3,087 research outputs found

    Cape Romain and the Charleston Bump: Historical and Recent Hydrographic Observations

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    A review and analysis of historical and new hydrographic data are presented for the Charleston Bump region. An area of doming isotherms is identified primarily between 31.5° and 34.5°N and the 200 and 400 m isobaths. The highest incidences of doming are found off Long Bay (86%), Cape Fear (38%), and Cape Romain (25%). Evidence suggests that low salinity shelf water collects in the doming area off Long Bay in July and that seasonal fluctuations in the depth of the main thermocline layer in this area are linked to Gulf Stream transport and local winds. At times there is a gradual offshore‐onshore movement of the Gulf Stream opposite Long Bay roughly following the 400 m isobath and at other times an abrupt eastward movement near 32°N. Much of the time there appears to be a direct seasonal relationship between historical seasonal velocity fields and offshore deflection with higher (lower) velocities corresponding to greater (lesser) deflection

    Ocean Chlorophyll Studies from a U-2 Aircraft Platform

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    Chlorophyll gradient maps of large ocean areas were generated from U-2 ocean color scanner data obtained over test sites in the Pacific and Atlantic Oceans. The delineation of oceanic features using the upward radiant intensity relies on an analysis method which presupposes that radiation backscattered from the atmosphere and ocean surface can be properly modeled using a measurement made at 778 nm. An estimation of the chlorophyll concentration was performed by properly ratioing radiances measured at 472 nm and 548 nm after removing the atmospheric effects. The correlation between the remotely sensed data and in-situ surface chlorophyll measurements was validated in two sets of data. The results show that the correlation between the in-situ measured chlorophyll and the derived quantity is a negative exponential function and the correlation coefficient was calculated to be -0.965

    Developmental and tissue-specific expression of NITRs

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    Novel immune-type receptors (NITRs) are encoded by large multi-gene families and share structural and signaling similarities to mammalian natural killer receptors (NKRs). NITRs have been identified in multiple bony fish species, including zebrafish, and may be restricted to this large taxonomic group. Thirty-nine NITR genes that can be classified into 14 families are encoded on zebrafish chromosomes 7 and 14. Herein, we demonstrate the expression of multiple NITR genes in the zebrafish ovary and during embryogenesis. All 14 families of zebrafish NITRs are expressed in hematopoietic kidney, spleen and intestine as are immunoglobulin and T cell antigen receptors. Furthermore, all 14 families of NITRs are shown to be expressed in the lymphocyte lineage, but not in the myeloid lineage, consistent with the hypothesis that NITRs function as NKRs. Sequence analyses of NITR amplicons identify known alleles and reveal additional alleles within the nitr1, nitr2, nitr3, and nitr5 families, reflecting the recent evolution of this gene family

    Yolk sac erythromyeloid progenitors expressing gain of function PTPN11 have functional features of JMML but are not sufficient to cause disease in mice

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    Background: Accumulating evidence suggests the origin of juvenile myelomonocytic leukemia (JMML) is closely associated with fetal development. Nevertheless, the contribution of embryonic progenitors to JMML pathogenesis remains unexplored. We hypothesized that expression of JMML-initiating PTPN11 mutations in HSC-independent yolk sac erythromyeloid progenitors (YS EMPs) would result in a mouse model of pediatric myeloproliferative neoplasm (MPN). Results: E9.5 YS EMPs from VavCre+;PTPN11D61Y embryos demonstrated growth hypersensitivity to granulocyte-macrophage colony-stimulating factor (GM-CSF) and hyperactive RAS-ERK signaling. Mutant EMPs engrafted the spleens of neonatal recipients, but did not cause disease. To assess MPN development during unperturbed hematopoiesis we generated CSF1R-MCM+;PTPN11E76K;ROSAYFP mice in which oncogene expression was restricted to EMPs. Yellow fluorescent protein-positive progeny of mutant EMPs persisted in tissues one year after birth and demonstrated hyperactive RAS-ERK signaling. Nevertheless, these mice had normal survival and did not demonstrate features of MPN. Conclusions: YS EMPs expressing mutant PTPN11 demonstrate functional and molecular features of JMML but do not cause disease following transplantation nor following unperturbed development

    3D integrated superconducting qubits

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    As the field of superconducting quantum computing advances from the few-qubit stage to larger-scale processors, qubit addressability and extensibility will necessitate the use of 3D integration and packaging. While 3D integration is well-developed for commercial electronics, relatively little work has been performed to determine its compatibility with high-coherence solid-state qubits. Of particular concern, qubit coherence times can be suppressed by the requisite processing steps and close proximity of another chip. In this work, we use a flip-chip process to bond a chip with superconducting flux qubits to another chip containing structures for qubit readout and control. We demonstrate that high qubit coherence (T1T_1, T2,echo>20μT_{2,\rm{echo}} > 20\,\mus) is maintained in a flip-chip geometry in the presence of galvanic, capacitive, and inductive coupling between the chips

    Distinguishing coherent and thermal photon noise in a circuit QED system

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    In the cavity-QED architecture, photon number fluctuations from residual cavity photons cause qubit dephasing due to the AC Stark effect. These unwanted photons originate from a variety of sources, such as thermal radiation, leftover measurement photons, and crosstalk. Using a capacitively-shunted flux qubit coupled to a transmission line cavity, we demonstrate a method that identifies and distinguishes coherent and thermal photons based on noise-spectral reconstruction from time-domain spin-locking relaxometry. Using these measurements, we attribute the limiting dephasing source in our system to thermal photons, rather than coherent photons. By improving the cryogenic attenuation on lines leading to the cavity, we successfully suppress residual thermal photons and achieve T1T_1-limited spin-echo decay time. The spin-locking noise spectroscopy technique can readily be applied to other qubit modalities for identifying general asymmetric non-classical noise spectra

    Hematopoietic-restricted Ptpn11E76K reveals indolent MPN progression in mice

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    Juvenile Myelomonocytic Leukemia (JMML) is a pediatric myeloproliferative neoplasm (MPN) that has a poor prognosis. Somatic mutations in Ptpn11 are the most frequent cause of JMML and they commonly occur in utero. Animal models of mutant Ptpn11 have probed the signaling pathways that contribute to JMML. However, existing models may inappropriately exacerbate MPN features by relying on non-hematopoietic-restricted Cre-loxP strains or transplantations into irradiated recipients. In this study we generate hematopoietic-restricted models of Ptpn11E76K-mediated disease using Csf1r-MCM and Flt3Cre. We show that these animals have indolent MPN progression despite robust GM-CSF hypersensitivity and Ras-Erk hyperactivation. Rather, the dominant pathology is pronounced thrombocytopenia with expanded extramedullary hematopoiesis. Furthermore, we demonstrate that the timing of tamoxifen administration in Csf1r-MCM mice can specifically induce recombinase activity in either fetal or adult hematopoietic progenitors. We take advantage of this technique to show more rapid monocytosis following Ptpn11E76K expression in fetal progenitors compared with adult progenitors. Finally, we demonstrate that Ptpn11E76K results in the progressive reduction of T cells, most notably of CD4+ and naïve T cells. This corresponds to an increased frequency of T cell progenitors in the thymus and may help explain the occasional emergence of T-cell leukemias in JMML patients. Overall, our study is the first to describe the consequences of hematopoietic-restricted Ptpn11E76K expression in the absence of irradiation. Our techniques can be readily adapted by other researchers studying somatically-acquired blood disorders
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