Extraction of Plumes in Turbulent Thermal Convection

We present a scheme to extract information about plumes, a prominent coherent structure in turbulent thermal convection, from simultaneous local velocity and temperature measurements. Using this scheme, we study the temperature dependence of the plume velocity and understand the results using the equations of motion. We further obtain the average local heat flux in the vertical direction at the cell center. Our result shows that heat is not mainly transported through the central region but instead through the regions near the sidewalls of the convection cell.Comment: 4 pages, 4 figures, submitted to Physical Review Letter

Gene editing: A new step and a new direction toward finding a cure for Duchenne muscular dystrophy (DMD)

AbstractDuchenne muscular dystrophy (DMD) is a progressive muscle degenerative disease affecting one out of 3500 male births. Patients usually succumb to the disease by age 25. It has been shown that skipping exons of the DMD gene that contain disease-causing mutations from the pre-mRNA can result in a shortened, but functional, dystrophin protein that could bring clinical benefits to patients. A recent breakthrough has been reported in Science by three groups who demonstrated that genetically deleting exon 23 by gene editing can restore the expression of dystrophin (albeit a shortened version) and improve the muscle function in a mouse model of DMD

Lung gene therapy—How to capture illumination from the light already present in the tunnel

AbstractGene therapy has been considered as the most ideal medical intervention for genetic diseases because it is intended to target the cause of diseases instead of disease symptoms. Availability of techniques for identification of genetic mutations and for in vitro manipulation of genes makes it practical and attractive. After the initial hype in 1990s and later disappointments in clinical trials for more than a decade, light has finally come into the tunnel in recent years, especially in the field of eye gene therapy where it has taken big strides. Clinical trials in gene therapy for retinal degenerative diseases such as Leber's congenital amaurosis (LCA) and choroideremia demonstrated clear therapeutic efficacies without apparent side effects. Although these successful examples are still rare and sporadic in the field, they provide the proof of concept for harnessing the power of gene therapy to treat genetic diseases and to modernize our medication. In addition, those success stories illuminate the path for the development of gene therapy treating other genetic diseases. Because of the differences in target organs and cells, distinct barriers to gene delivery exist in gene therapy for each genetic disease. It is not feasible for authors to review the current development in the entire field. Thus, in this article, we will focus on what we can learn from the current success in gene therapy for retinal degenerative diseases to speed up the gene therapy development for lung diseases, such as cystic fibrosis

Hidden Inequality: Financial Aid Information Available to College Students with Disabilities Attending Public Four-Year Institutions

College students with disabilities often encounter systems and processes that do not serve them well. Financial aid, structured in ways that can be particularly burdensome to students with disabilities, is one such system. This study used web-based content analysis of the largest public four-year institution in each state to explore how institutions explain and provide information and resources related to financial aid and whether they are equitable, consistent, and useful for students with disabilities specifically. The findings suggest that available information most often does not assist students in understanding how their disability-related needs can be supported or hindered by financial aid policies. The authors offer recommendations for practices that can improve equitable access to financial aid information

Applying novel tree-based frameworks to big data for classification of heart failure patients and prediction of clinical responses

Over 5 million Americans suffer from heart failure, a condition with a 5-year survival that eclipses all cancers apart from that of lung cancer. Conventional understanding of heart failure is simplistic: it is viewed as a single syndrome, despite real heterogeneity. In addition, models predicting outcomes focus on dichotomous results, like 30-day readmission. A novel approach to classification of heart failure may improve our ability to target interventions, improve patient experiences, and predict outcomes. The Healthcare Cost and Utilization Project is a family of administrative claims databases that describes patient demographics, comorbidities, procedures, acute care utilization and outcomes, such as mortality and readmission. Using the California datasets, which allow linkage of hospital admissions to emergency department visits, we sought to (1) develop a new classification tool for heart failure, (2) predict patient response based on previous visits, (3) predict survival time. In this pilot study, we propose novel tree-based frameworks for the classification of heart failure patients that can also be used to predict clinical response, health care utilization and mortality. The pilot sample contains 822 patients with heart failure who are randomly picked from a total sample of 211284 patients. The median number of encounters per patient was 3 (IQR: 5); each are associated with up to 168 variables. By applying random forest approaches to this pilot sample, we have performed classification of patients with heart failure and identified important predictors of outcomes. Going forward, we will refine the model and apply to the entire data set to produce broadly applicable insights

The number of inpatient consultations is negatively correlated with patient satisfaction in patients with prolonged hospital stays

Patient satisfaction is often measured using the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) Survey. Our aim was to examine the structural and clinical determinants of satisfaction among inpatients with prolonged lengths of stays (LOS)

Activation of plasma membrane H + -ATPases participates in dormancy alleviation in sunflower seeds

International audienceUsing various inhibitors and scavengers we took advantage of the size of sunflower (Helianthus annuus) seeds to investigate in vivo the effects of hormones, namely abscisic acid (ABA) and ethylene (ET), and reactive oxygen species (ROS) on the polarization of dormant (D) and non-dormant (ND) embryonic seed cells using microelectrodes. Our data show that D and ND seed cells present different polarization likely due to the regulation of plasma membrane (PM) H+-ATPase activity. The data obtained after addition of hormones or ROS scavengers further suggest that ABA dependent inhibition of PM H+-ATPases could participate in dormancy maintenance and that ET-and ROS-dependent PM H+-ATPase stimulation could participate in dormancy release in sunflower seeds

Estrogen transactivates EGFR via the sphingosine 1-phosphate receptor Edg-3: the role of sphingosine kinase-1

The transactivation of enhanced growth factor receptor (EGFR) by G protein–coupled receptor (GPCR) ligands is recognized as an important signaling mechanism in the regulation of complex biological processes, such as cancer development. Estrogen (E2), which is a steroid hormone that is intimately implicated in breast cancer, has also been suggested to function via EGFR transactivation. In this study, we demonstrate that E2-induced EGFR transactivation in human breast cancer cells is driven via a novel signaling system controlled by the lipid kinase sphingosine kinase-1 (SphK1). We show that E2 stimulates SphK1 activation and the release of sphingosine 1-phosphate (S1P), by which E2 is capable of activating the S1P receptor Edg-3, resulting in the EGFR transactivation in a matrix metalloprotease–dependent manner. Thus, these findings reveal a key role for SphK1 in the coupling of the signals between three membrane-spanning events induced by E2, S1P, and EGF. They also suggest a new signal transduction model across three individual ligand-receptor systems, i.e., “criss-cross” transactivation

Rescue of DNA damage after constricted migration reveals a mechano-regulated threshold for cell cycle.

Migration through 3D constrictions can cause nuclear rupture and mislocalization of nuclear proteins, but damage to DNA remains uncertain, as does any effect on cell cycle. Here, myosin II inhibition rescues rupture and partially rescues the DNA damage marker γH2AX, but an apparent block in cell cycle appears unaffected. Co-overexpression of multiple DNA repair factors or antioxidant inhibition of break formation also exert partial effects, independently of rupture. Combined treatments completely rescue cell cycle suppression by DNA damage, revealing a sigmoidal dependence of cell cycle on excess DNA damage. Migration through custom-etched pores yields the same damage threshold, with ∼4-µm pores causing intermediate levels of both damage and cell cycle suppression. High curvature imposed rapidly by pores or probes or else by small micronuclei consistently associates nuclear rupture with dilution of stiff lamin-B filaments, loss of repair factors, and entry from cytoplasm of chromatin-binding cGAS (cyclic GMP-AMP synthase). The cell cycle block caused by constricted migration is nonetheless reversible, with a potential for DNA misrepair and genome variation