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• Journal article
  Selimovic M, Bismarck A, Pfaffernoschke M, Springer Jet al., 1999,

  Grafted Carbon Fibers and their physico-chemical Properties; Part IV: Grafting of Cyano-Biphenyl containing Liquid-Crystalline Monomers onto modified Carbon Fibers

  , Acta Polymerica, Vol: 50, Pages: 156-162
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• Journal article
  Wuertz C, Bismarck A, Springer J, Koniger Ret al., 1999,

  Electrokinetic and Mechanical Characterization of UV Induced Crosslinked Acrylic Copolymers

  , Prog.Org.Coat., Vol: 37, Pages: 117-129
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• Journal article
  Scheid P, Griesenbach U, Davies J, Siddique Z, Gruenert DC, Geddes DM, Alton EWFWet al., 1998,

  Interleukin-8 production by airway epithelium and the effect of liposome-mediated IκB gene transfer

  , Thorax, Vol: 53, ISSN: 0040-6376

  Interleukin-8 (IL-8) is a major chemoattractant for neutrophils, present in the CF lung in large numbers. We measured basal and stimulated IL-8 secretion from CF and non CF airway epithelial cell lines (CFTE and 16HBE cells, respectively) as well as from Cos7 cells in a controlled in vitro environment. Basal IL-8 secretion was significantly higher in CFTE cells (8110 ± 2286 pg/mg protein) than in 16HBE (1113 ± 123 pg/mg protein) and Cos7 (497 ± 138 pg/mg protein) [n=6, p<0.05]. Following TNF-α stimulation IL-8 secretion increased 8 ± 0.9 fold in CFTE, 2 ± 0.4 fold in 16HBE and 2.7 ± 0.2 fold in Cos7 cells. Preliminary data in freshly obtained human nasal cells also indicate an increased basal secretion of IL-8 (non CF: 62 ± 10 pg/ml n=16, CF: 165 ± 37 pg/ml n=12, p<0.05). The response to addition of Pseudomonas aeruginosa to these cells as measured by IL-8 secretion was also increased in CF (3279 ± 656 pg/ml n=10, p<0.05) when compared to non CF samples (817 ± 143 pg/ml n=8). Thus it appears that the IL-8 response is disproportionately greater in CF cells. It is likely that new treatment aimed at reducing IL-8 levels will be beneficial in CF. Nuclear factor kappa B (NFκB) is a transcription factor that regulates expression of inflammatory mediators including IL-8. NFκB is kept in an inactive state by association with a specific inhibitor (IκB). We investigated the effects of liposome-mediated overexpression of IκB in CFTE and Cos7 cells. Despite successful transfection, as confirmed by RT-PCR in both cell types, we did not detect an alteration of basal or TNF-α stimulated IL-8 secretion. This is most likely related to low levels of gene expression. In conclusion, we have shown that CF cells lines as well as CF primary cells produce increased levels of secreted IL-8 in the basal as well as in a stimulated state. Reduction of IL-8 secretion is likely to b

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• Journal article
  Marshall R, Puddicombe A, Dinwiddie R, Crawford O, McAnulty R, Cookson W, Laurent GJet al., 1998,

  Familial pulmonary fibrosis in the UK

  , Thorax, Vol: 53, ISSN: 0040-6376

  A number of observations suggest a genetic influence in pulmonary fibrosis including the variation in response to profibrotic agents observed in both humans and certain animal strains. A rare familial form is well documented in the literature. However, no systematic investigation of the epidemiology of this disorder has been performed to our knowledge. We contacted 407 Adult Respiratory Physicians and also Respiratory Paediatricians in the UK to identify and characterise families in which two or more individuals have IPF. Occupational, clinical data and a family pedigree was obtained via a structured questionnaire. 84% of Adult Physicians responded identifying 63 individuals from 24 families to date. In adults, the average age of diagnosis was 56 years with an equal sex incidence. 74 % of patients had lived for the larger part of their lives in the Midlands, North or North-East of England. 44% had a potential occupational exposure to fibrogenic duts and 50% were never smokers. Inheritance, appears to be autosomal recessive. In an additional seven families, the onset of the disease occurred in infancy or childhood with a possible autosomal dominant mode of inheritance. Clinical parameters such as; symptomatology, natural history radiological and histological appearance were very similar to those seen in non-familial cases. Familial clustering in IPF is very rare in the UK. A genetic influence is suggested but not yet confirmed in 1-2 % of cases. The strength and exact mode of inheritance of a genetic predisposition remains to be determined however, its similarity to IPF and amenability to study using positional cloning techniques make this group an important target for genetic studies. We would like to identify further families in Europe.

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• Journal article
  Palmer LJ, Daniels SE, Rye PJ, Gibson NA, Tay GK, Cookson WO, Goldblatt J, Burton PR, LeSöuef PNet al., 1998,

  Linkage of chromosome 5q and 11q gene markers to asthma-associated quantitative traits in Australian children.

  , Am J Respir Crit Care Med, Vol: 158, Pages: 1825-1830, ISSN: 1073-449X

  Asthma is a genetically complex disease, and the investigation of putative linkages to candidate loci in independent populations is an important part of the gene discovery process. This study investigated the linkage of microsatellite markers in the 5q and 11q regions to asthma-associated quantitative traits in 121 Australian Caucasian nuclear families. The families were recruited on the basis of a child proband: a cohort of 95 randomly recruited families of unselected probands (n = 442 subjects) and a cohort of 26 families of probands selected on the basis of severe symptomatic asthma (n = 134 subjects). The quantitative traits assessed included serum levels of total IgE and specific IgE to house dust mite and mixed grass, blood eosinophil counts, and the dose-response slope (DRS) of FEV1 to histamine provocation. Multipoint linkage analysis using Haseman-Elston sib-pair methods provided evidence of significant linkage between the chromosome 5q markers and loge total serum IgE levels, specific serum IgE levels, and loge blood eosinophil counts. The chromosome 11q markers showed evidence of significant linkage to specific serum IgE levels. Neither region demonstrated significant linkage to the loge DRS to histamine. Phenotypes were residualized for age and sex. These data are consistent with the existence of loci regulating asthma-associated quantitative traits in both the 5q31-33 and 11q13 chromosomal regions.

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• Journal article
  Caddick MX, Arst HN, 1998,

  Deletion of the 389 N-terminal residues of the transcriptional activator AREA does not result in nitrogen metabolite derepression in <i>Aspergillus nidulans</i>

  , JOURNAL OF BACTERIOLOGY, Vol: 180, Pages: 5762-5764, ISSN: 0021-9193
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  • Citations: 18
• Journal article
  Hamada W, Spanu PD, 1998,

  Co-suppression of the hydrophobin gene <i>HCf-1</i> is correlated with antisense RNA biosynthesis in <i>Cladosporium fulvum</i>

  , MOLECULAR AND GENERAL GENETICS, Vol: 259, Pages: 630-638, ISSN: 0026-8925
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  • Citations: 32
• Journal article
  Denison SH, Negrete-Urtasun S, Mingot JR, Tilburn J, Mayer WA, Goel A, Espeso EA, Peñalva MA, Arst Net al., 1998,

  Putative membrane components of signal transduction pathways for ambient pH regulation in <i>Aspergillus</i> and meiosis in <i>Saccharomyces</i> are homologous

  , MOLECULAR MICROBIOLOGY, Vol: 30, Pages: 259-264, ISSN: 0950-382X
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  • Citations: 56
• Journal article
  Byrne B, Klahn S, Taylor PL, Eidne KAet al., 1998,

  Functional analysis of GnRH receptor ligand binding using biotinylated GnRH derivatives

  , MOLECULAR AND CELLULAR ENDOCRINOLOGY, Vol: 144, Pages: 11-19, ISSN: 0303-7207
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  • Citations: 4
• Journal article
  Wilson RA, Arst HN, 1998,

  Mutational analysis of AREA, a transcriptional activator mediating nitrogen metabolite repression in Aspergillus nidulans and a member of the "streetwise" GATA family of transcription factors.

  , Microbiol Mol Biol Rev, Vol: 62, Pages: 586-596, ISSN: 1092-2172

  The transcriptional activator AREA is a member of the GATA family of transcription factors and mediates nitrogen metabolite repression in the fungus Aspergillus nidulans. The nutritional versatility of A. nidulans and its amenability to classical and reverse genetic manipulations make the AREA DNA binding domain (DBD) a useful model for analyzing GATA family DBDs, particularly as structures of two AREA-DNA complexes have been determined. The 109 extant mutant forms of the AREA DBD surveyed here constitute one of the highest totals of eukaryotic transcription factor DBD mutants, are discussed in light of the roles of individual residues, and are compared to corresponding mutant sequence changes in other fungal GATA factor DBDs. Other topics include delineation of the DBD using both homology and mutational truncation, use of frameshift reversion to detect regions of tolerance to mutational change, the finding that duplication of the DBD can apparently enhance AREA function, and use of the AREA system to analyze a vertebrate GATA factor DBD. Some major points to emerge from work on the AREA DBD are (i) tolerance to sequence change (with retention of function) is surprisingly great, (ii) mutational changes in a transcription factor can have widely differing, even opposing, effects on expression of different structural genes so that monitoring expression of one or even several structural genes can be insufficient and possibly misleading, and (iii) a mutational change altering local hydrophobic packing and DNA binding target specificity can markedly influence the behavior of mutational changes elsewhere in the DBD.

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