Flow and Radiation Analyses for Stardust Entry at High Altitude

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76603/1/AIAA-2008-1215-337.pd

The formation of paranodal spirals at the ends of CNS myelin sheaths requires the planar polarity protein Vangl2

During axonal ensheathment, noncompact myelin channels formed at lateral edges of the myelinating process become arranged into tight paranodal spirals that resemble loops when cut in cross section. These adhere to the axon, concentrating voltage-dependent sodium channels at nodes of Ranvier and patterning the surrounding axon into distinct molecular domains. The signals responsible for forming and maintaining the complex structure of paranodal myelin are poorly understood. Here, we test the hypothesis that the planar cell polarity determinant Vangl2 organizes paranodal myelin. We show that Vangl2 is concentrated at paranodes and that, following conditional knockout of Vangl2 in oligodendrocytes, the paranodal spiral loosens, accompanied by disruption to the microtubule cytoskeleton and mislocalization of autotypic adhesion molecules between loops within the spiral. Adhesion of the spiral to the axon is unaffected. This results in disruptions to axonal patterning at nodes of Ranvier, paranodal axon diameter and conduction velocity. When taken together with our previous work showing that loss of the apico-basal polarity protein Scribble has the opposite phenotype—loss of axonal adhesion but no effect on loop–loop autotypic adhesion—our results identify a novel mechanism by which polarity proteins control the shape of nodes of Ranvier and regulate conduction in the CNS

Bacterial vs. zooplankton control of sinking particle flux in the ocean\u27s twilight zone

The downward flux of particulate organic carbon (POC) decreases significantly in the oceanÂs mesopelagic or ‘twilight’ zone due both to abiotic processes and metabolism by resident biota. Bacteria and zooplankton solubilize and consume POC to support their metabolism, but the relative importance of bacteria vs. zooplankton in the consumption of sinking particles in the twilight zone is unknown. We compared losses of sinking POC, using differences in export flux measured by neutrally buoyant sediment traps at a range of depths, with bacteria and zooplankton metabolic requirements at the Hawaii Ocean Time‐series station ALOHA in the subtropical Pacific and the Japanese times‐series site K2 in the subarctic Pacific. Integrated (150‐1,000 m) mesopelagic bacterial C demand exceeded that of zooplankton by up to 3‐fold at ALOHA, while bacteria and zooplankton required relatively equal amounts of POC at K2. However, sinking POC flux was inadequate to meet metabolic demands at either site. Mesopelagic bacterial C demand was 3‐ to 4‐fold (ALOHA), and 10‐fold (K2) greater than the loss of sinking POC flux, while zooplankton C demand was 1‐ to 2‐fold (ALOHA), and 3‐ to 9‐fold (K2) greater (using our ‘middle’ estimate conversion factors to calculate C demand). Assuming the particle flux estimates are accurate, we posit that this additional C demand must be met by diel vertical migration of zooplankton feeding at the surface and by carnivory at depth—with both processes ultimately supplying organic C to mesopelagic bacteria. These pathways need to be incorporated into biogeochemical models that predict global C sequestration in the deep sea

Time Protection: the Missing OS Abstraction

Timing channels enable data leakage that threatens the security of computer systems, from cloud platforms to smartphones and browsers executing untrusted third-party code. Preventing unauthorised information flow is a core duty of the operating system, however, present OSes are unable to prevent timing channels. We argue that OSes must provide time protection in addition to the established memory protection. We examine the requirements of time protection, present a design and its implementation in the seL4 microkernel, and evaluate its efficacy as well as performance overhead on Arm and x86 processors

Multiple uncontrolled conditions and blood pressure medication intensification: an observational study

Abstract Background Multiple uncontrolled medical conditions may act as competing demands for clinical decision making. We hypothesized that multiple uncontrolled cardiovascular risk factors would decrease blood pressure (BP) medication intensification among uncontrolled hypertensive patients. Methods We observed 946 encounters at two VA primary care clinics from May through August 2006. After each encounter, clinicians recorded BP medication intensification (BP medication was added or titrated). Demographic, clinical, and laboratory information were collected from the medical record. We examined BP medication intensification by presence and control of diabetes and/or hyperlipidemia. 'Uncontrolled' was defined as hemoglobin A1c ≥ for diabetes, BP ≥ 140/90 mmHg (≥ 130/80 mmHg if diabetes present) for hypertension, and low density lipoprotein cholesterol (LDL-c) ≥ 130 mg/dl (≥ 100 mg/dl if diabetes present) for hyperlipidemia. Hierarchical regression models accounted for patient clustering and adjusted medication intensification for age, systolic BP, and number of medications. Results Among 387 patients with uncontrolled hypertension, 51.4% had diabetes (25.3% were uncontrolled) and 73.4% had hyperlipidemia (22.7% were uncontrolled). The BP medication intensification rate was 34.9% overall, but higher in individuals with uncontrolled diabetes and uncontrolled hyperlipidemia: 52.8% overall and 70.6% if systolic BP ≥ 10 mmHg above goal. Intensification rates were lowest if diabetes or hyperlipidemia were controlled, lower than if diabetes or hyperlipidemia were not present. Multivariable adjustment yielded similar results. Conclusions The presence of uncontrolled diabetes and hyperlipidemia was associated with more guideline-concordant hypertension care, particularly if BP was far from goal. Efforts to understand and improve BP medication intensification in patients with controlled diabetes and/or hyperlipidemia are warranted.http://deepblue.lib.umich.edu/bitstream/2027.42/78266/1/1748-5908-5-55.xmlhttp://deepblue.lib.umich.edu/bitstream/2027.42/78266/2/1748-5908-5-55.pdfPeer Reviewe