107,372 research outputs found
Robinsonia boliviana Seitz 1921
No full textRobinsonia boliviana Seitz, 1921 Type locality. [Bolivia, La Paz], Songo river. Type specimens. Undisclosed number of syntypes (unknown repository). Taxonomic references. Seitz (1921), Watson & Goodger (1986) and Vincent & Laguerre (2014). Material not examined. Brazil, Maranhão: Açailândia, 4°57'14.17"S / 47°30'11.08"W. Light traps, 19– 27.xi.1990, V.O. Becker legit (VOB) (Teston & Ferro 2016). Month records in Maranhão. November. Geographical records in Brazil. Amapá, Pará and Rondônia (Amazon).Published as part of Silva, Karoline M. O., Câmara, Joseleide T. & Teston, José A., 2023, An annotated catalogue of the Phaegopterina (Erebidae, Arctiinae, Arctiini) of state of Maranhão, Brazil, pp. 1-40 in Zootaxa 5285 (1) on page 28, DOI: 10.11646/zootaxa.5285.1.1, http://zenodo.org/record/793572
Beilage zum Jahresbericht des Elberfelder Gymnasiums / Schulbücher des Gymnasiums, welche zu den beigesetzten Preisen dauerhaft gebunden in neuesten Auflagen bei den unterzeichneten Firmen vorrätig sind : [Katalog der Schulbibliothek]
No full text[von Oberlehrer Friedrich Seitz]Erschienen: T. 1 -
Bertholdia detracta Seitz 1921
No full text<i>Bertholdia detracta</i> Seitz, 1921 <p> <b>Type locality</b>. Colombia, [Boyacá], Muzo.</p> <p> <b>Type specimens</b>. Undisclosed number of syntypes (NHMUK; one ♁ syntype labeled TYPE).</p> <p> <b>Taxonomic references</b>. Seitz (1921), Watson & Goodger (1986), Vincent & Laguerre (2014).</p> <p> <b>Material examined</b>. <b>Brazil</b>, <i>Maranhão</i>: Açailândia, 4°57'14.17"S / 47°30'11.08"W. Light traps, 19–27.xi.1990, V.O. Becker legit, 1 specimen (VOB).</p> <p> <b>Month records in Maranhão</b>. November.</p> <p> <b>Geographical records in Brazil</b>. Pará and Rondônia (Amazon).</p>Published as part of <i>Silva, Karoline M. O., Câmara, Joseleide T. & Teston, José A., 2023, An annotated catalogue of the Phaegopterina (Erebidae, Arctiinae, Arctiini) of state of Maranhão, Brazil, pp. 1-40 in Zootaxa 5285 (1)</i> on page 9, DOI: 10.11646/zootaxa.5285.1.1, <a href="http://zenodo.org/record/7935723">http://zenodo.org/record/7935723</a>
Computational Representation of Wigner-Seitz Cell
No full textWigner-Seitz cell, theprimitive cell in reciprocal space was constructed computationally by joining the perpendicular bisectors of the line between the concerned point and its nearest neighbours. First of all, arrays of lattice points were constructed and the mid-point was identified. Then all the nearest points of the mid-point were joined and then perpendicular bisectors were drawn. At the last step, all the bisected points were joined to its adjacent lattice to form a closed region encompassing the mid-point. The innermost region is called the Wigner-Seitz cell in direct lattice and Brillouin zone in reciprocal lattic
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Search for hadronic resonance in multijet final states with the CDF detector
No full textThis thesis describes a search for a new hadronic resonance in 3.2 fb{sup -1} of data using the Collider Detector at Fermilab. The Fermilab Tevatron accelerator collides beams of protons and antiprotons at a center of mass energy of {radical}s = 1.96 TeV. A unique approach is presented to extract multijet resonances from the large QCD background. Although the search is model independent, a pair produced supersymmetric gluino decaying through R-parity violation into three partons each is used to test our sensitivity to new physics. We measure these partons as jets, and require a minimum of six jets in an event. We make use of the kinematic features and correlations and use an ensemble of jet combinations to distinguish signal from multijet QCD backgrounds. Our background estimates also include all-hadronic t{bar t} decays that have a signature similar to signal. We observe no significant excess in an invariant mass range of 77 GeV/c{sup 2} to 240 GeV/c{sup 2} and place 95% C.L. limits on {sigma}(p{bar p} {yields} {tilde g}{tilde g} {yields} 3jets + 3jets) as a function of gluino invariant mass
Cluster analysis of flowcytometric immunophenotyping with extended T cell subsets in suspected immunodeficiency
No full textAbstract Background Patients with immunodeficiencies commonly experience diagnostic delays resulting in morbidity. There is an unmet need to identify patients earlier, especially those with high risk for complications. Compared to immunoglobulin quantification and flowcytometric B cell subset analysis, expanded T cell subset analysis is rarely performed in the initial evaluation of patients with suspected immunodeficiency. The simultaneous interpretation of multiple immune variables, including lymphocyte subsets, is challenging. Objective To evaluate the diagnostic value of cluster analyses of immune variables in patients with suspected immunodeficiency. Methods Retrospective analysis of 38 immune system variables, including seven B cell and sixteen T cell subpopulations, in 107 adult patients (73 with immunodeficiency, 34 without) evaluated at a tertiary outpatient immunology clinic. Correlation analyses of individual variables, k‐means cluster analysis with evaluation of the classification into “no immunodeficiency” versus “immunodeficiency” and visual analyses of hierarchical heatmaps were performed. Results Binary classification of patients into groups with and without immunodeficiency was correct in 54% of cases with the full data set and increased to 69% and 75% of cases, respectively, when only 16 variables with moderate (p < .05) or 7 variables with strong evidence (p < .01) for a difference between groups were included. In a cluster heatmap with all patients but only moderately differing variables and a heatmap with only immunodeficient patients restricted to T cell variables alone, segregation of most patients with common variable immunodeficiency and combined immunodeficiency was observed. Conclusion Cluster analyses of immune variables, including detailed lymphocyte flowcytometry with T cell subpopulations, may support clinical decision making for suspected immunodeficiency in daily practice
Lineage stability and effector function of CD4+FOXP3+ regulatory T cells
No full textThis work focuses on regulatory T (Treg) cell biology in the context of defining the role of forkhead box protein 3 (FOXP3) isoform expression and Treg mediated suppression via CTLA-4 (cytotoxic T-lymphocyte-associated protein 4). Treg cells are crucial in maintaining immunological tolerance and they in part act by suppressing dendritic cells (DCs). Previous studies have demonstrated that Treg cells express the co-inhibitory receptor CTLA-4, which is essential for Treg cells ability to control the expression of the costimulatory molecules CD80/CD86 on DCs. In study I we generated a novel mouse strain that exclusively expresses the naturally occurring ligand-independent CTLA-4 isoform (liCTLA-4) in Treg cells only. This isoform cannot control CD80/CD86 expression by direct binding to these molecules. One of the key findings in this study is that these Ctla4ex2fl/flFoxp3-Cre mice did not develop a lymphoproliferative phenotype early in life. When we extended our study, we saw that older Ctla4ex2fl/flFoxp3-Cre mice (6 months) developed an inflammatory phenotype in the lung. Interestingly, Ctla4ex2fl/flFoxp3-Cre mice had an increased number of Treg cells, in particular Treg cells lacking CD25 expression. The dramatic increase of Treg cells could potentially compensate for any functional impairment due to altered CTLA-4 expression. Thus, we isolated Treg cells for in vitro assays to further investigate Treg cell function using an DC suppression assay that we established. We found that Treg cells isolated from Ctla4ex2fl/flFoxp3-Cre were able to control CD80 and CD86 expression. However, Treg cells isolated from Ctla4ex2fl/flFoxp3-Cre failed to support upregulation of PD-L2 on suppressed DCs.The transcription factor FOXP3 is a key regulator for Treg cell differentiation and is required to maintain their suppressive phenotype. FOXP3 occurs as four distinct isoforms, full-length FOXP3 and isoforms lacking exon 2 and or exon 7. In study II we determined the FOXP3 isoform expression in plaques and blood from patients suffering from atherosclerotic disease. We found a positive correlation between FOXP3D2 splice variant expression and plaque stability in plaque tissue that was not apparent in blood. Another key finding from this study is that during Treg cell activation the overall upregulation of FOXP3 expression is mainly due to an increased expression of the isoform FOXP3D2. In study III and IV we reported on two patients with a novel frameshift mutation in the FOXP3 gene (NM_014009.3:c.305delT) located in exon 2 which results in a premature stop codon and consequently the loss of any isoforms expressing exon 2. Both patients had a very mild IPEX phenotype, which strongly suggests FOXP3D2 alone is able to at least partially maintain Treg cell development and function. Investigating the female carrier, we saw approximately 20% of the Treg pool had the c.305delT mutation not matching the expected 50% from random X-chromosome inactivation. RNA sequencing allowed us to identify a set of genes, several which previously have been demonstrated to regulate FOPX3 expression, that are specifically regulated by full-length FOXP3. This gene set may explain the loss of c.305delT Treg cells and we currently favor the view that they regulate the lineage stability of Treg cells.List of scientific papersI. Christina Seitz*, Sang Liu*, Katrin Klocke, Anne-Laure Joly, Paulo V Czarnewski, Christopher A Tibbitt, Sara M Parigi, Lisa S Westerberg, Jonathan M Coquet, Eduardo J Villablanca, Kajsa Wing, John Andersson. Multi-faceted inhibition of dendritic cell function by CD4+Foxp3+ regulatory T cells. Journal of Autoimmunity. 98:86-94, 2019. *Authors contributed equally. https://doi.org/ II. Anne-Laure Joly, Christina Seitz*, Sang Liu*, Nikolai V Kuznetsov, Karl Gertow, Lisa S Westerberg, Gabrielle Paulsson-Berne, Göran K Hansson, John Andersson. Alternative splicing of FOXP3 controls regulatory T cell effector functions and is associated with human atherosclerotic plaque stability. Circulation Research. 122:1385–1394, 2018. *Authors contributed equally. https://doi.org/10.1161/CIRCRESAHA.117.312340 III. Katie Frith, Anne-Laure Joly, Cindy S Ma, Stuart G Tangye, Christina Seitz, Zuzana Lohse, Charles F Verge, John Andersson & Paul Gray. The FOXP3Δ2 isoform supports regulatory T cell development and protects against severe IPEX. The Journal of Allergy and Clinical Immunology. 144:317-320, 2019. https://doi.org/10.1016/j.jaci.2019.03.003 IV. Christina Seitz, Anne-Laure Joly, Katie Frith, Zuzanna Lohse, Paul Gray, John Andersson. FOXP3fl controls the lineage-stability of CD4+FOXP3+ regulatory T cells. [Manuscript]</p
Handwritten biographical information on Paulina T. McClung Merritt
No full textA handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
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