Notes: The genetic element for periodontal disease, a central pathogenic role for cytokines, as well as the principle of individual variation in disease experience are tenets of periodontal research. However, a role for cytokine gene polymorphism in immunoregulation in periodontal disease remains suggestive rather than being firmly established. The problems (and some potential solutions) relating to association analyses and experimental studies of cytokine gene polymorphisms at the molecular genetic level are outlined in the preceding sections. Our response to these challenges will be aided by the recent and rapidly developing fields of genomics, proteomics and bioinformatics.Developments in genomics are providing fundamental structural information about the human genome and genomic variation, e.g. dbSNP (Table 1)(155, 163). Analysis of the entire genomic complement of individual human SNPs in population studies of genetic association remains beyond our technical and economic resources. However, the increasing availability of high throughput technologies should make analysis of SNPs across multiple gene loci a fairly routine matter and association studies incorporating the analysis of several thousand gene polymorphisms are beginning to be done (18). Characterization of the physical relationship between individual SNPs in the genome and development of a genome-wide haplotype map will facilitate more detailed studies of genetic basis for human disease (61). For example, genotyping studies within individual loci have revealed that haplotypes within particular genetic regions contain informative SNPs and redundant SNPs; determination of the genotype of informative SNPs identifies the haplotype in that gene or region of the genome and these have been termed ‘haplotype tag SNPs’ (htSNPs) (97). Genotyping htSNPs promises to reduce the genotyping effort required and to aid investigations of the role of polymorphism and linkage disequilibrium across wide regions of the genome.Developments in technologies able to provide mRNA profiles (transcriptomics) and protein profiles (proteomics) at the cellular level are providing comprehensive phenotypic information with a wide range of applications in immunologic and pathologic studies of human disease. Cellular immune responses can now be mapped to changes in regulatory networks, rather than individual mediators, in response to defined stimuli (161). These technologies promise to facilitate comprehensive studies of genotype/phenotype relationships and will provide more sophisticated models for analyzing complex elements of human diseases (25). There is an increasing appreciation that biological research relies on efficient and imaginative information processing, especially in the post-genomic era. Bioinformatic approaches have evolved from demands of handling nucleic acid and protein sequences in molecular biological research and have now expanded to other areas such as immunologic research, where analysis of complex regulatory networks is critical to understanding immune responses in health and disease (2).There is no doubt that we now have the technologic basis to generate and analyze large volumes of information in the pursuit of understanding complex diseases such as periodontal disease at the molecular genetic level. However, in order to successfully exploit these developments there needs to be a move away from the reductionist view, which supports a central role for individual gene variants and loci in genetic susceptibility to complex diseases. Periodontal disease should be viewed as a polygenic disease in which many interacting gene variants contribute to disease susceptibility. Also, sophisticated models need to be developed which integrate modern perspectives on genetic variation at the genomic level, the dynamic nature of host immune responses and the relationship between immune parameters and disease activity (25, 147). These models must also consider the multifactorial nature of periodontal disease and in particular the contribution of environmental factors such as smoking. However, given the critical role of cytokines in immune responses, the limited information concerning the role of cytokine polymorphisms outside the IL-1 cluster, and our restricted understanding of cytokine regulation, cytokine genes and immune regulation are likely to remain an important field of investigation in periodontal research.

Notes: [Auszug] Four groups of healthy chickens (32 experimental, 11 control) between the ages of 1 and 5 weeks were used. Each of the experimental chickens was injected with poly I o poly C (1-0 mg/kg) by way of a wing vein. When symptoms of cerebellar ataxia appeared, the experimental chickens, along with normal ...

Notes: Background, aims: Early onset periodontal diseases (EOP) are a group of inflammatory disorders characterised by a rapid rate of periodontal tissue destruction, in young individuals who are otherwise healthy. There is now substantial evidence to suggest that genetic factors play a rôle in the pathogenesis of EOP but the precise nature of these factors remains unclear. Polymorphisms in cytokine genes which may underpin inter-individual differences in cytokine synthesis and secretion have been associated with other diseases which have an inflammatory pathogenesis, including chronic adult periodontal disease (CAPD).Method: We therefore investigated the frequency of polymorphisms in the genes encoding interleukin-1β (IL-1β) and its receptor antagonist (IL-1RA) in 70 EOP patients, including a subgroup of 21 localised EOP (L-EOP) patients and 72 periodontally healthy controls. All subjects were of Caucasian heritage and systemically healthy. A single nucleotide polymorphism (SNP) in exon 5 of the IL-1β gene (IL-1β+3953) was analysed by amplifying the polymorphic region using PCR, followed by restriction digestion with Taq1 and gel electrophoresis.Results: The frequency of IL-1β genotypes homozygous for allele 1 (corresponding to the presence of a restriction site) of the IL-1β+3953 SNP was found to be significantly increased in EOP patients (χ2 test, p=0.025). Upon stratification for smoking status a significant difference was found in the IL-1β genotype distribution between EOP smokers compared to control smokers (F-exact test, p=0.02), but not between EOP non-smokers and control non-smokers. The IL-1β 1/1 genotype occurred at a higher frequency in EOP smokers (odds ratio=4.9) compared to control smokers. A variable number tandem repeat polymorphism (VNTR) in intron 2 of the IL-1RA gene was analysed by amplifying the polymorphic region using PCR and fragment size analysis by gel electrophoresis. There was no evidence for an association of an IL-1RA genotype with EOP. However the combination of IL-1β allele 1 and IL-1RA allele 1 (corresponding to 4 repeats) was associated with EOP (Clump, p=0.01).Conclusions: These findings suggest that an IL-1β genotype in combination with smoking, and a combined IL-1β and IL-1RA genotype are risk factors for EOP and support a role for genetic and environmental factors in susceptibility to EOP.

Notes: Abstract Observations of secondary conidium production in an African strain ofS. schenckii revealed that secondary conidia are produced (1) acropetally on short sterigmata, (2) sympodially on short conidial appendages, and/or (3) sympodially or acropetally on short sporogenous cells which arise directly from the primary conidium. The secondary conidia therefore appear also to be sympodulospores.

Notes: Abstract One-day-old chicks were infected by aerosolized conidia ofAspergillus fumigatus orA. flavus. Plaques containing viable organisms were observed on the third day of infection. Although plaques persisted for several weeks, cultures could not be recovered from them after about ten days. Flourescent antibody methods revealed an immune response to both agents within three days of challenge. Precipitin titers againstAspergillus active protein (AAP) did not appear until the tenth day, and was not detected after seven weeks. Aspergillus polysaccharide (APS) failed to react antigenically in infected birds. AAP was separated by Sephadex chromatography into nine distinct fractions. One fraction from each species was associated with an immediate and one with a delayed type of skin response in wattles. A low molecular weight fraction which lacked skin reactivity was an effective antigen in precipitin tests. Except for a weak skin reaction toA. fumigatus APS in rabbits, skin tests with extracts and APP fractions correlated with wattle reactions in chicks.

Notes: Abstract Hyphae from 30 isolants ofSporothrix andOphiostoma species were washed, dried and pyrolyzed at 350°C. Pyrolysis products were separated on a Carbowax column heated 7.5°C/min to and maintained for 50 min at 160°C. Hydrogen flame detector responses were recorded graphically. Fifteen clinical isolants ofS. schenckii from geographically separated sources produced qualitatively identical pyrograms.S. foliorum, 8 avirulentS. schenckii and otherSporothrix species isolants from soils, andSporothrix states of 6Ophiostoma species yielded pyrograms readily distinguished from each other and from those of virulentS. schenckii. Taxonomic and clinical implications of the pyrograms are mentioned.