74 research outputs found
The Collmann gear : patents in England, united States of America, France, Belgium, Austria & Hungary, Germany, Russia & Poland etc
No full textby A. CollmannExlibrisetikette: "Geschenk aus dem Nachlasse von August Waldner" 002230265_0001 Exemplar der ETH-BI
Role of phosphoinositide 3-kinases in mast cell activation
No full textMast cells are primary effector cells in allergy and chronic inflammation. Class IB (PI3Kγ)
and class IA (PI3Kδ) PI3K have been shown to play major roles in mast cell activation:
antigen/IgE stimulation triggers autocrine/paracrine activation of mast cells through G
protein-coupled receptors (GPCRs) and PI3Kγ, e.g. by adenosine through the A3 adenosine
receptor. PI3Kδ acts downstream of c-kit to promote mast cell growth and differentiation.
Presently, data concerning the relative importance of PI3Kγ and PI3Kδ are controversial.
Here we investigate the role of PI3Kγ and PI3Kδ during mast cell activation and allergic
responses. From blood to tissues, we demonstrate that PI3Kγ is a major player in mast cell
adhesion to endothelia involving α4β1 integrin whereas adhesion to fibronectin is mediated
by α5β1 integrin. VCAM-1 and ICAM-1 upregulation and mast cell-derived TNF-α-
mediated activation of endothelia also require functional PI3Kγ. Genetic and pharmacologic
approaches confirm the role of PI3Kδ in stem factor signaling (SCF) signaling. However,
IgE/antigen signaling and mast cell degranulation are driven by PI3Kγ. Finally, in vivo mast
cell recruitment as well as passive cutaneous anaphylaxis experiments are severely impaired
by absence or pharmacological inhibition of PI3Kγ. Altogether, modulation of PI3Kγ and
TNF-α affect mast cell function in crucial phases, rendering them appropriated targets for
allergic diseases
Members of the Hermann Sons of San Antonio holding bags with their names and fictitious addresses on each, ca. 1900
No full textPhotograph shows members of the Hermann Sons dressed in costumes. Each is holding a bag with lettering reading: (L. to r.): (?) Glockner from Dal Salado; A. Rummel from Post Oak Creek; A. Collmann from Punkin Center; H. Hoefting from Rattlesnake Hill; H. Koepp from Cibilo (sic) Valley; F. Hummerl from Coon Holler; and William Dobrowolski from Onion Creek. Photo is torn at Dobrowolski
Members of the Hermann Sons of San Antonio holding bags with their names and fictitious addresses on each, ca. 1900
No full textPhotograph shows members of the Hermann Sons dressed in costumes. Each is holding a bag with lettering reading: (L. to r.): (?) Glockner from Dal Salado; A. Rummel from Post Oak Creek; A. Collmann from Punkin Center; H. Hoefting from Rattlesnake Hill; H. Koepp from Cibilo (sic) Valley; F. Hummerl from Coon Holler; and William Dobrowolski from Onion Creek. Photo is torn at Dobrowolski
Untersuchungen zur Proliferationskinetik der Erythropoese von gefrierkonserviertem Knochenmark <em>in vitro</em>.
No full textMenschliche Knochenmarkzellsuspensionen wurden unter Verwendung von Dimethylsulfoxyd als Gefrierschutzstoff bei −88° C eingefroren und nach Auftauen 48 h lang in Flüssigkeitskulturen beobachtet. An Hand von Kammerzählungen und Differentialzählungen gefärbter Ausstriche konnte gezeigt werden, daß die Erythropoese nach Gefrierkonservierung proliferationsfähig blieb und in vitro sogar Zeichen einer leichten Stimulierung aufwies. Abgesehen von einer etwas erhöhten Fragilität der Zellen wurden an der Erythroposese keine wesentlichen, durch den Gefrierprozeß bedingsten Schädigungen festgestellt. Große basophile «Blasten» traten in den Kulturen gefrorener Knochenmarkzellen auf, die sonst nicht in Kultur gefunden werden konnten
Contiguous gene deletions involving EFNB1, OPHN1, PJA1 and EDA in patients with craniofrontonasal syndrome.
No full textCraniofrontonasal syndrome (CFNS [MIM 304110]) is an X-linked malformation syndrome characterized by craniofrontonasal dysplasia and extracranial manifestations in heterozygous females. In the majority of patients CFNS is caused by mutations in the EFNB1 gene (MIM 300035). We identified three girls with classical CFNS and mild developmental delay harboring de novo deletions of the EFNB1 gene. Applying haplotype analysis, Southern blot hybridization and array-comparative genomic hybridization, deletion of EFNB1 was found to be part of contiguous gene deletions in the patients. In one patient the deletion interval includes the genes for oligophrenin-1 (OPHN1 [MIM 300127]) and praja 1 (PJA1 [MIM 300420]). In the second patient the deletion includes OPHN1, PJA1 and the gene for ectodysplasin A (EDA [MIM 300451]). In the third patient EFNB1 gene deletion may include deletion of regulatory regions 5' of OPHN1. Previously, the OPHN1 gene has been shown to be responsible for recessive X-linked mental retardation. Although it is too early to predict the future cognitive performance of the two infant patients with contiguous gene deletions of OPHN1-EFNB1-PJA1, mild learning disabilities have been recognized in the older, third patient. It is important for genetic counseling to be aware that their male offspring may not only be carriers of CFNS but may also be affected by mental retardation and anhidrotic ectodermal dysplasia
Contiguous gene deletions involving EFNB1, OPHN1, PJA1 and EDA in patients with craniofrontonasal syndrome.
No full text
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