Randomized trial of use of incentive to increase the response rate to a mailed survey

Author name used in this publication: Tong M. F. ChanAuthor name used in this publication: Sonny H. M. TseAuthor name used in this publication: Mary C. DayAuthor name used in this publication: Edmond T. F. TongAuthor name used in this publication: Lorna K. P. Suen2003-2004 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Airborne measurements of western U.S. wildfire emissions: Comparison with prescribed burning and air quality implications

Wildfires emit significant amounts of pollutants that degrade air quality. Plumes from three wildfires in the western U.S. were measured from aircraft during the Studies of Emissions and Atmospheric Composition, Clouds and Climate Coupling by Regional Surveys (SEAC4RS) and the Biomass Burning Observation Project (BBOP), both in summer 2013. This study reports an extensive set of emission factors (EFs) for over 80 gases and 5 components of submicron particulate matter (PM1) from these temperate wildfires. These include rarely, or never before, measured oxygenated volatile organic compounds and multifunctional organic nitrates. The observed EFs are compared with previous measurements of temperate wildfires, boreal forest fires, and temperate prescribed fires. The wildfires emitted high amounts of PM1 (with organic aerosol (OA) dominating the mass) with an average EF that is more than 2 times the EFs for prescribed fires. The measured EFs were used to estimate the annual wildfire emissions of carbon monoxide, nitrogen oxides, total nonmethane organic compounds, and PM1 from 11 western U.S. states. The estimated gas emissions are generally comparable with the 2011 National Emissions Inventory (NEI). However, our PM1 emission estimate (1530 ± 570 Gg yr-1) is over 3 times that of the NEI PM2.5 estimate and is also higher thanthe PM2.5 emitted from all other sources in these states in the NEI. This study indicates that the source of OA from biomass burning in the western states is significantly underestimated. In addition, our results indicate that prescribed burning may be an effective method to reduce fine particle emissions

FMRFamide-Like Peptides (FLPs) Enhance Voltage-Gated Calcium Currents to Elicit Muscle Contraction in the Human Parasite Schistosoma mansoni

Schistosomes are amongst the most important and neglected pathogens in the world, and schistosomiasis control relies almost exclusively on a single drug. The neuromuscular system of schistosomes is fertile ground for therapeutic intervention, yet the details of physiological events involved in neuromuscular function remain largely unknown. Short amidated neuropeptides, FMRFamide-like peptides (FLPs), are distributed abundantly throughout the nervous system of every flatworm examined and they produce potent myoexcitation. Our goal here was to determine the mechanism by which FLPs elicit contractions of schistosome muscle fibers. Contraction studies showed that the FLP Tyr-Ile-Arg-Phe-amide (YIRFamide) contracts the muscle fibers through a mechanism that requires Ca2+ influx through sarcolemmal voltage operated Ca2+ channels (VOCCs), as the contractions are inhibited by classical VOCC blockers nicardipine, verapamil and methoxyverapamil. Whole-cell patch-clamp experiments revealed that inward currents through VOCCs are significantly and reversibly enhanced by the application of 1 µM YIRFamide; the sustained inward currents were increased to 190% of controls and the peak currents were increased to 180%. In order to examine the biochemical link between the FLP receptor and the VOCCs, PKC inhibitors calphostin C, RO 31–8220 and chelerythrine were tested and all produced concentration dependent block of the contractions elicited by 1 µM YIRFamide. Taken together, the data show that FLPs elicit contractions by enhancing Ca2+ influx through VOCC currents using a PKC-dependent pathway

DNA Methylation of the ABO Promoter Underlies Loss of ABO Allelic Expression in a Significant Proportion of Leukemic Patients

Background: Loss of A, B and H antigens from the red blood cells of patients with myeloid malignancies is a frequent occurrence. Previously, we have reported alterations in ABH antigens on the red blood cells of 55% of patients with myeloid malignancies. Methodology/Principal Findings: To determine the underlying molecular mechanisms of this loss, we assessed ABO allelic expression in 21 patients with ABH antigen loss previously identified by flow cytometric analysis as well as an additional 7 patients detected with ABH antigen changes by serology. When assessing ABO mRNA allelic expression, 6/12 (50%) patients with ABH antigen loss detected by flow cytometry and 5/7 (71%) of the patients with ABH antigen loss detected by serology had a corresponding ABO mRNA allelic loss of expression. We examined the ABO locus for copy number and DNA methylation alterations in 21 patients, 11 with loss of expression of one or both ABO alleles, and 10 patients with no detectable allelic loss of ABO mRNA expression. No loss of heterozygosity (LOH) at the ABO locus was observed in these patients. However in 8/11 (73%) patients with loss of ABO allelic expression, the ABO promoter was methylated compared with 2/10 (20%) of patients with no ABO allelic expression loss (P = 0.03). Conclusions/Significance: We have found that loss of ABH antigens in patients with hematological malignancies is associated with a corresponding loss of ABO allelic expression in a significant proportion of patients. Loss of ABO allelic expression was strongly associated with DNA methylation of the ABO promoter.Tina Bianco-Miotto, Damian J. Hussey, Tanya K. Day, Denise S. O'Keefe and Alexander Dobrovi

Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo

Tissue inhibitor of metalloproteinases-3 (TIMP-3) regulates extracellular matrix via its inhibition of matrix metalloproteinases and membrane-bound sheddases. Timp-3 is expressed at multiple sites of extensive tissue remodelling. This extends to bone where its role, however, remains largely unresolved. In this study, we have used Micro-CT to assess bone mass and architecture, histological and histochemical evaluation to characterise the skeletal phenotype of Timp-3 KO mice and have complemented this by also examining similar indices in mice harbouring a Timp-3 transgene driven via a Col-2a-driven promoter to specifically target overexpression to chondrocytes. Our data show that Timp-3 deficiency compromises tibial bone mass and structure in both cortical and trabecular compartments, with corresponding increases in osteoclasts. Transgenic overexpression also generates defects in tibial structure predominantly in the cortical bone along the entire shaft without significant increases in osteoclasts. These alterations in cortical mass significantly compromise predicted tibial load-bearing resistance to torsion in both genotypes. Neither Timp-3 KO nor transgenic mouse growth plates are significantly affected. The impact of Timp-3 deficiency and of transgenic overexpression extends to produce modification in craniofacial bones of both endochondral and intramembranous origins. These data indicate that the levels of Timp-3 are crucial in the attainment of functionally-appropriate bone mass and architecture and that this arises from chondrogenic and osteogenic lineages

Teachers' resilience: conceived, perceived or lived-in

[Extract] Schools in Western countries are places where work related conditions lead to teacher disaffection and attrition. To mitigate this employers and scholars advocate fostering teacher resilience. This chapter presents a critical examination of teacher resilience. Originally conceived as a personal trait, later research showed human resilience is an attribute that can be developed. Resilience is one’s ability to manage stressors and maintain adaptive functioning across all domains of life. Latterly, scholars investigated resilience in teachers, mainly through qualitative or quantitative self-report studies. This research constitutes perceived teacher resilience, because as formulated, teacher resilience is conceptually flawed, limited in scope, based on teachers’ functioning within their professional lives. We do not know what constitutes long serving teachers’ actual, lived-in resilience: what enables teachers to maintain their wellbeing and effectiveness in the classroom, reflecting human resilience as originally conceived. For an accurate profile of teacher resilience we must study those still teaching, and teachers who have exited the profession to determine why they left. Perhaps exiting the profession signals a resilient person who does accept working conditions that do not support wellbeing or teaching effectiveness. Perhaps ‘teacher resilience’ is inaccurately used in the context of teacher attrition and disaffection

Some Like It Fat: Comparative Ultrastructure of the Embryo in Two Demosponges of the Genus Mycale (Order Poecilosclerida) from Antarctica and the Caribbean

0000-0002-7993-1523© 2015 Riesgo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License [4.0], which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. The attached file is the published version of the article

Increased Dickkopf-1 expression in breast cancer bone metastases

The aim of this study was to determine whether Dickkopf-1 (Dkk-1) expression in breast cancer was associated with bone metastases. We first analysed Dkk-1 expression by human breast cancer cell lines that induce osteolytic or osteoblastic lesions in animals. Dickkopf-1 levels were then measured in the bone marrow aspirates of hind limbs from eight NMRI mice inoculated with breast cancer cells that induced bone metastases and 11 age-matched non-inoculated control animals. Finally, Dkk-1 was measured in the serum of 17 women with breast cancer in complete remission, 19 women with breast cancer and bone metastases, 16 women with breast cancer and metastases at non-bone sites and 16 healthy women. Only breast cancer cells that induce osteolytic lesions in animals produced Dkk-1. There was a six-fold increase in Dkk-1 levels in the bone marrow from animals inoculated with MDA-B02 cells when compared with that of control non-inoculated animals (P=0.003). Median Dkk-1 levels in the serum of patients with breast cancer and bone metastases were significantly higher than levels of patients in complete remission (P=0.016), patients with breast cancer having metastases at non-bone sites (P<0.0001) and healthy women (P=0.047), although there was a large overlap in individual levels between the different groups. In conclusion, Dkk-1 is secreted by osteolytic human breast cancer cells lines and increased circulating levels are associated with the presence of bone metastases in patients with breast cancer. Measurements of circulating Dkk-1 levels may be useful for the clinical investigation of patients with breast cancer and bone metastases