197 research outputs found
Bio-inspired design of ice-retardant devices based on benthic marine invertebrates: the effect of surface texture
Growth of ice on surfaces poses a challenge for both organisms and for
devices that come into contact with liquids below the freezing point.
Resistance of some organisms to ice formation and growth, either in subtidal
environments (e.g. Antarctic anchor ice), or in environments with moisture and
cold air (e.g. plants, intertidal) begs examination of how this is
accomplished. Several factors may be important in promoting or mitigating ice
formation. As a start, here we examine the effect of surface texture alone. We
tested four candidate surfaces, inspired by hard-shelled marine invertebrates
and constructed using a three-dimensional printing process. We screened
biological and artifical samples for ice formation and accretion in submerged
conditions using previous methods, and developed a new test to examine ice
formation from surface droplets as might be encountered in environments with
moist, cold air. It appears surface texture plays only a small role in delaying
the onset of ice formation: a stripe feature (corresponding to patterning found
on valves of blue mussels, Crassostrea gigas, or on the spines of the Antarctic
sea urchin, Sterechinus neumayeri) slowed ice formation an average of 25%
compared to a grid feature (corresponding to patterning found on sub-polar
butterclams, Saxidomas). The geometric dimensions of the features have only a
small (~6%) effect on ice formation. Surface texture affects ice formation, but
does not explain by itself the large variation in ice formation and
species-specific ice resistance observed in other work. This suggests future
examination of other factors, such as material elastic properties and coatings,
and their interaction with surface pattern
The effect of single‐component sleep restriction therapy on depressive symptoms: A systematic review and meta‐analysis
Summary: Sleep restriction therapy is a behavioural component within cognitive behavioural therapy for insomnia and is an effective standalone treatment for insomnia, but its effect on depressive symptoms remains unclear. This review aimed to synthesise and evaluate the impact of single‐component sleep restriction therapy on depressive symptoms relative to a control intervention. We searched electronic databases and sleep‐related journals for randomised controlled trials and uncontrolled clinical trials, published from 1 January 1986 until 19 August 2023, that delivered sleep restriction therapy to adults with insomnia. Random‐effects meta‐analysis of standardised mean differences and Cochrane risk of bias assessment were performed on randomised controlled trials, while uncontrolled clinical trials were discussed narratively. The meta‐analysis was pre‐registered on PROSPERO (ID: CRD42020191803). We identified seven randomised controlled trials (N = 1102) and two uncontrolled clinical trials (N = 22). Findings suggest that sleep restriction therapy is associated with a medium effect for improvement in depressive symptoms at post‐treatment (N c = 6, g = −0.45 [95% confidence interval = −0.70 to −0.21], p < 0.001) and a small effect at follow‐up (N c = 4, g = −0.31 [95% confidence interval = −0.45 to −0.16], p < 0.001). Five of the seven included randomised controlled trials were judged to have a high risk of bias. Standalone sleep restriction therapy appears to be efficacious for improving depressive symptoms at post‐treatment and follow‐up. However, conclusions are tentative due to the small number of trials and because none of the trials was performed in a population with clinically defined depression. Large‐scale trials are needed to test the effect of sleep restriction therapy in patients experiencing depression and insomnia. Findings also highlight the need to improve the standardisation and reporting of sleep restriction therapy procedures, and to design studies with more rigorous control arms to reduce potential bias
Shifts in stability and control effectiveness during evolution of Paraves support aerial maneuvering hypotheses for flight origins
The capacity for aerial maneuvering shaped the evolution of flying animals.
Here we evaluate consequences of aviaian morphology for aerial performance
(1,2) by quantifying static stability and control effectiveness of physical
models (3) for numerous taxa sampled from within the lineage leading to birds
(Paraves, 4). Results of aerodynamic testing are mapped phylogenetically (5-9)
to examine how maneuvering characteristics correlate with tail shortening,
fore- and hindwing elaboration, and other morphological features (10). In the
evolution of the Avialae we observe shifts from static stability to inherently
unstable aerial planforms; control effectiveness also migrated from tails to
the forewings. These shifts suggest that some degree of aerodynamic control and
and capacity for maneuvering preceded the evolution of strong power stroke. The
timing of shifts also suggests some features normally considered in light of
development of a power stroke may play important roles in control.Comment: 12 pages, 6 figures, 1 supplemental figures and 5 supplemental table
Major adverse cardiovascular events of enzalutamide versus abiraterone in prostate cancer: a retrospective cohort study.
Background
While the cardiovascular risks of androgen receptor pathway inhibitors have been studied, they were seldom compared directly. This study compares the risks of major adverse cardiovascular events (MACE) between enzalutamide and abiraterone among prostate cancer (PCa) patients.
Methods
Adult PCa patients receiving either enzalutamide or abiraterone in addition to androgen deprivation therapy in Hong Kong between 1 December 1999 and 31 March 2021 were identified in this retrospective cohort study. Patients who switched between enzalutamide and abiraterone, initiated abiraterone used without steroids, or experienced prior cardiac events were excluded. Patients were followed-up until 30 September 2021. The primary outcomes were MACE, a composite of stroke, myocardial infarction (MI), Heart failure (HF), or all-cause mortality and a composite of adverse cardiovascular events (CACE) not including all-cause mortality. The secondary outcomes were individual components of MACE. Inverse probability treatment weighting was used to balance covariates between treatment groups.
Results
In total, 1015 patients were analyzed (456 enzalutamide users and 559 abiraterone users; mean age 70.6 ± 8.8 years old) over a median follow-up duration of 11.3 (IQR: 5.3–21.3) months. Enzalutamide users had significantly lower risks of 4P-MACE (weighted hazard ratio (wHR) 0.71 [95% confidence interval (CI) 0.59–0.86], p < 0.001) and CACE (wHR 0.63 [95% CI: 0.42–0.96], p = 0.031), which remained consistent in multivariable analysis. Such an association may be stronger in patients aged ≥65 years or without diabetes mellitus and was independent of bilateral orchidectomy. Enzalutamide users also had significantly lower risks of MI (wHR 0.57 [95% CI: 0.33–0.97], p = 0.040) and all-cause mortality (wHR 0.71 [95% CI: 0.59–0.85], p < 0.001).
Conclusion
Enzalutamide was associated with lower cardiovascular risks than abiraterone in PCa patients
Results from the centers for disease control and prevention's predict the 2013-2014 Influenza Season Challenge
Background: Early insights into the timing of the start, peak, and intensity of the influenza season could be useful in planning influenza prevention and control activities. To encourage development and innovation in influenza forecasting, the Centers for Disease Control and Prevention (CDC) organized a challenge to predict the 2013-14 Unites States influenza season. Methods: Challenge contestants were asked to forecast the start, peak, and intensity of the 2013-2014 influenza season at the national level and at any or all Health and Human Services (HHS) region level(s). The challenge ran from December 1, 2013-March 27, 2014; contestants were required to submit 9 biweekly forecasts at the national level to be eligible. The selection of the winner was based on expert evaluation of the methodology used to make the prediction and the accuracy of the prediction as judged against the U.S. Outpatient Influenza-like Illness Surveillance Network (ILINet). Results: Nine teams submitted 13 forecasts for all required milestones. The first forecast was due on December 2, 2013; 3/13 forecasts received correctly predicted the start of the influenza season within one week, 1/13 predicted the peak within 1 week, 3/13 predicted the peak ILINet percentage within 1 %, and 4/13 predicted the season duration within 1 week. For the prediction due on December 19, 2013, the number of forecasts that correctly forecasted the peak week increased to 2/13, the peak percentage to 6/13, and the duration of the season to 6/13. As the season progressed, the forecasts became more stable and were closer to the season milestones. Conclusion: Forecasting has become technically feasible, but further efforts are needed to improve forecast accuracy so that policy makers can reliably use these predictions. CDC and challenge contestants plan to build upon the methods developed during this contest to improve the accuracy of influenza forecasts. © 2016 The Author(s)
Autophosphorylation-based calcium (Ca2+) sensitivity priming and Ca2+/Calmodulin inhibition of Arabidopsis thaliana Ca2+-dependent protein kinase 28 (CPK28)
Plant calcium (Ca2+) dependent protein kinases (CPKs) are composed of a dual specificity (Ser/Thr and Tyr) kinase domain tethered to a Calmodulin-like domain (CLD) via an autoinhibitory junction (J) and represent the primary Ca2+-dependent protein kinase activities in plant systems. While regulation of CPKs by Ca2+ has been extensively studied, the contribution of autophosphorylation in the control of CPK activity is less well understood. Furthermore, whether Calmodulin (CaM) contributes to CPK regulation, as is the case for Ca2+/CaM-dependent protein kinases (CaMKs) outside the plant lineage, remains an open question. We screened a subset of plant CPKs for CaM-binding and found that CPK28 is a high-affinity Ca2+/CaM-binding protein. Using synthetic peptides and native gel electrophoresis, we coarsely mapped the CaM-binding domain to a site within the CPK28 J domain that overlaps with the known site of intramolecular interaction between the J domain and CLD. Peptide kinase activity of fully dephosphorylated CPK28 was Ca2+-responsive and inhibited by Ca2+/CaM. Using in situ autophosphorylated protein, we expand on the known set of CPK28 autophosphorylation sites, and demonstrate that, unexpectedly, autophosphorylated CPK28 had enhanced activity at physiological concentrations of Ca2+ compared to dephosphorylated protein, suggesting that autophosphorylation functions to prime CPK28 for Ca2+-activation. Furthermore, CPK28 autophosphorylation substantially reduced sensitivity of the kinase to Ca2+/CaM inhibition. Overall, our analyses uncover new complexities in the control of CPK28 and provide mechanistic support for Ca2+ signaling specificity through Ca2+ sensor priming
Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context
Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts
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