRK2 mutations. Penetrance was estimated in families of LRRK2 carriers with consideration of the inherent bias towards increased penetrance in a familial sample. Results: Thirty-one out of 509 families with multiple cases of PD (6.1%) were found to have 58 LRRK2 mutation carriers (6.4%). Twenty-nine of the 31 families had G2019S mutations while two had R1441C mutations. No mutations were identified among controls or unaffected relatives of PD cases. Nine PD-affected relatives of G2019S carriers did not carry the LRRK2 mutation themselves. At the maximum observed age range of 90 to 94 years, the unbiased estimated penetrance was 67% for G2019S families, compared with a baseline PD risk of 17% seen in the non-LRRK2-related PD families. Conclusion: Lifetime penetrance of LRRK2 estimated in the unascertained relatives of multiplex PD families is greater than that reported in studies of sporadically ascertained LRRK2 cases, suggesting that inherited susceptibility factors may modify the penetrance of LRRK2 mutations. In addition, the presence of nine PD phenocopies in the LRRK2 families suggests that these susceptibility factors may also increase the risk of non-LRRK2-related PD. No differences in penetrance were found between men and women, suggesting that the factors that influence penetrance for LRRK2 carriers are independent of the factors which increase PD prevalence in men