209 research outputs found

    End Calorimeter Warm Tube Heater

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    The Tevatron accelerator beam tube must pass through the End Calorimeter cryostats of the D-Zero Collider Detector. Furthermore, the End Calorimeter cryostats must be allowed to roll back forty inches without interruption of the vacuum system; hence, the Tev tube must slide through the End Calorimeter cryostat as it is rolled back. The Tev pass through the End Calorimeter can actually be thought of as a cluster of concentric tubes: Tev tube, warm (vacuum vessel) tube, IS layers of superinsulation, cold tube (argon vessel), and Inner Hadronic center support tube. M. Foley generated an ANSYS model to study the heat load. to the cryostat. during collider physics studies; that is, without operation of the heater. A sketch of the model is included in the appendix. The vacuum space and superinsulation was modeled as a thermal solid, with conductivity derived from tests performed at Fermilab. An additional estimate was done. by this author, using data supplied by NR-2. a superinsulation manufacturer. The ANSYS result and hand calculation are in close agreement. The ANSYS model was modified. by this author. to incorporate the effect of the heater. Whereas the earlier model studied steady state operation only. the revised model considers the heater-off steady state mode as the initial condition. then performs a transient analysis with a final load step for time tending towards infinity. Results show the thermal gradient as a function of time and applied voltage. It should be noted that M. Foley's model was generated for one half the warm tube. implying the tube to be symmetric. In reality. the downstream connection (relative to the collision point) attachment to the vacuum shell is via several convolutions of a 0.020-inch wall bellows; hence. a nearly adiabatic boundary condition. Accordingly. the results reported in the table reflect extrapolation of the curves to the downstream end of the tube. Using results from the ANSYS analysis, that is, tube temperature and corresponding heat flux, temperature of the nichrome wire can be estimated. The possibility of frost is of genuine concern, as evidenced by the 250 K minimum temperature for the warm tube while heaters are not operating. Noting that steady state operation at 1 Amp (40 volts) allows the nichrome wire to stay below the critical temperature for Kapton, a conservative plan is to allow several days of heater operation, at 1 Amp (40 volts), before roll-back. Warm-up can be accelerated by operating the heaters in excess of 1 Amp, as evidenced by the test where a maximum of 3.2 Amp was supplied. Operating the heaters in excess of 1 Amp must be done with care since a rapid rise in temperature will likely occur once any ice present has been melted

    D0-EC RTD Wiring Layout (North Calorimeter)

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    The temperature of the North End-Calorimeter of the D-Zero detector is to be monitored by several RTD temperature sensors. The location and other important information pertaining to each individual RTD is included in the following tables, which are grouped by bundle number. There are mne 60 pIll port connectors. Each connector corresponds to a bundle of twisted pairs. Twisted pairs, of one of eight colors along with either a black or white wire, run to 10-pin connectors which have a mate on the module or cryostat wall. In general, all 60 pins, or all 10 pins are not used. The color scheme of the wires was designed so that all the twisted pairs with white run West from the instrumentation port, and twisted pairs with black run East. This scheme proved to be very successful and efficient during the installation process. After being installed, every RTD connection was checked and their corresponding resistances were recorded by Jerry Blazey. All the RTD's tested successfully, except for 2. The 2 dead RTD's were: Channel 17 on bundle 4, which is located on the front of MH module 8L; and Channel 13 on bundle 5, which is located on the Bottom of the Middle Coarse Plate of the IH

    Methodology for environmental assessment of agri-environment schemes: the Agri Environmental Footprint Index

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    End of project reportAgri-environment schemes pay farmers for the provision of environmental services. Such schemes tend to have multiple measures that deliver multiple environmental objectives, and there is a lack of consistent methodology with which to measure the environmental benefits of such schemes. Funded by EU FP6, the Agri-Environment Footprint project (www.footprint.rdg.ac.uk) aimed to address this challenge, and this report provides results from selected components of the project.European Unio

    Propagation and dispersion of electrostatic waves in the ionospheric E region

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    Crit II Electric, Magnetic, and Density Measurements Within an Ionizing Neutral Stream

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    Measurements from rocket borne sensors inside a high velocity neutral barium beam show a factor of six increasei n plasmad ensityi n a movingi onizingf ront. This region-wacso -locatedw ith intensef luctuatinge lectric fields( $E • 300m V/m) at frequenciewse llu ndert he lower hybrid frequency for a barium plasina. Large quasi-DC electric and magnetic field fluctuations were also detected with a large componento f the current and the electricf ield. parallelt o Bo. An Alfv6n wavew ith a finite electricf ield componentp arallel to the geomagneticfi eld was observed to propagatea longB o, wherei t wasd etectedb y ami nstrumented sub-payload

    Comparative analysis of discrete exosome fractions obtained by differential centrifugation

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    Background: Cells release a mixture of extracellular vesicles, amongst these exosomes, that differ in size, density and composition. The standard isolation method for exosomes is centrifugation of fluid samples, typically at 100,000×g or above. Knowledge of the effect of discrete ultracentrifugation speeds on the purification from different cell types, however, is limited. Methods: We examined the effect of applying differential centrifugation g-forces ranging from 33,000×g to 200,000×g on exosome yield and purity, using 2 unrelated human cell lines, embryonic kidney HEK293 cells and bladder carcinoma FL3 cells. The fractions were evaluated by nanoparticle tracking analysis (NTA), total protein quantification and immunoblotting for CD81, TSG101, syntenin, VDAC1 and calreticulin. Results: NTA revealed the lowest background particle count in Dulbecco's Modified Eagle's Medium media devoid of phenol red and cleared by 200,000×g overnight centrifugation. The centrifugation tube fill level impacted the sedimentation efficacy. Comparative analysis by NTA, protein quantification, and detection of exosomal and contamination markers identified differences in vesicle size, concentration and composition of the obtained fractions. In addition, HEK293 and FL3 vesicles displayed marked differences in sedimentation characteristics. Exosomes were pelleted already at 33,000×g, a g-force which also removed most contaminating microsomes. Optimal vesicle-to-protein yield was obtained at 67,000×g for HEK293 cells but 100,000×g for FL3 cells. Relative expression of exosomal markers (TSG101, CD81, syntenin) suggested presence of exosome subpopulations with variable sedimentation characteristics. Conclusions: Specific g-force/k factor usage during differential centrifugation greatly influences the purity and yield of exosomes. The vesicle sedimentation profile differed between the 2 cell lines

    Microsatellite alteration and immunohistochemical expression profile of chromosome 9p21 in patients with sporadic renal cell carcinoma following surgical resection.

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    BACKGROUND: Long-term prognostic significance of loss of heterozygosity on chromosome 9p21 for localized renal cell carcinoma following surgery remains unreported. The study assessed the frequency of deletions of different loci of chromosome 9p along with immunohistochemical profile of proteins in surgically resected renal cancer tissue and correlated this with long-term outcomes. METHODS: DNA was extracted from renal tumours and corresponding normal kidney tissues in prospectively collected samples of 108 patients who underwent surgical resection for clinically localized disease between January 2001 and December 2005, providing a minimum of 9 years follow-up for each participant. After checking quality of DNA, amplified by PCR, loss of heterozygosity (LOH) on chromosome 9p was assessed using 6 microsatellite markers in 77 clear cell carcinoma. Only 5 of the markers showed LOH (D9S1814, D9S916, D9S974, D9S942, and D9S171). Protein expression of p15(INK4b), p16(INK4a), p14(ARF), CAIX, and adipose related protein (ADFP) were demonstrated by immunostaining in normal and cancer tissues. Loss of heterozygosity for microsatellite analysis was correlated with tumour characteristics, recurrence free, cancer specific, and overall survival, including significance of immunohistochemical profile of protein expressions. RESULTS: The main deletion was found at loci telomeric to CDKN2A region at D9S916. There was a significant correlation between frequency of LOH stage (p = 0.005) and metastases (p = 0.006) suggesting a higher LOH for advanced and aggressive renal cell carcinoma. Most commonly observed LOH in the 3 markers: D9S916, D9S974, and D9S942 were associated with poor survival, and were statistically significant on multivariate analysis. Immunohistochemical expression of p14, p15, and p16 proteins were either low or absent in cancer tissue compared to normal. CONCLUSIONS: Loss of heterozygosity of p921 chromosome is associated with aggressive tumours, and predicts cancer specific or recurrence free survival on long-term follow-up. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12885-016-2514-8) contains supplementary material, which is available to authorized users

    Mutations in the WTX - gene are found in some high-grade microsatellite instable (MSI-H) colorectal cancers

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    Background: Genetically, colorectal cancers (CRCs) can be subdivided into tumors with chromosomal instability (CIN) or microsatellite instability (MSI). In both types of CRCs genes that are involved in the degradation of beta-CATENIN are frequently mutated. Whereas in CIN CRCs APC (Adenomatous Polyposis Coli) is affected in most cases, high grade MSI (MSI-H) CRCs frequently display mutations in various genes, like the APC-, AXIN2- or CTNNBI (beta-CATENIN) gene itself. Recently in Wilms tumors, WTX (Wilms tumor gene on the X-chromosome) was discovered as another gene involved in the destruction of beta-CATENIN. As the WTX-gene harbors a short T(6)-microsatellite in its N-terminal coding region, we hypothesized that frameshift-mutations might occur in MSI-H CRCs in the WTX gene, thus additionally contributing to the stabilization of beta-CATENIN in human CRCs. Methods: DNA was extracted from 632 formalin-fixed, paraffin-embedded metastatic CRCs (UICCIV) and analyzed for MSI-H by investigating the stability of the highly sensitive microsatellite markers BAT25 and BAT26 applying fluorescence capillary electrophoresis (FCE). Then, in the MSI-H cases, well described mutational hot spot regions from the APC-, AXIN2- and CTNNBI genes were analyzed for genomic alterations by didesoxy-sequencing while the WTX T(6)-microsatellite was analyzed by fragment analysis. Additionally, the PCR products of T(5)-repeats were subcloned and mutations were validated using didesoxy-sequencing. Furthermore, the KRAS and the BRAF proto-oncogenes were analyzed for the most common activating mutations applying pyro-sequencing. mRNA expression of WTX from MSI-H and MSS cases and a panel of colorectal cancer cell lines was investigated using reverse transcription (RT-) PCR and FCE. Results: In our cohort of 632 metastatic CRCs (UICCIV) we identified 41 MSI-H cases (6.5%). Two of the 41 MSI-H cases (4.8%) displayed a frameshift mutation in the T(6)-repeat resulting in a T(5) sequence. Only one case, a male patient, expressed the mutated WTX gene while being wild type for all other investigated genes. Conclusion: Mutations in the WTX-gene might compromise the function of the beta-CATENIN destruction complex in only a small fraction of MSI-H CRCs thus contributing to the process of carcinogenesis
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