Credit Union Division Activities, April 2003, Issue 6

Newsletter for Iowa Credit Union Division

Estudi dels fenòmens de contacte de llengües en el lèxic d'escolars de primera llengua castellana i la seva l'evolució lingüística (de 6è de primària a 1r d'ESO)

Aquest treball estudia els fenòmens de contacte de llengües que apareixen a la llengua oral catalana d'una mostra d'adolescents de primera llengua castellana de Manlleu en dos punts temporals (6è de primària i 1r d'ESO) i compara els resultats obtinguts amb dos estudis precedents (Vila, 1996; Galindo, 2006)

Histoire du dix-neuvième siècle depuis les traités de Vienne. Tome 6 / G. G. Gervinus,... ; traduit de l'allemand par J.-F. Minssen,...

Collection : Collection d'historiens contemporains

Iowa Community Empowerment Newsletter, October 2003, Vol. 4, No. 6

Monthly newsletter for the Iowa Department of Public Health

Iowa Community Empowerment Newsletter, December 2002, Vol. 3, no. 6

Monthly newsletter for the Iowa Department of Public Health

Iowa Community Empowerment Newsletter, December 2001, Vol. 2, no. 6

Monthly newsletter for the Iowa Department of Public Health

Species-Specific Recognition of Aspergillus fumigatus by Toll-like Receptor 1 and Toll-like Receptor 6.

Background. Aspergillus fumigatus causes invasive aspergillosis, a potentially fatal infection in oncohematological patients. Innate immune detection of A. fumigatus involves Toll-like receptor (TLR) 4 and TLR2, which forms a heterodimer with either TLR1 or TLR6. The role of those coreceptors in Aspergillus sensing is unknown. Methods. Cytokine production was measured in bone marrow-derived macrophages (BMDMs) from wild-type (WT) and TLR-deficient mice after incubation with a WT and an immunogenic RodA-deficient ([6;rodA-47) strain of A. fumigatus and in lungs from these mice after intranasal mold inoculation. Aspergillus fumigatus-mediated NF-κB activation was measured in HEK293T cells transfected with plasmids expressing mouse or human TLRs. Results. Bone marrow-derived macrophages from TLR1- and TLR6-deficient mice produced lower amounts of interleukin 12p40, CXCL2, interleukin 6, and tumor necrosis factor α than BMDMs from WT mice after stimulation with A. fumigatus. Lungs from TLR1- and TLR6-deficient mice had diminished CXCL1 and CXCL2 production and increased fungal burden after intranasal inoculation of [6;rodA A. fumigatus compared with lungs from WT mice. [6;rodA strain-mediated NF-κB activation was observed in HEK293T cells expressing mouse TLR2/1, mouse TLR2/6, and human TLR2/1 but not human TLR2/6. Conclusions. Innate immune detection of A. fumigatus is mediated by TLR4 and TLR2 together with TLR1 or TLR6 in mice and TLR1 but not TLR6 in humans.

IoWoman, November/December 2004, Vol.34, no.6

Newsletter for the Iowa Commission on the Status of Women

Iowa Community Empowerment Newsletter, December 2004, Vol.5, no.6

Monthly newsletter for the Iowa Department of Public Health

The Security Blanket, Febraury 2002, Vol.1, no.6

Newsletter for Information Technology Department

Lottery Action, January 26 - February 6, 2005, Vol. 12, No. 2

Iowa Lottery Newsletter for Retailers

Iowa Community Empowerment Newsletter, February 2005, Vol.6, no.1

Monthly newsletter for the Iowa Department of Public Health

Mutations in the heparan-sulfate proteoglycan glypican 6 (GPC6) impair endochondral ossification and cause recessive omodysplasia.

Glypicans are a family of glycosylphosphatidylinositol (GPI)-anchored, membrane-bound heparan sulfate (HS) proteoglycans. Their biological roles are only partly understood, although it is assumed that they modulate the activity of HS-binding growth factors. The involvement of glypicans in developmental morphogenesis and growth regulation has been highlighted by Drosophila mutants and by a human overgrowth syndrome with multiple malformations caused by glypican 3 mutations (Simpson-Golabi-Behmel syndrome). We now report that autosomal-recessive omodysplasia, a genetic condition characterized by short-limbed short stature, craniofacial dysmorphism, and variable developmental delay, maps to chromosome 13 (13q31.1-q32.2) and is caused by point mutations or by larger genomic rearrangements in glypican 6 (GPC6). All mutations cause truncation of the GPC6 protein and abolish both the HS-binding site and the GPI-bearing membrane-associated domain, and thus loss of function is predicted. Expression studies in microdissected mouse growth plate revealed expression of Gpc6 in proliferative chondrocytes. Thus, GPC6 seems to have a previously unsuspected role in endochondral ossification and skeletal growth, and its functional abrogation results in a short-limb phenotype.