79 research outputs found
Seasonal Movements and Distribution of Steller’s Eiders (Polysticta stelleri) Wintering at Kodiak Island, Alaska
We used satellite telemetry in 2004–06 to describe the annual movements and habitat use of a segment of the Pacific population of Steller’s Eiders (Polysticta stelleri) that winters at Kodiak Island, Alaska. Information about broad-scale patterns of seasonal distribution and links among annual cycle stages is critical for interpreting population trends and developing conservation strategies. We captured birds in Chiniak Bay at Kodiak Island in late February and early March and monitored the movements after departure from Kodiak Island of 24 satellite-tagged birds: 16 after-second-year (ASY) age class females, one second-year age class female, and seven ASY males. All birds used the same intercontinental migration corridor during spring, but routes and chronology of spring migration appeared to vary by year and among individuals. Sixteen of the 24 birds that were tracked migrated to breeding areas along the Arctic coast of Russia from the Chukotka Peninsula to the Taymyr Peninsula; five birds, assumed to be non-breeding, spent the summer in nearshore waters of Russia and Alaska; and the remaining three birds either died during spring migration or had failed transmitters. Thirteen birds were tracked to molt sites that were broadly distributed along the coast of Alaska. Molt sites included St. Lawrence Island, the Kuskokwim Shoals, Kamishak Bay, and three sites along the Alaska Peninsula. Twelve of these 13 birds returned to Kodiak Island to winter, and a single male wintered on the Alaska Peninsula. Steller’s Eiders marked during winter at Kodiak Island were widely distributed during the breeding season, but a large proportion of marked birds returned to molting and wintering areas in two years of the study.De 2004 à 2006, nous avons recouru à la télémétrie satellitaire pour décrire l’utilisation de l’habitat et les mouvements annuels d’un segment de la population d’eiders de Steller (Polysticta stelleri) dans la région du Pacifique, eiders qui hivernent sur l’île Kodiak, en Alaska. Il est essentiel d’obtenir des données sur les tendances à grande échelle de la répartition saisonnière et des liens entre les divers stades du cycle annuel de ces oiseaux afin d’être en mesure d’interpréter leurs tendances démographiques et d’élaborer des stratégies de conservation. Nous avons capturé des oiseaux dans la baie Chiniak de l’île Kodiak vers la fin février et le début mars. Après notre départ de l’île Kodiak, nous avons surveillé les mouvements de 24 oiseaux pistés par satellite : 16 femelles de plus de deux ans, une femelle de deux ans et sept mâles de plus de deux ans. Tous les oiseaux ont emprunté le même couloir de migration intercontinental au printemps, mais les routes et la chronologie de la migration printanière semblaient varier d’une année à l’autre et d’un individu à l’autre. Seize des24 oiseaux pistés ont migré vers des aires de reproduction situées le long de la côte arctique de la Russie, depuis la presqu’île de Tchoukotkae jusqu’à la presqu’île de Taïmyr; cinq oiseaux, probablement non reproducteurs, ont passé l’été dans les eaux côtières de la Russie et de l’Alaska, tandis que les trois autres oiseaux sont morts pendant la migration printanière ou étaient dotés de transmetteurs défectueux. Treize oiseaux ont été repérés à des sites de mue largement répartis le long de la côte de l’Alaska. Parmi ces sites, notons ceux de l’île Saint-Laurent, du haut-fond de Kuskokwim, de la baie de Kamishak et de trois autres sites le long de la péninsule de l’Alaska. Douze de ces 13 oiseaux sont retournés à l’île Kodiak pour passer l’hiver, et un seul mâle a hiverné dans la péninsule de l’Alaska. Les eiders de Steller qui ont été marqués à l’île Kodiak pendant l’hiver étaient largement répartis pendant la saison de reproduction, mais une grande proportion d’oiseaux pistés sont retournés aux aires de mue et d’hivernage au cours des deux années visées par l’étude
Tradable Pollution Permits and the Regulatory Game
This paper analyzes polluters\u27 incentives to move from a traditional command and control (CAC) environmental regulatory regime to a tradable permits (TPP) regime. Existing work in environmental economics does not model how firms contest and bargain over actual regulatory implementation in CAC regimes, and therefore fail to compare TPP regimes with any CAC regime that is actually observed. This paper models CAC environmental regulation as a bargaining game over pollution entitlements. Using a reduced form model of the regulatory contest, it shows that CAC regulatory bargaining likely generates a regulatory status quo under which firms with the highest compliance costs bargain for the smallest pollution reductions, or even no reduction at all. As for a tradable permits regime, it is shown that all firms are better off under such a regime than they would be under an idealized CAC regime that set and enforced a uniform pollution standard, but permit sellers (low compliance cost firms) may actually be better off under a TPP regime with relaxed aggregate pollution levels. Most importantly, because high cost firms (or facilities) are the most weakly regulated in the equilibrium under negotiated or bargained CAC regimes, they may be net losers in a proposed move to a TPP regime. When equilibrium costs under a TPP regime are compared with equilibrium costs under a status quo CAC regime, several otherwise paradoxical aspects of firm attitudes toward TPP type reforms can be explained. In particular, the otherwise paradoxical pattern of allowances awarded under Phase II of the 1990 Clean Air Act\u27s acid rain program, a pattern tending to favor (in Phase II) cleaner, newer generating units, is explained by the fact that under the status quo regime, a kind of bargained CAC, it was the newer cleaner units that were regulated, and which therefore had higher marginal control costs than did the largely unregulated older, plants. As a normative matter, the analysis here implies that the proper baseline for evaluating TPP regimes such as those contained in the Bush Administration\u27s recent Clear Skies initiative is not idealized, but nonexistent CAC regulatory outcomes, but rather the outcomes that have resulted from the bargaining game set up by CAC laws and regulations
The tip of the iceberg: challenges of accessing hospital electronic health record data for biological data mining
Distribution and seasonality of rhinovirus and other respiratory viruses in a cross-section of asthmatic children in Trinidad, West Indies
<p>Abstract</p> <p>Background</p> <p>Childhood asthma in the Caribbean is advancing in prevalence and morbidity. Though viral respiratory tract infections are reported triggers for exacerbations, information on these infections with asthma is sparse in Caribbean territories. We examined the distribution of respiratory viruses and their association with seasons in acute and stable asthmatic children in Trinidad.</p> <p>Methods</p> <p>In a cross-sectional study of 70 wheezing children attending the emergency department for nebulisation and 80 stable control subjects (2 to 16 yr of age) in the asthma clinic, nasal specimens were collected during the dry (<it>n </it>= 38, January to May) and rainy (<it>n </it>= 112, June to December) seasons. A multitarget, sensitive, specific high-throughput Respiratory MultiCode assay tested for respiratory-virus sequences for eight distinct groups: human rhinovirus, respiratory syncytial virus, parainfluenza virus, influenza virus, metapneumovirus, adenovirus, coronavirus, and enterovirus.</p> <p>Results</p> <p>Wheezing children had a higher [χ<sup>2 </sup>= 5.561, <it>p </it>= 0.018] prevalence of respiratory viruses compared with stabilized asthmatics (34.3% (24) versus (vs.) 17.5% (14)). Acute asthmatics were thrice as likely to be infected with a respiratory virus (OR = 2.5, 95% CI = 1.2 – 5.3). The predominant pathogens detected in acute versus stable asthmatics were the rhinovirus (RV) (<it>n </it>= 18, 25.7% vs. <it>n </it>= 7, 8.8%; <it>p </it>= 0.005), respiratory syncytial virus B (RSV B) (<it>n </it>= 2, 2.9% vs. <it>n </it>= 4, 5.0%), and enterovirus (<it>n </it>= 1, 1.4% vs. <it>n </it>= 2, 2.5%). Strong odds for rhinoviral infection were observed among nebulised children compared with stable asthmatics (<it>p </it>= 0.005, OR = 3.6, 95% CI = 1.4 – 9.3,). RV was prevalent throughout the year (Dry, <it>n </it>= 6, 15.8%; Rainy, <it>n </it>= 19, 17.0%) and without seasonal association [χ<sup>2 </sup>= 0.028, <it>p </it>= 0.867]. However it was the most frequently detected virus [Dry = 6/10, (60.0%); Rainy = 19/28, (67.9%)] in both seasons.</p> <p>Conclusion</p> <p>Emergent wheezing illnesses during childhood can be linked to infection with rhinovirus in Trinidad's tropical environment. Viral-induced exacerbations of asthma are independent of seasons in this tropical climate. Further clinical and virology investigations are recommended on the role of infections with the rhinovirus in Caribbean childhood wheeze.</p
Encoding optical control in LCK kinase to quantitatively investigate its activity in live cells.
LCK is a tyrosine kinase that is essential for initiating T-cell antigen receptor (TCR) signaling. A complete understanding of LCK function is constrained by a paucity of methods to quantitatively study its function within live cells. To address this limitation, we generated LCK*, in which a key active-site lysine is replaced by a photocaged equivalent, using genetic code expansion. This strategy enabled fine temporal and spatial control over kinase activity, thus allowing us to quantify phosphorylation kinetics in situ using biochemical and imaging approaches. We find that autophosphorylation of the LCK active-site loop is indispensable for its catalytic activity and that LCK can stimulate its own activation by adopting a more open conformation, which can be modulated by point mutations. We then show that CD4 and CD8, T-cell coreceptors, can enhance LCK activity, thereby helping to explain their effect in physiological TCR signaling. Our approach also provides general insights into SRC-family kinase dynamics
Loss of Caveolin-1 Accelerates Neurodegeneration and Aging
The aged brain exhibits a loss in gray matter and a decrease in spines and synaptic densities that may represent a sequela for neurodegenerative diseases such as Alzheimer's. Membrane/lipid rafts (MLR), discrete regions of the plasmalemma enriched in cholesterol, glycosphingolipids, and sphingomyelin, are essential for the development and stabilization of synapses. Caveolin-1 (Cav-1), a cholesterol binding protein organizes synaptic signaling components within MLR. It is unknown whether loss of synapses is dependent on an age-related loss of Cav-1 expression and whether this has implications for neurodegenerative diseases such as Alzheimer's disease.We analyzed brains from young (Yg, 3-6 months), middle age (Md, 12 months), aged (Ag, >18 months), and young Cav-1 KO mice and show that localization of PSD-95, NR2A, NR2B, TrkBR, AMPAR, and Cav-1 to MLR is decreased in aged hippocampi. Young Cav-1 KO mice showed signs of premature neuronal aging and degeneration. Hippocampi synaptosomes from Cav-1 KO mice showed reduced PSD-95, NR2A, NR2B, and Cav-1, an inability to be protected against cerebral ischemia-reperfusion injury compared to young WT mice, increased Aβ, P-Tau, and astrogliosis, decreased cerebrovascular volume compared to young WT mice. As with aged hippocampi, Cav-1 KO brains showed significantly reduced synapses. Neuron-targeted re-expression of Cav-1 in Cav-1 KO neurons in vitro decreased Aβ expression.Therefore, Cav-1 represents a novel control point for healthy neuronal aging and loss of Cav-1 represents a non-mutational model for Alzheimer's disease
Fine-mapping type 2 diabetes loci to single-variant resolution using high-density imputation and islet-specific epigenome maps
We expanded GWAS discovery for type 2 diabetes (T2D) by combining data from 898,130 European-descent individuals (9% cases), after imputation to high-density reference panels. With these data, we (i) extend the inventory of T2D-risk variants (243 loci,135 newly implicated in T2D predisposition, comprising 403 distinct association signals); (ii) enrich discovery of lower-frequency risk alleles (80 index variants with minor allele frequency 2); (iii) substantially improve fine-mapping of causal variants (at 51 signals, one variant accounted for >80% posterior probability of association (PPA)); (iv) extend fine-mapping through integration of tissue-specific epigenomic information (islet regulatory annotations extend the number of variants with PPA >80% to 73); (v) highlight validated therapeutic targets (18 genes with associations attributable to coding variants); and (vi) demonstrate enhanced potential for clinical translation (genome-wide chip heritability explains 18% of T2D risk; individuals in the extremes of a T2D polygenic risk score differ more than ninefold in prevalence).Peer reviewe
Robot-assisted Transplant Ureteral Repair to treat transplant ureteral strictures in patients after Robot-assisted Kidney Transplant: a case series
OBJECTIVE: To describe the use of robotic-assisted transplant ureteral repair (RATUR) for treating transplant ureteral stricture (TUS) in 3 patients who had undergone robot assisted kidney transplant (RAKT).
METHOD: We reviewed the medical records of 3 patients who experienced TUS after RAKT and who underwent RATUR between 2017 and 2020. The patients\u27 RAKT, post-transplant clinical course, endourological interventions, reoperation, and recovery were assessed.
RESULTS: All patients diagnosed with TUS presented with deterioration of kidney function after RAKT. Method of diagnosis included ultrasound, antegrade ureterogram, and CT scan. All 3 patients had a short (\u3c1 \u3ecm) area of TUS and underwent RATUR. For 2 patients, distal strictures were bypassed with modified Lich-Gregoir ureteroneocystostomy reimplantation. One patient was treated with pyelo-ureterostomy to the contralateral native ureter. No intraoperative complications, conversions to open surgery, or significant operative blood loss requiring blood transfusion for any patient were observed. Also, no patients had urine leaks in the immediate or late postoperative period. After RATUR, 2 patients developed Clavien grade II complications with rectus hematoma or urinary tract infection.
CONCLUSION: RATUR is a technically feasible operation for kidney transplant patients with TUS after RAKT. This procedure may provide the same benefits of open operation without promoting certain comorbidities that may occur from open surgical procedures
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