2,643 research outputs found

    Fellows as teachers: a model to enhance pediatric resident education

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    Pressures on academic faculty to perform beyond their role as educators has stimulated interest in complementary approaches in resident medical education. While fellows are often believed to detract from resident learning and experience, we describe our preliminary investigations utilizing clinical fellows as a positive force in pediatric resident education. Our objectives were to implement a practical approach to engage fellows in resident education, evaluate the impact of a fellow-led education program on pediatric resident and fellow experience, and investigate if growth of a fellowship program detracts from resident procedural experience.This study was conducted in a neonatal intensive care unit (NICU) where fellows designed and implemented an education program consisting of daily didactic teaching sessions before morning clinical rounds. The impact of a fellow-led education program on resident satisfaction with their NICU experience was assessed via anonymous student evaluations. The potential value of the program for participating fellows was also evaluated using an anonymous survey.The online evaluation was completed by 105 residents. Scores were markedly higher after the program was implemented in areas of teaching excellence (4.44 out of 5 versus 4.67, p<0.05) and overall resident learning (3.60 out of 5 versus 4.61, p<0.001). Fellows rated the acquisition of teaching skills and enhanced knowledge of neonatal pathophysiology as the most valuable aspects of their participation in the education program. The anonymous survey revealed that 87.5% of participating residents believed that NICU fellows were very important to their overall training and education.While fellows are often believed to be a detracting factor to residency training, we found that pediatric resident attitudes toward the fellows were generally positive. In our experience, in the specialty of neonatology a fellow-led education program can positively contribute to both resident and fellow learning and satisfaction. Further investigation into the value of utilizing fellows as a positive force in resident education in other medical specialties appears warranted

    Incorporation of albumin fusion proteins into fibrin clots in vitro and in vivo: comparison of different fusion motifs recognized by factor XIIIa

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    <p>Abstract</p> <p>Background</p> <p>The transglutaminase activated factor XIII (FXIIIa) acts to strengthen pathological fibrin clots and to slow their dissolution, in part by crosslinking active α<sub>2</sub>-antiplasmin (α<sub>2</sub>AP) to fibrin. We previously reported that a yeast-derived recombinant fusion protein comprising α<sub>2</sub>AP residues 13-42 linked to human serum albumin (HSA) weakened <it>in vitro </it>clots but failed to become specifically incorporated into <it>in vivo </it>clots. In this study, our aims were to improve both the stability and clot localization of the HSA fusion protein by replacing α<sub>2</sub>AP residues 13-42 with shorter sequences recognized more effectively by FXIIIa.</p> <p>Results</p> <p>Expression plasmids were prepared encoding recombinant HSA with the following N-terminal 23 residue extensions: H<sub>6</sub>NQEQVSPLTLLAG<sub>4</sub>Y (designated XL1); H<sub>6</sub>DQMMLPWAVTLG<sub>4</sub>Y (XL2); H<sub>6</sub>WQHKIDLPYNGAG<sub>4</sub>Y (XL3); and their 17 residue non-His-tagged equivalents (XL4, XL5, and XL6). The HSA moiety of XL4- to XL6-HSA proteins was C-terminally His-tagged. All chimerae were efficiently secreted from transformed <it>Pichia pastoris </it>yeast except XL3-HSA, and following nickel chelate affinity purification were found to be intact by amino acid sequencing, as was an N-terminally His-tagged version of α<sub>2</sub>AP(13-42)-HSA. Of the proteins tested, XL5-HSA was cross-linked to biotin pentylamine (BPA) most rapidly by FXIIIa, and was the most effective competitor of α<sub>2</sub>AP crosslinking not only to BPA but also to plasma fibrin clots. In the mouse ferric chloride <it>vena cava </it>thrombosis model, radiolabeled XL5-HSA was retained in the clot to a greater extent than recombinant HSA. In the rabbit jugular vein stasis thrombosis model, XL5-HSA was also retained in the clot, in a urea-insensitive manner indicative of crosslinking to fibrin, to a greater extent than recombinant HSA.</p> <p>Conclusions</p> <p>Fusion protein XL5-HSA (DQMMLPWAVTLG<sub>4</sub>Y-HSAH<sub>6</sub>) was found to be more active as a substrate for FXIIIa-mediated transamidation than seven other candidate fusion proteins <it>in vitro</it>. The improved stability and reactivity of this chimeric protein was further evidenced by its incorporation into <it>in vivo </it>clots formed in thrombosis models in both mice and rabbits.</p

    Galactic and Extragalactic Samples of Supernova Remnants: How They Are Identified and What They Tell Us

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    Supernova remnants (SNRs) arise from the interaction between the ejecta of a supernova (SN) explosion and the surrounding circumstellar and interstellar medium. Some SNRs, mostly nearby SNRs, can be studied in great detail. However, to understand SNRs as a whole, large samples of SNRs must be assembled and studied. Here, we describe the radio, optical, and X-ray techniques which have been used to identify and characterize almost 300 Galactic SNRs and more than 1200 extragalactic SNRs. We then discuss which types of SNRs are being found and which are not. We examine the degree to which the luminosity functions, surface-brightness distributions and multi-wavelength comparisons of the samples can be interpreted to determine the class properties of SNRs and describe efforts to establish the type of SN explosion associated with a SNR. We conclude that in order to better understand the class properties of SNRs, it is more important to study (and obtain additional data on) the SNRs in galaxies with extant samples at multiple wavelength bands than it is to obtain samples of SNRs in other galaxiesComment: Final 2016 draft of a chapter in "Handbook of Supernovae" edited by Athem W. Alsabti and Paul Murdin. Final version available at https://doi.org/10.1007/978-3-319-20794-0_90-

    Three geographically separate domestications of Asian rice

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    Domesticated rice (Oryza sativa L.) accompanied the dawn of Asian civilization(1) and has become one of world's staple crops. From archaeological and genetic evidence various contradictory scenarios for the origin of different varieties of cultivated rice have been proposed, the most recent based on a single domestication(2,3). By examining the footprints of selection in the genomes of different cultivated rice types, we show that there were three independent domestications in different parts of Asia. We identify wild populations in southern China and the Yangtze valley as the source of the japonica gene pool, and populations in Indochina and the Brahmaputra valley as the source of the indica gene pool. We reveal a hitherto unrecognized origin for the aus variety in central India or Bangladesh. We also conclude that aromatic rice is a result of a hybridization between japonica and aus, and that the tropical and temperate versions of japonica are later adaptations of one crop. Our conclusions are in accord with archaeological evidence that suggests widespread origins of rice cultivation(1,4). We therefore anticipate that our results will stimulate a more productive collaboration between genetic and archaeological studies of rice domestication, and guide utilization of genetic resources in breeding programmes aimed at crop improvement.European Research Council [339941]info:eu-repo/semantics/publishedVersio

    Performance Analysis of Dual-Hop MIMO AF Relaying Network with Multiple Interferences

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    In this paper, we investigate the performance of a dual-hop multiple-input-multiple-output (MIMO) amplify-and-forward (AF) relay network, where the source, relay, and destination are all equipped with multiple antennas. By using maximum ratio transmission (MRT) at the transmitter and maximum ratio combining (MRC) at the receiver, we first obtain the output signal-to-interference-plus-noise ratio (SINR) of the dual-hop AF relay system, considering multiple cochannel interferences (CCIs), as well as noise at the relay. Then, we derive an exact closed-form expression for the outage probability (OP), and the asymptotic result of OP at high SNR, which can be used to calculate the array gain and diversity order. Finally, computer simulations are conducted to validate the performance analysis. Our new analytical expressions not only provide a fast and efficient method to evaluate the system performance but enable us to gain valuable insights into the effects of key parameters on the MIMO AF relaying network performance that benefits from implementing multiple antennas at each of the three nodes as well

    Cyclooxygenase-2 Induction by Arsenite through the IKKβ/NFκB Pathway Exerts an Antiapoptotic Effect in Mouse Epidermal Cl41 cells

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    BACKGROUND: Arsenic contamination has become a major public health concern worldwide. Epidemiologic data show that long-term arsenic exposure results in the risk of skin cancer. However, the mechanisms underlying carcinogenic effects of arsenite on skin remain to be studied. OBJECTIVES: In the present study we evaluated cyclooxygenase-2 (COX-2) expression, the signaling pathways leading to COX-2 induction, and its antiapoptotic function in the response to arsenite exposure in mouse epidermal JB6 Cl41 cells. METHODS: We used the luciferase reporter assay and Western blots to determine COX-2 induction by arsenite. We utilized dominant negative mutant, genetic knockout, gene knockdown, and gene overexpression approaches to elucidate the signaling pathway involved in COX-2 induction and its protective effect on cell apoptosis. RESULTS: The induction of COX-2 by arsenite was inhibited in Cl41 cells transfected with IKKβ-KM, a dominant mutant inhibitor of kβ (Ikβ) kinase (IKKβ), and in IKKβ-knockout (IKKβ(−/−)) mouse embryonic fibroblasts (MEFs). IKKβ/nuclear factor κB (NFκB) pathway-mediated COX-2 induction exerted an antiapoptotic effect on the cells exposed to arsenite because cell apoptosis was significantly enhanced in the Cl41 cells transfected with IKKβ-KM or COX-2 small interference RNA (siCOX-2). In addition, IKKβ(−/−) MEFs stably transfected with COX-2 showed more resistance to arsenite-induced apoptosis compared with the same control vector–transfected cells. CONCLUSIONS: These results demonstrate that arsenite exposure can induce COX-2 expression through the IKKβ/NFκB pathway, which thereby exerts an antiapoptotic effect in response to arsenite. In light of the importance of apoptosis evasion during carcinogenesis, we anticipate that COX-2 induction may be at least partially responsible for the carcinogenic effect of arsenite on skin
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