Funerals: Alternatives and Arrangements.

10 p

Orthography influences the perception and production of speech.

One intriguing question in language research concerns the extent to which orthographic information impacts on spoken word processing. Previous research has faced a number of methodological difficulties and has not reached a definitive conclusion. Our research addresses these difficulties by capitalizing on recent developments in the area of word learning. Participants were trained to criterion on a set of associations between novel pictures and novel spoken words. Spelling-sound consistent or spelling-sound inconsistent spellings were introduced on the 2nd day, and the influence of these spellings on speech processing was assessed on the 3rd day. Results showed significant orthographic effects on speech perception and speech production in a situation in which spelling–sound consistency was manipulated with perfect experimental control. Results are discussed in terms of a highly interactive language system in which there is a rapid and automatic flow of activation in both directions between orthographic and phonological representations

Fundamental Defect in Appellate Review of Error in the Texas Jury Charge Procedure Forum.

Abstract Forthcoming

Strategies to Reduce the Harmful Effects of Extreme Heat Events: A Four-City Study

Extreme heat events (EHEs) are becoming more intense, more frequent and longer lasting in the 21st century. These events can disproportionately impact the health of low-income, minority, and urban populations. To better understand heat-related intervention strategies used by four U.S. cities, we conducted 73 semi-structured interviews with government and non-governmental organization leaders representing public health, general social services, emergency management, meteorology, and the environmental planning sectors in Detroit, MI; New York City, NY; Philadelphia, PA and Phoenix, AZ—cities selected for their diverse demographics, climates, and climate adaptation strategies. We identified activities these leaders used to reduce the harmful effects of heat for residents in their city, as well as the obstacles they faced and the approaches they used to evaluate these efforts. Local leaders provided a description of how local context (e.g., climate, governance and city structure) impacted heat preparedness. Despite the differences among study cities, political will and resource access were critical to driving heat-health related programming. Upon completion of our interviews, we convened leaders in each city to discuss these findings and their ongoing efforts through day-long workshops. Our findings and the recommendations that emerged from these workshops could inform other local or national efforts towards preventing heat-related morbidity and mortality

Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.

The inhibition of death-receptor apoptosis is a conserved viral function. The murine cytomegalovirus (MCMV) gene M36 is a sequence and functional homologue of the human cytomegalovirus gene UL36, and it encodes an inhibitor of apoptosis that binds to caspase-8, blocks downstream signaling and thus contributes to viral fitness in macrophages and in vivo. Here we show a direct link between the inability of mutants lacking the M36 gene (ΔM36) to inhibit apoptosis, poor viral growth in macrophage cell cultures and viral in vivo fitness and virulence. ΔM36 grew poorly in RAG1 knockout mice and in RAG/IL-2-receptor common gamma chain double knockout mice (RAGγC(-/-)), but the depletion of macrophages in either mouse strain rescued the growth of ΔM36 to almost wild-type levels. This was consistent with the observation that activated macrophages were sufficient to impair ΔM36 growth in vitro. Namely, spiking fibroblast cell cultures with activated macrophages had a suppressive effect on ΔM36 growth, which could be reverted by z-VAD-fmk, a chemical apoptosis inhibitor. TNFα from activated macrophages synergized with IFNγ in target cells to inhibit ΔM36 growth. Hence, our data show that poor ΔM36 growth in macrophages does not reflect a defect in tropism, but rather a defect in the suppression of antiviral mediators secreted by macrophages. To the best of our knowledge, this shows for the first time an immune evasion mechanism that protects MCMV selectively from the antiviral activity of macrophages, and thus critically contributes to viral pathogenicity in the immunocompromised host devoid of the adaptive immune system

The association between low level exposures to ambient air pollution and term low birth weight: a retrospective cohort study

BACKGROUND: Studies in areas with relatively high levels of air pollution have found some positive associations between exposures to ambient levels of air pollution and several birth outcomes including low birth weight (LBW). The purpose of this study was to examine the association between LBW among term infants and ambient air pollution, by trimester of exposure, in a region of lower level exposures. METHODS: The relationship between LBW and ambient levels of particulate matter up to 10 um in diameter (PM(10)), sulfur dioxide (SO(2)) and ground-level ozone (O(3)) was evaluated using the Nova Scotia Atlee Perinatal Database and ambient air monitoring data from the Environment Canada National Air Pollution Surveillance Network and the Nova Scotia Department of Environment. The cohort consisted of live singleton births (≥37 weeks of gestation) between January1,1988 and December31,2000. Maternal exposures to air pollution were assigned to women living within 25 km of a monitoring station at the time of birth. Air pollution was evaluated as a continuous and categorical variable (using quartile exposures) for each trimester and relative risks were estimated from logistic regression, adjusted for confounding variables. RESULTS: There were 74,284 women with a term, singleton birth during the study period and with exposure data. In the analyses unadjusted for year of birth, first trimester exposures in the highest quartile for SO(2 )and PM(10)suggested an increased risk of delivering a LBW infant (relative risk = 1.36, 95% confidence interval = 1.04 to 1.78 for SO(2 )exposure and relative risk = 1.33, 95% confidence interval = 1.02 to 1.74 for PM(10)). After adjustment for birth year, the relative risks were attenuated somewhat and not statistically significant. A dose-response relationship for SO(2 )was noted with increasing levels of exposure. No statistically significant effects were noted for ozone. CONCLUSION: Our results suggest that exposure during the first trimester to relatively low levels of some air pollutants may be associated with a reduction in birth weight in term-born infants. These findings have implications for the development of effective risk management strategies to minimize the public health impacts for pregnant women

Seeking and sharing: why the pulmonaryn fibrosis community engages the web 2.0 environment

Background Pulmonary fibrosis (PF) is a rare, progressive disease that affects patients and their loved ones on many levels. We sought to better understand the needs and interests of PF patients and their loved ones (collectively “reader-participants”) by systematically analyzing their engagement with the World Wide Web (the current version referred to as Web 2.0). Methods Data were collected from three PF-focused, interactive websites hosted by physician-investigators with expertise in PF. All data generated by reader-participants for approximately 10 months were downloaded and then analyzed using qualitative content analysis methods. Results PF experts posted 38 blog entries and reader-participants posted 40 forum entries. Blogs received 363 responses, and forum entries received 108 responses from reader-participants. Reader-participants primarily used the three websites to seek information from or offer a contribution to the PF community. Information was sought about PF symptoms, diagnosis, prognosis, treatments, research, pathophysiology, and disease origin; reader-participants also made requests for new posts and pleas for research and sought clarification on existing content. Contributions included personal narratives about experiences with PF, descriptions of activities or behaviors found to be helpful with PF symptoms, resources or information about PF, and supportive comments to other PF sufferers. Conclusions PF patients and their loved ones engage the Web 2.0 environment at these PF-focused sites to satisfy their needs to better understand PF and its impacts and to support others facing similar challenges. Clinicians may find it beneficial to encourage PF patients’ involvement in internet forums that foster dynamic, bi-directional information sharing

HtrA2/Omi Terminates Cytomegalovirus Infection and Is Controlled by the Viral Mitochondrial Inhibitor of Apoptosis (vMIA)

Viruses encode suppressors of cell death to block intrinsic and extrinsic host-initiated death pathways that reduce viral yield as well as control the termination of infection. Cytomegalovirus (CMV) infection terminates by a caspase-independent cell fragmentation process after an extended period of continuous virus production. The viral mitochondria-localized inhibitor of apoptosis (vMIA; a product of the UL37x1 gene) controls this fragmentation process. UL37x1 mutant virus-infected cells fragment three to four days earlier than cells infected with wt virus. Here, we demonstrate that infected cell death is dependent on serine proteases. We identify mitochondrial serine protease HtrA2/Omi as the initiator of this caspase-independent death pathway. Infected fibroblasts develop susceptibility to death as levels of mitochondria-resident HtrA2/Omi protease increase. Cell death is suppressed by the serine protease inhibitor TLCK as well as by the HtrA2-specific inhibitor UCF-101. Experimental overexpression of HtrA2/Omi, but not a catalytic site mutant of the enzyme, sensitizes infected cells to death that can be blocked by vMIA or protease inhibitors. Uninfected cells are completely resistant to HtrA2/Omi induced death. Thus, in addition to suppression of apoptosis and autophagy, vMIA naturally controls a novel serine protease-dependent CMV-infected cell-specific programmed cell death (cmvPCD) pathway that terminates the CMV replication cycle

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy