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The Hurricane Forecast Improvement Project (HFIP; renamed the "Hurricane Forecast Improvement Program" in 2017) was established by the U.S. National Oceanic and Atmospheric Administration (NOAA) in 2007 with a goal of improving tropical cyclone (TC) track and intensity predictions. A major focus of HFIP has been to increase the quality of guidance products for these parameters that are available to forecasters at the National Weather Service National Hurricane Center (NWS/NHC). One HFIP effort involved the demonstration of an operational decision process, named Stream 1.5, in which promising experimental versions of numerical weather prediction models were selected for TC forecast guidance. The selection occurred every year from 2010 to 2014 in the period preceding the hurricane season (defined as August–October), and was based on an extensive verification exercise of retrospective TC forecasts from candidate experimental models run over previous hurricane seasons. As part of this process, user-responsive verification questions were identified via discussions between NHC staff and forecast verification experts, with additional questions considered each year. A suite of statistically meaningful verification approaches consisting of traditional and innovative methods was developed to respond to these questions. Two examples of the application of the Stream 1.5 evaluations are presented, and the benefits of this approach are discussed. These benefits include the ability to provide information to forecasters and others that is relevant for their decision-making processes, via the selection of models that meet forecast quality standards and are meaningful for demonstration to forecasters in the subsequent hurricane season; clarification of user-responsive strengths and weaknesses of the selected models; and identification of paths to model improvement. Significance Statement: The Hurricane Forecast Improvement Project (HFIP) tropical cyclone (TC) forecast evaluation effort led to innovations in TC predictions as well as new capabilities to provide more meaningful and comprehensive information about model performance to forecast users. Such an effort—to clearly specify the needs of forecasters and clarify how forecast improvements should be measured in a "user-oriented" framework—is rare. This project provides a template for one approach to achieving that goal. [ABSTRACT FROM AUTHOR]

The validity of the traditional balance approximation for the asymmetric flow above the boundary layer generally in hurricanes is examined here. Scaling considerations of the divergence equation show that the validity of the balance approximation hinges on the smallness of the nondimensional product [Mathematical Expression Omitted]. The first term represents the ratio of asymmetric horizontal divergence to asymmetric vertical vorticity for azimuthal wavenumber n, while the second term represents a Rossby number based upon the azimuthal mean tangential wind and absolute vertical vorticity of the hurricane vortex. Wind observations of Hurricane Gloria (1985) indicate that this product is not at all small in the near-vortex region (several hundred kilometers beyond the radius of maximum tangential winds) where asymmetric convergence forced by surface friction and cumulus convection is typically large. Although the Gloria observations represent only a single case, there are dynamical reasons to expect this product to be O(1) just above the hurricane boundary layer in steadily translating hurricanes. The meteorological relevance of these results to the problem of balance dynamics in hurricanes is briefly discussed.

The Hurricane Research Division (HRD) is NOAA's primary component for research on tropical cyclones. In accomplishing research goals, many staff members have developed analysis procedures and forecast models that not only help improve the understanding of hurricane structure, motion, and intensity change, but also provide operational support for forecasters at the National Hurricane Center (NHC). During the 1993 hurricane season, HRD demonstrated three important real-time capabilities for the first time. These achievements included the successful transmission of a series of color radar reflectivity images from the NOAA research aircraft to NHC, the operational availability of objective mesoscale streamline and isotach analyses of a hurricane surface wind field, and the transition of the experimental dropwindsonde program on the periphery of hurricanes to a technology capable of supporting operational requirements. Examples of these and other real-time capabilities are presented for Hurricane Emily.

Almost half of vertebrate neurons die before reaching maturity due to a process called programmed cell death. Essential to the survival of neurons during this stage of development is the availability of certain neurotrophic substances. However, studies conducted in vitro reveal that chronic depolarization can take the place of these substances in enhancing neuronal survival by virtue of their ability to suppress programmed neuronal death. Evidence suggests that the rise of cytoplasmic free calcium through voltage-activated channels is responsible for mediating the effects of chronic depolarization.

Withdrawal of nerve growth factor (NGF) from sympathetic neurons causes their apoptotic death. Activation of c-Jun NH2-terminal kinase (JNK) may contribute to this death by the induction and phosphorylation of pro-apoptotic Bcl-2 proteins, such as Bax, that are involved in cytochrome c release from mitochondria and reactive oxygen species (ROS) production. Induction of either JNK or ROS may stimulate the other, and both may regulate release of apoptogenic factors from the mitochondria. In order to discern the relationship between JNK and ROS in apoptosis, we treated NGF-deprived, mouse sympathetic neurons with a JNK inhibitor and examined the effect on several important apoptotic events. Block of JNK activation prevented induction of c-Jun expression and resulted in a dose-dependent, yet surprisingly modest, increase in cell survival after 48 h of NGF deprivation. JNK suppression was also not sufficient to prevent the elevation in ROS or the release of cytochrome c from the mitochondria in NGF-deprived sympathetic neurons. Bax deletion prevents apoptotic death of NGF-deprived neurons by preventing release of cytochrome c from their mitochondria. It also prevents increased ROS on NGF deprivation. However, we found that induction of c-Jun in cells lacking Bax was equivalent to that in wild-type neurons. Our results suggest that while JNK activation plays an important role in many forms of apoptosis, it may not be a crucial regulator of Bax-dependent events involved in the apoptotic death of mouse sympathetic neurons deprived of NGF and that ROS is not involved in its activation in these cells. [ABSTRACT FROM AUTHOR]