Best tracks'' are National Hurricane Center (NHC) poststorm analyses of the intensity, central pressure, position, and size of Atlantic and eastern North Pacific basin tropical and subtropical cyclones. This paper estimates the uncertainty (average error) for Atlantic basin best track parameters through a survey of the NHC Hurricane Specialists who maintain and update the Atlantic hurricane database. A comparison is then made with a survey conducted over a decade ago to qualitatively assess changes in the uncertainties. Finally, the implications of the uncertainty estimates for NHC analysis and forecast products as well as for the prediction goals of the Hurricane Forecast Improvement Program are discussed.1 Maximum 1-min-average wind associated with the tropical cyclone at an elevation of 10 m with an unobstructed exposure (Office of the Federal Coordinator for Meteorological Services and Supporting Research 2012). 2 Cyclone size is described by the maximum extent of winds of 34, 50, and 64 kt in each of four quadrants about the center.

No abstract

The National Center for Atmospheric Research (NCAR), in a joint effort with the National Oceanic and Atmospheric Administration (NOAA) and the German Aerospace Research Establishment, has developed a dropwindsonde based on the Global Positioning System (GPS) satellite navigation. The NCAR GPS dropwindsonde represents a major advance in both accuracy and resolution for atmospheric measurements over data-sparse oceanic areas of the globe, providing wind accuracies of 0.5-2.0 m s _1 with a vertical resolution of-5 m. One important advance over previous generations of sondes is the ability to measure surface (10 m) winds. The new dropwindsonde has already been used extensively in one major international research field experiment (Fronts and Atlantic Storm Track Experiment), in operational and research hurricane flights from NOAA's National Weather Service and Hurricane Research Division, during NCAR's SNOWBAND experiment, and in recent CALJET and NORPEX El Nino experiments. The sonde has been deployed from a number of different aircraft, including NOAA's WP-3Ds and new Gulf stream IV jet, the Air Force C-130s, NCAR's Electra, and a leased Lear-36. This paper describes the characteristics of the new dropwindsonde and its associated aircraft data system, details the accuracy of its measurements, and presents examples from its initial applications.

Bax is required for the apoptotic death of sympathetic neurons deprived of nerve growth factor (NGF). After NGF withdrawal, Bax translocates from the cytoplasm to the mitochondria of these cells and induces release of the proapoptotic protein cytochrome c. Here, we report that withdrawing NGF from mouse sympathetic neurons caused an increase of mitochondria-derived reactive oxygen species (ROS). Suppressing these ROS inhibited apoptosis. Bax deletion blocked death and prevented the ROS burst. Inducing a pro-oxidant state similar to that in NGF-deprived, wild-type cells caused cytochrome c release even in neurons lacking Bax. A similar ROS burst in cerebellar granule neurons undergoing apoptosis was also blocked by Bax deletion. These findings indicate that Bax lies upstream from increased ROS in NGF-deprived neurons and suggest that the Bax-induced ROS burst is both necessary and sufficient for cytochrome c redistribution in these cells.

Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer’s disease (AD). We examined the ability of the novel mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienlyl) decyl triphenylphosphonium methanesulfonate]) to prevent AD-like pathology in mouse cortical neurons in cell culture and in a triple transgenic mouse model of AD (3xTg-AD). MitoQ attenuated β-amyloid (Aβ)-induced neurotoxicity in cortical neurons and also prevented increased production of reactive species and loss of mitochondrial membrane potential (Δψm) in them. To determine whether the mitochondrial protection conferred by MitoQ was sufficient to prevent the emergence of AD-like neuropathology in vivo, we treated young female 3xTg-AD mice with MitoQ for 5 months and analyzed the effect on the progression of AD-like pathologies. Our results show that MitoQ prevented cognitive decline in these mice as well as oxidative stress, Aβ accumulation, astrogliosis, synaptic loss, and caspase activation in their brains. The work presented herein suggests a central role for mitochondria in neurodegeneration and provides evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative stress and metabolic failure, namely AD.

No abstract

The National Hurricane Center issues analyses, forecasts, and warnings over large parts of the North Atlantic and Pacific Oceans, and in support of many nearby countries. Advances in observational capabilities, operational numerical weather prediction, and forecaster tools and support systems over the past 15-20 yr have enabled the center to make more accurate forecasts, extend forecast lead times, and provide new products and services. Important limitations, however, persist. This paper discusses the current workings and state of the nation's hurricane warning program, and highlights recent improvements and the enabling science and technology. It concludes with a look ahead at opportunities to address challenges.

Nephrotoxicity induced by cisplatin involves tubular cell necrosis and apoptosis; the latter of which may be initiated by multiple mechanisms including activation of the intrinsic mitochondrial pathway. In cultured tubular epithelial cells, cisplatin can activate the proapoptotic protein Bax resulting in cytochrome c release, caspase activation, and apoptosis. Definitive evidence for the involvement of Bax in cisplatin nephrotoxicity in vivo, however, is lacking. We analyzed Bax regulation during cisplatin nephrotoxicity in wild-type mice and determined the pathological role of Bax using mice in which this gene was knocked out. In wild-type mice, cisplatin induced Bax in renal tubular cells which became active, accumulated in the mitochondria, and was accompanied by acute kidney injury. Compared with the wild-type mice renal function, as measured by blood urea nitrogen and serum creatinine, was partially but significantly preserved in Bax knockout mice. The number of apoptotic cells was decreased as was general tissue damage. Additionally, cisplatin-induced cytochrome c release was attenuated in the Bax-deficient mice. This significant decrease in apoptosis and in cytochrome c release was also mirrored in primary cultures of proximal tubular cells prepared from Bax knockout animals. Collectively, our results provide compelling evidence for a role of Bax and its related apoptotic pathway in cisplatin nephrotoxicity.