The RTC and the escalating costs of the thrift insurance mess

An examination of the structure of the Resolution Trust Corporation and of its performance in resolving the savings and loan insurance crisis, defining the obstacles that may be impeding the RTC's effectiveness in closing insolvent thrifts and returning their assets to the private sector.Resolution Trust Corporation (U.S.) ; Savings and loan associations

FDICIA's prompt corrective action provisions

A review of the origins of FDICIA's early intervention policy and the political economy arguments for supporting it, with emphasis on the specific sections of the law that pertain to this policy and the ways in which the new guidelines will impact the future of the nation's depositories.Deposit insurance ; Federal Deposit Insurance Corporation Improvement Act of 1991

Stable isotope evidence for crustal recycling as recorded by superdeep diamonds

Sub-lithospheric diamonds from the Juina-5 and Collier-4 kimberlites and the Machado River alluvial deposit in Brazil have carbon isotopic compositions that co-vary with the oxygen isotopic compositions of their inclusions, which implies that they formed by a mixing process. The proposed model for this mixing process, based on interaction of slab-derived carbonate melt with reduced (carbide- or metal-bearing) ambient mantle, explains these isotopic observations. It is also consistent with the observed trace element chemistries of diamond inclusions from these localities and with the experimental phase relations of carbonated subducted crust. The 18O-enriched nature of the inclusions demonstrates that they incorporate material from crustal protoliths that previously interacted with seawater, thus confirming the subduction-related origin of superdeep diamonds. These samples also provide direct evidence of an isotopically anomalous reservoir in the deep (≥350 km) mantle

Cattle handling technique can induce fatigued cattle syndrome in cattle not fed a beta adrenergic agonist

Citation: Frese, D. A., Reinhardt, C. D., Bartle, S. J., Rethorst, D. N., Hutcheson, J. P., Nichols, W. T., . . . Thomson, D. U. (2016). Cattle handling technique can induce fatigued cattle syndrome in cattle not fed a beta adrenergic agonist. Journal of Animal Science, 94(2), 581-591. doi:10.2527/jas2015-9824Angus crossbred steers (n = 40; 563 +/- 44 kg) were used to examine the effects of handling method and fat thickness on the blood chemistry and physiology of market steers. Steers were blocked by backfat (BF) thickness and were randomly assigned to treatment groups: low-stress handling (LSH) and aggressive handling (AH). Cattle were then ran-domly assigned to one of 5 blocks containing 4 steers from the LSH and AH treatments. Steers in the LSH treatment were walked and AH cattle were run through a course of 1,540 m. Blood samples were obtained via jugular venipuncture before handling (BASE), at 770 m (LAP1), at 1,540 m (LAP2), and at1 h (1H) and 2 h (2H) after finishing the course. Blood samples were analyzed for plasma lactate (LAC), creatinine kinase (CK), base excess (BE), blood pH (pH), serum cortisol (CORT) concentrations, and venous carbon dioxide (PvCO2) and oxygen (PvO2) pressures. Heart rate (HR), respiratory rate (RR), and rectal temperature (TEMP) were measured at the same intervals. Cattle in the AH treatment had greater (P 0.14). Blood pH in AH cattle was decreased compared with that in LSH cattle (P 0.13) at BASE, 1H, or 2H. Heart rate and TEMP were increased in AH cattle compared to LSH (P > 0.01). Serum cortisol was increased (P < 0.05) in AH compared to that in LSH cattle at LAP1 (87.5 vs. 58.9 nmol/ L), LAP2 (144.4 vs. 93.1 nmol/ L), and 1H (113.5 vs. 53.1 nmol/ L). Although RR was not differ-ent between LSH and AH, PvCO2 was decreased in AH compared to that in LSH (P < 0.05) at LAP2 (30.6 vs. 39.3 mmHg) and PvO2 was increased at LAP1 (42.7 vs. 33.5 mmHg) and at LAP2 (51.5 vs. 36.6 mmHg). Lactate was increased in AH cattle in the thicker BF group at 1H (P < 0.05), and blood pH was decreased at LAP1, LAP2, and 1H (P < 0.05) compared to the thinner BF cohorts. Four AH steers became exhausted (EXH) and did not complete the course. Increased CK, decreased PvCO2, and muscle tremors occurred in EXH steers compared to non-exhausted AH cohorts. Results of this study show that AH causes physiologic and blood chemistry changes in steers, which can be potentially detrimental to cattle, emphasizing the need for lowstress handling practices

Smoking in asthma is associated with elevated levels of corticosteroid resistant sputum cytokines—an exploratory study

&lt;p&gt;Background: Current cigarette smoking is associated with reduced acute responses to corticosteroids and worse clinical outcomes in stable chronic asthma. The mechanism by which current smoking promotes this altered behavior is currently unclear. Whilst cytokines can induce corticosteroid insensitivity in-vitro, how current and former smoking affects airway cytokine concentrations and their responses to oral corticosteroids in stable chronic asthma is unclear.&lt;/p&gt; &lt;p&gt;Objectives: To examine blood and sputum cytokine concentrations in never, ex and current smokers with asthma before and after oral corticosteroids.&lt;/p&gt; &lt;p&gt;Methods: Exploratory study utilizing two weeks of oral dexamethasone (equivalent to 40 mg/day prednisolone) in 22 current, 21 never and 10 ex-smokers with asthma. Induced sputum supernatant and plasma was obtained before and after oral dexamethasone. 25 cytokines were measured by multiplex microbead system (Invitrogen, UK) on a Luminex platform.&lt;/p&gt; &lt;p&gt;Results: Smokers with asthma had elevated sputum cytokine interleukin (IL) -6, -7, and -12 concentrations compared to never smokers with asthma. Few sputum cytokine concentrations changed in response to dexamethasone IL-17 and IFNα increased in smokers, CCL4 increased in never smokers and CCL5 and CXCL10 reduced in ex-smokers with asthma. Ex-smokers with asthma appeared to have evidence of an ongoing corticosteroid resistant elevation of cytokines despite smoking cessation. Several plasma cytokines were lower in smokers wi&lt;/p&gt; &lt;p&gt;Conclusion: Cigarette smoking in asthma is associated with a corticosteroid insensitive increase in multiple airway cytokines. Distinct airway cytokine profiles are present in current smokers and never smokers with asthma and could provide an explanatory mechanism for the altered clinical behavior observed in smokers with asthma.&lt;/p&gt

Canvass: a crowd-sourced, natural-product screening library for exploring biological space

NCATS thanks Dingyin Tao for assistance with compound characterization. This research was supported by the Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH). R.B.A. acknowledges support from NSF (CHE-1665145) and NIH (GM126221). M.K.B. acknowledges support from NIH (5R01GM110131). N.Z.B. thanks support from NIGMS, NIH (R01GM114061). J.K.C. acknowledges support from NSF (CHE-1665331). J.C. acknowledges support from the Fogarty International Center, NIH (TW009872). P.A.C. acknowledges support from the National Cancer Institute (NCI), NIH (R01 CA158275), and the NIH/National Institute of Aging (P01 AG012411). N.K.G. acknowledges support from NSF (CHE-1464898). B.C.G. thanks the support of NSF (RUI: 213569), the Camille and Henry Dreyfus Foundation, and the Arnold and Mabel Beckman Foundation. C.C.H. thanks the start-up funds from the Scripps Institution of Oceanography for support. J.N.J. acknowledges support from NIH (GM 063557, GM 084333). A.D.K. thanks the support from NCI, NIH (P01CA125066). D.G.I.K. acknowledges support from the National Center for Complementary and Integrative Health (1 R01 AT008088) and the Fogarty International Center, NIH (U01 TW00313), and gratefully acknowledges courtesies extended by the Government of Madagascar (Ministere des Eaux et Forets). O.K. thanks NIH (R01GM071779) for financial support. T.J.M. acknowledges support from NIH (GM116952). S.M. acknowledges support from NIH (DA045884-01, DA046487-01, AA026949-01), the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program (W81XWH-17-1-0256), and NCI, NIH, through a Cancer Center Support Grant (P30 CA008748). K.N.M. thanks the California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board for support. B.T.M. thanks Michael Mullowney for his contribution in the isolation, elucidation, and submission of the compounds in this work. P.N. acknowledges support from NIH (R01 GM111476). L.E.O. acknowledges support from NIH (R01-HL25854, R01-GM30859, R0-1-NS-12389). L.E.B., J.K.S., and J.A.P. thank the NIH (R35 GM-118173, R24 GM-111625) for research support. F.R. thanks the American Lebanese Syrian Associated Charities (ALSAC) for financial support. I.S. thanks the University of Oklahoma Startup funds for support. J.T.S. acknowledges support from ACS PRF (53767-ND1) and NSF (CHE-1414298), and thanks Drs. Kellan N. Lamb and Michael J. Di Maso for their synthetic contribution. B.S. acknowledges support from NIH (CA78747, CA106150, GM114353, GM115575). W.S. acknowledges support from NIGMS, NIH (R15GM116032, P30 GM103450), and thanks the University of Arkansas for startup funds and the Arkansas Biosciences Institute (ABI) for seed money. C.R.J.S. acknowledges support from NIH (R01GM121656). D.S.T. thanks the support of NIH (T32 CA062948-Gudas) and PhRMA Foundation to A.L.V., NIH (P41 GM076267) to D.S.T., and CCSG NIH (P30 CA008748) to C.B. Thompson. R.E.T. acknowledges support from NIGMS, NIH (GM129465). R.J.T. thanks the American Cancer Society (RSG-12-253-01-CDD) and NSF (CHE1361173) for support. D.A.V. thanks the Camille and Henry Dreyfus Foundation, the National Science Foundation (CHE-0353662, CHE-1005253, and CHE-1725142), the Beckman Foundation, the Sherman Fairchild Foundation, the John Stauffer Charitable Trust, and the Christian Scholars Foundation for support. J.W. acknowledges support from the American Cancer Society through the Research Scholar Grant (RSG-13-011-01-CDD). W.M.W.acknowledges support from NIGMS, NIH (GM119426), and NSF (CHE1755698). A.Z. acknowledges support from NSF (CHE-1463819). (Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH); CHE-1665145 - NSF; CHE-1665331 - NSF; CHE-1464898 - NSF; RUI: 213569 - NSF; CHE-1414298 - NSF; CHE1361173 - NSF; CHE1755698 - NSF; CHE-1463819 - NSF; GM126221 - NIH; 5R01GM110131 - NIH; GM 063557 - NIH; GM 084333 - NIH; R01GM071779 - NIH; GM116952 - NIH; DA045884-01 - NIH; DA046487-01 - NIH; AA026949-01 - NIH; R01 GM111476 - NIH; R01-HL25854 - NIH; R01-GM30859 - NIH; R0-1-NS-12389 - NIH; R35 GM-118173 - NIH; R24 GM-111625 - NIH; CA78747 - NIH; CA106150 - NIH; GM114353 - NIH; GM115575 - NIH; R01GM121656 - NIH; T32 CA062948-Gudas - NIH; P41 GM076267 - NIH; R01GM114061 - NIGMS, NIH; R15GM116032 - NIGMS, NIH; P30 GM103450 - NIGMS, NIH; GM129465 - NIGMS, NIH; GM119426 - NIGMS, NIH; TW009872 - Fogarty International Center, NIH; U01 TW00313 - Fogarty International Center, NIH; R01 CA158275 - National Cancer Institute (NCI), NIH; P01 AG012411 - NIH/National Institute of Aging; Camille and Henry Dreyfus Foundation; Arnold and Mabel Beckman Foundation; Scripps Institution of Oceanography; P01CA125066 - NCI, NIH; 1 R01 AT008088 - National Center for Complementary and Integrative Health; W81XWH-17-1-0256 - Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program; P30 CA008748 - NCI, NIH, through a Cancer Center Support Grant; California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board; American Lebanese Syrian Associated Charities (ALSAC); University of Oklahoma Startup funds; 53767-ND1 - ACS PRF; PhRMA Foundation; P30 CA008748 - CCSG NIH; RSG-12-253-01-CDD - American Cancer Society; RSG-13-011-01-CDD - American Cancer Society; CHE-0353662 - National Science Foundation; CHE-1005253 - National Science Foundation; CHE-1725142 - National Science Foundation; Beckman Foundation; Sherman Fairchild Foundation; John Stauffer Charitable Trust; Christian Scholars Foundation)Published versionSupporting documentatio

Individual common variants exert weak effects on the risk for autism spectrum disorders.

While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm&lt; 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest

Framing research on school principals' identities

This paper provides a basis for a tentative framework for guiding future research into principals’ identity construction and development. It is situated in the context of persisting emphases placed by government policies on the need for technocratic competencies in principals as a means of demonstrating success defined largely as compliance with demands for the improvement in student test scores. Often this emphasis is at the expense of forwarding a broader view of the need, alongside these, for clear educational values, beliefs and practices that are associated with these. The framework is informed by the theoretical work of Wenger and Bourdieu as well as recent empirical research on the part played by professional identity and emotions in school leadership. In the paper, we highlight different lines of inquiry and the issues they raise for researchers. We argue that the constructions of school leadership identities are located in time, space and place, and emotions reflect complex leadership identities situated within social hierarchies which are part of wider structures and social relations of power and control