A single fast radio burst localized to a massive galaxy at cosmological distance.

Fast radio bursts (FRBs) are brief radio emissions from distant astronomical sources. Some are known to repeat, but most are single bursts. Nonrepeating FRB observations have had insufficient positional accuracy to localize them to an individual host galaxy. We report the interferometric localization of the single-pulse FRB 180924 to a position 4 kiloparsecs from the center of a luminous galaxy at redshift 0.3214. The burst has not been observed to repeat. The properties of the burst and its host are markedly different from those of the only other accurately localized FRB source. The integrated electron column density along the line of sight closely matches models of the intergalactic medium, indicating that some FRBs are clean probes of the baryonic component of the cosmic web.

Why consumers misattribute sponsorships to non-sponsor brands: Differential roles of item and relational communications.

Brands engaged in sponsorship of events commonly have objectives that depend on consumer memory for the sponsor-event relationship (e.g., sponsorship awareness). Consumers however, often misattribute sponsorships to nonsponsor competitor brands, indicating erroneous memory for these relationships. The current research uses an item and relational memory framework to reveal sponsor brands may inadvertently foster this misattribution when they communicate relational linkages to events. Effects can be explained via differential roles of communicating item information (information that supports processing item distinctiveness) versus relational information (information that supports processing relationships among items) in contributing to memory outcomes. Experiment 1 uses event-cued brand recall to show that correct memory retrieval is best supported by communicating relational information when sponsorship relationships are not obvious (low congruence). In contrast, correct retrieval is best supported by communicating item information when relationships are obvious (high congruence). Experiment 2 uses brand-cued event recall to show that, against conventional marketing recommendations, relational information increases misattribution, whereas item information guards against misattribution. Results suggest sponsor brands must distinguish between item and relational communications to enhance correct retrieval and limit misattribution. Methodologically, the work shows that choice of cueing direction is critical in differentially revealing patterns of correct and incorrect retrieval with pair relationships. (PsycINFO Database Record

Children's knowledge of packaged and fast food brands and their BMI. Why the relationship matters for policy makers.

Studies regarding the advancing challenges of obesity in many countries are beginning to converge on the importance of early food exposure and consumption patterns. Across two studies (Study 1, 34 boys, 35 girls; Study 2, 40 boys, 35 girls, ages 3-6), child knowledge of brands offering products high in sugar, salt and fat was shown to be a significant predictor of child BMI, even after controlling for their age and gender and when also considering the extent of their TV viewing. Additionally, two different collage measures of brand knowledge (utilized across the two studies) performed similarly, suggesting that this measure may be serving as a surrogate indicator of an overall pattern of product exposure and consumption. Policy implications are discussed.

The contribution of estuary-resident life histories to the return of adult Oncorhynchus kisutch.

This study evaluated estuarine habitat use, life-history composition, growth and survival of four successive broods of coho salmon Oncoryhnchus kisutch in Salmon River, Oregon, U.S.A. Subyearling and yearling O. kisutch used restored and natural estuarine wetlands, particularly in the spring and winter. Stream-reared yearling smolts spent an average of 2 weeks in the estuary growing rapidly before entering the ocean. Emergent fry also entered the estuary in the spring, and some resided in a tidal marsh throughout the summer, even as salinities increased to >20. A significant portion of the summer stream-resident population of juvenile O. kisutch migrated out of the catchment in the autumn and winter and used estuary wetlands and adjacent streams as alternative winter-rearing habitats until the spring when they entered the ocean as yearling smolts. Passive integrated transponder (PIT) tag returns and juvenile life-history reconstructions from otoliths of returning adults revealed that four juvenile life-history types contributed to the adult population. Estuarine-associated life-history strategies accounted for 20-35% of the adults returning to spawn in the four brood years, indicating that a sizable proportion of the total O. kisutch production is ignored by conventional estimates based on stream habitat capacity. Juvenile O. kisutch responses to the reconnection of previously unavailable estuarine habitats have led to greater life-history diversity in the population and reflect greater phenotypic plasticity of the species in the U.S. Pacific Northwest than previously recognized.

Predictors of behavior change intention using health risk appraisal data.

OBJECTIVES: To investigate predictors of behavior change intention and discuss potential implications for practitioners. METHODS: Health risk appraisal (HRA) data from 2 organizations were used to develop and confirm a path analysis model for predictors of intention to change behavior. RESULTS: Lower self-rated health perception and higher ratings of stress corresponded to higher behavior-change intention scores. Stress was associated with poorer health perception. CONCLUSIONS: Higher stress and lower perception of health status were directly associated with intention to change behavior. Incorporating stress management and awareness of health perception into health promotion strategies could enhance wellness programs by aligning programs with motivating factors.

Contingent choice. Exploring the relationship between sweetened beverages and vegetable consumption.

Adults and children are repeatedly exposed to the pairing of food and drink as found in meal deals and "combos". There may arise from this indoctrination, a contingent relationship between drink context and food preference. Our multi-method research examines food and drink combining. A survey-based study examines the food and drink pairing preferences of adults (N=60), while a laboratory study with young children (N=75, aged three to five) examines the role of drink context on vegetable consumption. The adult survey finds strong food and drink combining preferences. The pairing of soft drinks with calorie dense foods is regarded favorably, while the pairing of soft drinks with vegetables is not. In child food trials, vegetable consumption is not influenced by the child's fussiness but is influenced by the drink accompaniment. In limited contexts, these findings demonstrate the contingent relationship between drink context and food consumption. Both palate preference and associative learning may be mechanisms driving the effects of drink context on food consumption. The findings suggest simple consumer strategies that might be employed to change dietary patterns (e.g., drink water with meals), and hold straightforward policy implications (e.g., increase water as the default option in meal deals).

Collectible toys and decisions to share: I will gift you one to expand my set.

Two studies were used to examine the collecting behaviour of preschool children. Prior studies of collecting have defined the behaviour as exhibited by older children and adults. To understand childhood collecting, existing theoretical perspectives were discussed in terms of how they might apply to children's behaviour as collectors. Results showed that some preschool children are motivated to engage in collecting and possess the developmental capacities required for successful collecting. Individual differences in executive functioning (Study 1, N= 57) and theory of mind (Study 2, N= 46) explained why some preschoolers were more oriented towards collecting than others. Study 2 showed that the motivational pull of collectible toys can be very strong, with some children agreeing to pay the 'cost' of sharing with a confederate child in order to obtain a collectible toy. This research highlights similarities and differences between adult and child collecting. Suggestions are provided for parents and for policy considerations regarding the appropriateness of marketing collectible toys to preschoolers.

Alternative thinking about starting points of obesity. Development of child taste preferences.

Food marketers are at the epicenter of criticism for the unfolding obesity epidemic as societies consider banning advertising to children and taxing "junk" foods. While marketing's role in obesity is not well understood, there is clear evidence that children are regularly targeted with calorie-dense, nutrient-poor food. Much of the past research seeks to understand how marketing influences brand preference and child requests. The authors argue that understanding palate development offers new insights for discussion. Two studies consider whether a sugar/fat/salt (SFS) palate is linked to children's knowledge of food brands, experience with products, and advertising. In study 1, the authors develop a survey measure of taste preferences and find that a child's SFS palate (as reported by parents) relates significantly to children's self-reported food choices. Study 2 examines how knowledge of certain branded food and drinks is related to palate. Findings show that children with detailed mental representations of fast-food and soda brands--developed via advertising and experience--have higher scores on the SFS palate scale.

Sponsorship, ambushing, and counter-strategy: effects upon memory for sponsor and event.

Corporate sponsorship of sports, causes, and the arts has become a mainstream communications tool worldwide. The unique marketing opportunities associated with major events also attract nonsponsoring companies seeking to form associations with the event (ambushing). There are strategies available to brands and events which have been ambushed; however, there is only limited information about the effects of those strategies on attainment of sponsorship objectives. In Experiment 1, university staff and students participated by studying paragraphs linking a sponsor to a novel event. Relative to each sponsor-event pair, they then studied one of three different messages about a competitor. Results find a message which linked the competitor and the event increased competitor recall given the event as a cue and event recall given the competitor as a cue. These effects were moderated if there was information about the competitor not being the sponsor. In Experiment 2 ambushing and counter-ambushing information was presented over 2 days. Both types of messages increased competitor recall given the event as a cue and event recall given the competitor as a cue. In addition, "not sponsor" information was not always used even when it should have been recallable. The results can be explained if participants are using three cues: a specific cue such as a brand name, a contextual cue, and a category cue, such as the concept of an event. Findings suggest to sponsoring firms and event properties that counter-ambushing communications may have the unintended effect of strengthening an ambusher-event relationship in memory.

Reorganization of myofilament proteins and decreased cGMP-dependent protein kinase in the human uterus during pregnancy.

Excessive or premature contractions of uterine smooth muscle may contribute to preterm labor. Contractile stimuli induce myosin and actin filament interactions through calcium-dependent myosin phosphorylation. The mechanisms that maintain myometrial quiescence until term are not well established, but may include control of calcium levels by nitric oxide and cGMP signaling and thin filament (caldesmon and calponin) regulation. Previously, we reported that myometrial tissues from pregnant rats are not responsive to cGMP due to decreases in cGMP-dependent protein kinase. Considering the well documented differences in the endocrinology of parturition among species, this study was conducted to test the hypothesis that the levels and subcellular distribution of caldesmon, calponin, and cGMP-dependent protein kinase are regulated with the hormonal milieu of human pregnancy. Whereas cGMP-dependent protein kinase was significantly reduced in the human uterus during pregnancy, caldesmon expression was significantly increased, and both caldesmon and calponin were redistributed to a readily extractable subcellular pool. These data suggest that cGMP-dependent protein kinase does not mediate gestational quiescence. Redistribution of thin filament-associated proteins, however, may alter uterine smooth muscle tone or the cytoskeletal framework of myocytes to maintain gestation despite the substantial distention that accompanies all intrauterine pregnancies.

Regulation of cyclic guanosine monophosphate-dependent protein kinase in human uterine tissues during the menstrual cycle.

Contractility of uterine smooth muscle is essential for the cyclic shedding of the endometrial lining and also for expulsion of the fetus during parturition. The nitric oxide (NO)-cGMP signaling pathway is involved in smooth muscle relaxation. The downstream target of this pathway essential for decreasing cytoplasmic calcium and muscle tone is the cGMP-dependent protein kinase (PKG). The present study was undertaken to localize expression of PKG in tissues of the female reproductive tract and to test the hypothesis that uterine smooth muscle PKG levels vary with the human menstrual cycle. Immunohistochemistry was used to localize PKG in myometrium, cervix, and endometrium obtained during proliferative and secretory phases. The PKG was localized to uterine and vascular smooth muscle cells in myometrium, stromal cells in endometrium, and a small percentage of cervical stromal cells. Using Western blot analysis and protein kinase activity assays, the expression of PKG was reduced significantly in progesterone-dominated uteri compared with myometrium from postmenopausal women or women in the proliferative phase. These findings support a role for PKG in the control of uterine and vascular smooth muscle contractility during the menstrual cycle.

Cyclic GMP-dependent protein kinase expression in coronary arterial smooth muscle in response to balloon catheter injury.

Arterial smooth muscle cells undergo phenotypic and proliferative changes in response to balloon catheter injury. Nitric oxide (NO) and cGMP have been implicated in the inhibition of vascular smooth muscle cell proliferation and phenotypic modulation in cultured-cell studies. We have examined the expression of the major cGMP receptor protein in smooth muscle, cGMP-dependent protein kinase I (PKG), in response to balloon catheter injury in the swine coronary artery. On injury, there was a transient decrease in the expression of PKG in neointimal smooth muscle cells when compared with medial smooth muscle cells. The decrease in PKG expression was observed in the population of proliferating cells expressing the extracellular matrix protein osteopontin but not in cells present in the uninjured portion of the media. Coincident with the suppression of PKG expression in neointimal cells after injury, there was a marked increase in the expression of type II NO synthase (inducible NOS [iNOS], NOS-II) in the neointimal cells. These results suggest that PKG expression is transiently reduced in response to injury in the population of coronary arterial smooth muscle cells that are actively proliferating and producing extracellular matrix proteins. The reduction in PKG expression is also correlated temporally with increases in inflammatory activity in the injured vessels as assessed by iNOS expression. Coupled with our current knowledge regarding the role of PKG in the regulation of cultured cell phenotypes, these results imply that PKG may also regulate phenotypic modulation of vascular smooth muscle cells in vivo as well.

The development of a health policy for the Army.

This paper describes the development of the Army Health Policy (AHP), which is a key component of the Army Human Resources Strategy (AHRS). The work on the AHP provided an opportunity for a fundamental review of the delivery of health support to the Army. The AHP will provide the strategic framework by which the Army will ensure the health of its workforce and, where appropriate, their dependents. The methodology used for this work may be a useful model for the development of a health policy for occupational populations.

Nitric oxide regulation of cGMP production in osteoclasts.

Bone resorption by osteoclasts is modified by agents that affect cyclic guanosine monophosphate (cGMP), but their relative physiological roles, and what components of the process are present in osteoclasts or require accessory cells such as osteoblasts, are unclear. We studied cGMP regulation in avian osteoclasts, and in particular the roles of nitric oxide and natriuretic peptides, to clarify the mechanisms involved. C-type natriuretic peptide drives a membrane guanylate cyclase, and increased cGMP production in mixed bone cells. However, C-type natriuretic peptide did not increase cGMP in purified osteoclasts. By contrast, osteoclasts did produce cGMP in response to nitric oxide (NO) generators, sodium nitroprusside or 1-hydroxy-2-oxo-3,3-bis(3-aminoethyl)-1-triazene. These findings indicate that C-type natriuretic peptide and NO modulate cGMP in different types of bone cells. The activity of the osteoclast centers on HCI secretion that dissolves bone mineral, and both NO generators and hydrolysis-resistant cGMP analogues reduced bone degradation, while cGMP antagonists increased activity. NO synthase agonists did not affect activity, arguing against autocrine NO production. Osteoclasts express NO-activated guanylate cyclase and cGMP-dependent protein kinase (G-kinase). G-kinase reduced membrane HCI transport activity in a concentration-dependent manner, and phosphorylated a 60-kD osteoclast membrane protein, which immunoprecipitation showed is not an H+-ATPase subunit. We conclude that cGMP is a negative regulator of osteoclast activity. cGMP is produced in response to NO made by other cells, but not in response to C-type natriuretic peptide. G-kinase modulates osteoclast membrane HCI transport via intermediate protein(s) and may mediate cGMP effects in osteoclasts.

Nitric oxide-dependent induction of glutathione synthesis through increased expression of gamma-glutamylcysteine synthetase.

The nitric oxide (NO) donors S-nitrosopenicillamine or DetaNONOate, which release NO at a rate of 0-15 nM sec-1, were exposed to rat aortic vascular smooth muscle cells for a period of 0-24 h. This treatment resulted in an increase in total glutathione levels of two- to threefold under conditions where no cytotoxicity was detected. The signaling pathways do not involve activation of protein kinase G Ialpha nor are they cGMP dependent. Oxidation of reduced glutathione (GSH) was found after exposure to NO for 3-4 h at rates of formation at or above 8 nM sec-1. Increased intracellular GSH was due to enhanced expression of the rate-limiting enzyme for GSH synthesis, gamma-glutamylcysteine synthetase. Since NO has been shown previously to protect cells against oxidative stress, we propose that the increase in GSH by NO is a potential mechanism for enhancing the antioxidant defenses of the cell. This result also has important implications for identifying redox-sensitive cell signaling pathways that can be activated by NO.

Alpha-adrenergic receptors regulate human lymphocyte amiloride-sensitive sodium channels.

Two independent signal transduction pathways regulate lymphocyte amiloride-sensitive sodium channels (ASSCs), one utilizing cAMP as a second messenger and the other utilizing a GTP-binding protein. This implies that two plasma membrane receptors play a role in the regulation of lymphocyte ASSCs. In this study, we tested the hypothesis that alpha1- and alpha2-adrenergic receptors independently regulate lymphocyte ASSCs via the two previously identified second messengers. Direct measurements indicated that norepinephrine increased lymphocyte cAMP and activated ASSCs. The alpha2-specific inhibitor, yohimbine, blocked this activation, thereby linking alpha2-adrenergic receptors to ASSC regulation via cAMP. The alpha1-specific ligand, terazosin, acted as an agonist and activated lymphocyte ASSCs but inhibited ASSC current that had been preactivated by norepinephrine or 8-(4-chlorophenylthio) (CPT)-cAMP. Terazosin had no effect on the lymphocyte whole cell ASSC currents preactivated by treatment with pertussis toxin. This finding indirectly links alpha1-adrenergic receptors to lymphocyte ASSC regulation via GTP-binding proteins. Terazosin had no direct inhibitory or stimulatory effects on alpha,beta,gamma-endothelial sodium channels reconstituted into planar lipid bilayers and expressed in Xenopus oocytes, ruling out a direct interaction between terazosin and the channels. These findings support the hypothesis that both alpha1- and alpha2-adrenergic receptors independently regulate lymphocyte ASSCs via GTP-binding proteins and cAMP, respectively.

Nitric oxide-dependent production of cGMP supports the survival of rat embryonic motor neurons cultured with brain-derived neurotrophic factor.

Trophic factor deprivation induces neuronal nitric oxide synthase (NOS) and apoptosis of rat embryonic motor neurons in culture. We report here that motor neurons constitutively express endothelial NOS that helps support the survival of motor neurons cultured with brain-derived neurotrophic factor (BDNF) by activating the nitric oxide-dependent soluble guanylate cyclase. Exposure of BDNF-treated motor neurons to nitro-L-arginine methyl ester (L-NAME) decreased cell survival 40-50% 24 hr after plating. Both low steady-state concentrations of exogenous nitric oxide (<0.1 microM) and cGMP analogs protected BDNF-treated motor neurons from death induced by L-NAME. Equivalent concentrations of cAMP analogs did not affect cell survival. Inhibition of nitric oxide-sensitive guanylate cyclase with 2 microM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) reduced the survival of BDNF-treated motor neurons by 35%. cGMP analogs also protected from ODQ-induced motor neuron death, whereas exogenous nitric oxide did not. In all cases, cell death was prevented with caspase inhibitors. Our results suggest that nitric oxide-stimulated cGMP synthesis helps to prevent apoptosis in BDNF-treated motor neurons.

Regulation of cGMP-induced relaxation and cGMP-dependent protein kinase in rat myometrium during pregnancy.

Increases in guanosine 3',5'-cyclic monophosphate (cGMP) induced by nitric oxide (NO), nitrovasodilators, and atrial peptides correlate with relaxation of vascular smooth muscle. Relaxation of myometrial smooth muscle by increases in cGMP, however, has required unusually high concentrations of the cyclic nucleotide. We tested the hypothesis that the sensitivity of myometrium to relaxation by cGMP is increased during pregnancy. Aortic smooth muscle was more sensitive to relaxation by cGMP than myometrial tissues, and, contrary to our hypothesis, myometrium from pregnant rats was least sensitive. Although levels of cGMP were elevated after treatment with the NO donor, S-nitroso-N-acetylpenicillamine, relaxation of myometrial tissues obtained from pregnant rats occurred only at extraordinarily high concentrations. The levels of cGMP-dependent protein kinase (PKG) were significantly decreased in myometrium from pregnant rats compared with myometrium from nonpregnant cycling animals or aortic smooth muscle. Administration of estradiol to ovariectomized rats increased myometrial PKG expression, and progesterone antagonized this response. We conclude that 1) myometrial tissues from pregnant rats are not sensitive to relaxation by cGMP and 2) this insensitivity to cGMP is accompanied by progesterone-mediated decreases in the level of PKG expression.

Nitric oxide--cyclic GMP pathway regulates vascular smooth muscle cell phenotypic modulation: implications in vascular diseases.

The role of cGMP-dependent protein kinase (PKG) in the regulation of rat aortic vascular smooth muscle cells (VSMC) phenotype was examined using a transfected cell culture system. Repetitively passaged VSMC do not express PKG and exist in the synthetic phenotype. Transfection of PKG-l alpha cDNA, or the active catalytic domain of PKG-l alpha, resulted in the appearance of VSMC having a morphology consistent with the contractile phenotype. PKG-expressing cells also contained markers for the contractile phenotype (for example, smooth muscle specific myosin heavy chain, calponin, alpha-actin) and reduced levels of synthetic phenotype markers (osteopontin, thrombospondin). PKG-transfected VSMC have also reduced the levels of fibroblast growth factor receptors 1 and 2, consistent with the establishment of a more contractile phenotype. The regulation of PKG expression in VSMC is largely undefined; however, continuous exposure of cultured bovine aortic smooth muscle cells with nitric oxide (NO)-donor drugs or cyclic nucleotide analogues reduced the expression of PKG. These results suggest that PKG occupies a critical role in VSMC phenotype and that suppression of PKG expression during inflammation or injury promotes a more synthetic state of the VSMC.

Smooth muscle cell expression of type I cyclic GMP-dependent protein kinase is suppressed by continuous exposure to nitrovasodilators, theophylline, cyclic GMP, and cyclic AMP.

A key component of the nitric oxide-cyclic guanosine monophosphate (cGMP) pathway in smooth muscle cells (SMC) is the type I GMP-dependent protein kinase (PK-G I). Activation of PK-G I mediates the reduction of cytoplasmic calcium concentrations and vasorelaxation. In this manuscript, we demonstrate that continuous exposure of SMC in culture to the nitrovasodilators S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP) results in approximately 75% suppression of PK-G I mRNA by 48 h. PK-G I mRNA and protein were also suppressed by continuous exposure to cGMP analogues 8-bromo- and 8-(4-chlorophenylthio) guanosine-3,5-monophosphate or the cAMP analogue dibutyryl cAMP. These results suggest that activation of one or both of the cyclic nucleotide-dependent protein kinases mediates PK-G I mRNA suppression. Using isoform-specific cDNA probes, only the PK-G I alpha was detected in SMC, either at baseline or after suppression, while PK-G I beta was not detected, indicating that isoform switch was not contributing to the gene regulation. Using the transcription inhibitor actinomycin D, the PK-G I mRNA half-life in bovine SMC was observed to be 5 h. The half-life was not affected by the addition of SNAP to actinomycin D, indicating no effect on PK-G I mRNA stability. Nuclear runoff studies indicated a suppression of PK-G I gene transcription by SNAP. PK-G I suppression was also observed in vivo in rats given isosorbide dinitrate in the drinking water, with a dose-dependent suppression of PK-G I protein in the aorta. PK-G I antigen in whole rat lung extract was also suppressed by administration of isosorbide or theophylline in the drinking water. These data may contribute to our understanding of nitrovasodilator resistance, a phenomenon resulting from continuous exposure to nitroglycerin or other nitrovasodilators.