Keck NIRSPEC Radial Velocity Observations of Late-M dwarfs

We present the results of an infrared spectroscopic survey of 23 late-M dwarfs with the NIRSPEC echelle spectrometer on the Keck II telescope. Using telluric lines for wavelength calibration, we are able to achieve measurement precisions of down to 45 m/s for our late-M dwarfs over a one to four year-long baseline. Our sample contains two stars with RV variations of >1000 m/s. While we require more measurements to determine whether these RV variations are due to unseen planetary or stellar companions or are the result of starspots known to plague the surface of M dwarfs, we can place upper limits of <40 MJsini on the masses of any companions around those two M dwarfs with RV variations of <160 m/s at orbital periods of 10-100 days. We have also measured the rotational velocities for all the stars in our late-M dwarf sample and offer our multi-order, high-resolution spectra over 2.0 to 2.4 micron to the atmospheric modeling community to better understand the atmospheres of late-M dwarfs.Comment: Accepted to Ap

Salvaging the Speaker Clause: The Constitutional Case Against Nonmember Speakers of the House

As the Founding generation understood the word, “Speaker” meant an elected member of the House. Yet modern representatives nominate non-House-members for the speakership—and many argue the practice is constitutional. To correct this constitutional drift, this Article closely analyzes the text of the Speaker Clause, the structure of the Constitution, and 700 years of history and tradition to show that the Constitution requires the Speaker of the House to be a member of the House. It also considers the practicalities of correcting this drift. If, as this Article argues, the Constitution bars nonmembers from the speakership, who can enforce that rule, especially if Congress itself is the one violating it? Though the Speaker Clause likely is not justiciable, Congress has an independent duty—equally important to that of the judiciary—to uphold the Constitution. This Article’s conclusion is significant. It clarifies the procedure and rationale involved in choosing a Speaker of the House. And by excluding nonmembers as candidates for the speakership, this Article’s conclusion promises to make future speakership negotiations and votes smoother, eliminating one avenue for meaningless protest votes

Slowly cycling Rho kinase-dependent actomyosin cross-bridge slippage explains intrinsic high compliance of detrusor smooth muscle

Biological soft tissues are viscoelastic because they display timeindependent pseudoelasticity and time-dependent viscosity. However, there is evidence that the bladder may also display plasticity, defined as an increase in strain that is unrecoverable unless work is done by the muscle. In the present study, an electronic lever was used to induce controlled changes in stress and strain to determine whether rabbit detrusor smooth muscle (rDSM) is best described as viscoelastic or viscoelastic plastic. Using sequential ramp loading and unloading cycles, stress-strain and stiffness-stress analyses revealed that rDSM displayed reversible viscoelasticity, and that the viscous component was responsible for establishing a high stiffness at low stresses that increased only modestly with increasing stress compared with the large increase produced when the viscosity was absent and only pseudoelasticity governed tissue behavior. The study also revealed that rDSM underwent softening correlating with plastic deformation and creep that was reversed slowly when tissues were incubated in a Ca2+ -containing solution. Together, the data support a model of DSM as a viscoelastic-plastic material, with the plasticity resulting from motor protein activation. This model explains the mechanism of intrinsic bladder compliance as slipping cross bridges, predicts that wall tension is dependent not only on vesicle pressure and radius but also on actomyosin cross-bridge activity, and identifies a novel molecular target for compliance regulation, both physiologically and therapeutically

Wireless Bus Interconnects for Flexible and Reliable CubeSat Signal Integrations

One of the largest, yet easily forgotten, aspects of constructing any complex system is the effort needed to integrate several subsystems. One common way to do this is to standardize the interface between subsystems, whether that is a physical standard, such as USB, or protocol standards, such as Wi-Fi and Bluetooth. In our previous implementations of CubeSat systems and subsystems we have found the PC/104 bus to be volume and mass inefficient while allowing too many potential conflicts to be considered a \u27standard\u27. Our research proposes to implement a wireless, Bluetooth based, communication interface between subsystems to minimize the physical and logistical effort required to build CubeSat systems. By completely removing the need for physical/electrical connections between the subsystems, the barrier to entry for making custom modules for CubeSats can be lowered dramatically. Throughout the course of this research, the applicability of Bluetooth Low-Energy (BLE) utilizing the Generic Attribute (GATT) protocol is investigated

The DEAD-box helicase Ded1 from yeast is an mRNP cap-associated protein that shuttles between the cytoplasm and nucleus

International audienceThe DEAD-box helicase Ded1 is an essential yeast protein that is closely related to mammalian DDX3 and to other DEAD-box proteins involved in developmental and cell cycle regulation. Ded1 is considered to be a translation-initiation factor that helps the 40S ribosome scan the mRNA from the 5 7-methylguanosine cap to the AUG start codon. We used IgG pull-down experiments, mass spectrom-etry analyses, genetic experiments, sucrose gradients , in situ localizations and enzymatic assays to show that Ded1 is a cap-associated protein that actively shuttles between the cytoplasm and the nucleus. NanoLC-MS/MS analyses of purified complexes show that Ded1 is present in both nuclear and cytoplasmic mRNPs. Ded1 physically interacts with purified components of the nuclear CBC and the cytoplasmic eIF4F complexes, and its enzymatic activity is stimulated by these factors. In addition, we show that Ded1 is genetically linked to these factors. Ded1 comigrates with these proteins on sucrose gradients, but treatment with rapamycin does not appreciably alter the distribution of Ded1; thus, most of the Ded1 is in stable mRNP complexes. We conclude that Ded1 is an mRNP cofactor of the cap complex that may function to remodel the different mRNPs and thereby regulate the expression of the mRNAs

Generalizability of SPRINT Results to the U.S. Adult Population

Background In SPRINT (Systolic Blood Pressure Intervention Trial), a systolic blood pressure (SBP) goal of <120 mm Hg resulted in lower cardiovascular disease (CVD) risk compared with an SBP goal of <140 mm Hg. Objectives The purpose of this study was to estimate the prevalence, number, and characteristics of U.S. adults meeting SPRINT eligibility criteria and determine the broader population to whom SPRINT could be generalized. Methods We conducted a cross-sectional, population-based study using data from the National Health and Nutrition Examination Survey, 2007 to 2012. The SPRINT inclusion criteria were age ≥50 years, SBP 130 to 180 mm Hg depending on the number of antihypertensive medication classes being taken, and high CVD risk (history of coronary heart disease, estimated glomerular filtration rate of 20 to 59 ml/min/1.73 m2, 10-year CVD risk ≥15%, or age ≥75 years). Exclusion criteria were diabetes, history of stroke, >1 g in 24 h of proteinuria daily, heart failure, estimated glomerular filtration rate <20 ml/min/1.73 m2, or receiving dialysis. Treated hypertension was defined by self-reported use of medication to lower blood pressure with ≥1 class of antihypertensive medication identified through a pill bottle review. Results Overall, 7.6% (95% confidence interval [CI]: 7.0% to 8.3%) or 16.8 million (95% CI: 15.7 to 17.8 million) U.S. adults, and 16.7% (95% CI: 15.2% to 18.3%) or 8.2 million (95% CI: 7.6 to 8.8 million) adults with treated hypertension met the SPRINT eligibility criteria. Among both the overall U.S. population and adults with treated hypertension, the percentage meeting SPRINT eligibility criteria increased with older age, was higher among males than females, and was higher among non-Hispanic whites compared with non-Hispanic blacks or Hispanics. Of U.S. adults eligible for SPRINT, 51.0% (95% CI: 47.8% to 54.1%) or 8.6 million (95% CI: 8.0 to 9.1 million) were not treated for hypertension. Conclusions A substantial percentage of U.S. adults meet the eligibility criteria for SPRINT

A specific amino acid motif of HLA-DRB1 mediates risk and interacts with smoking history in Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disease in which genetic risk has been mapped to HLA, but precise allelic associations have been difficult to infer due to limitations in genotyping methodology. Mapping PD risk at highest possible resolution, we performed sequencing of 11 HLA genes in 1,597 PD cases and 1,606 controls. We found that susceptibility to PD can be explained by a specific combination of amino acids at positions 70-74 on the HLA-DRB1 molecule. Previously identified as the primary risk factor in rheumatoid arthritis and referred to as the "shared epitope" (SE), the residues Q/R-K/R-R-A-A at positions 70-74 in combination with valine at position 11 (11-V) is highly protective in PD, while risk is attributable to the identical epitope in the absence of 11-V. Notably, these effects are modified by history of cigarette smoking, with a strong protective effect mediated by a positive history of smoking in combination with the SE and 11-V (P = 10-4; odds ratio, 0.51; 95% confidence interval, 0.36-0.72) and risk attributable to never smoking in combination with the SE without 11-V (P = 0.01; odds ratio, 1.51; 95% confidence interval, 1.08-2.12). The association of specific combinations of amino acids that participate in critical peptide-binding pockets of the HLA class II molecule implicates antigen presentation in PD pathogenesis and provides further support for genetic control of neuroinflammation in disease. The interaction of HLA-DRB1 with smoking history in disease predisposition, along with predicted patterns of peptide binding to HLA, provide a molecular model that explains the unique epidemiology of smoking in PD