This study is the first, to our knowledge, suggesting that the -572 G/C polymorphism of the IL-6 gene may be one of the protective factors associated with lower susceptibility to chronic periodontitis.

The precentral P22/N30 cortical component of the median nerve somatosensory evoked potentials (SEPs) was recorded in 16 patients (11 women and five men) suffering from cervical dystonia before and after botulinum toxin therapy. Cervical dystonia was diagnosed as idiopathic in all patients: 13 patients suffered from right-sided torticollis, and three suffered from left-sided torticollis. The amplitude of the P22/N30 component and the side-to-side ratio of amplitude values were measured. Normal values were obtained by acquiring measurements in two groups of healthy volunteers (n1 = 20 and n2 = 20). The recordings in the first control group were done with the patient's head in a normal position, whereas, in the second control group, the patient kept the head intentionally rotated 60 degrees to the right. Patients were treated with local injections of botulinum toxin A (BTX-A). The mean duration of treatment was 8.3 months, and the mean total amount of BTX injected was 295 U. The P22/N30 precentral component was repeatedly recorded in patients after head posture had been corrected to the normal plane by BTX-A treatment. The recordings showed that the amplitude of the P22/N30 precentral component recorded contralaterally to the direction of head deviation was significantly higher in patients before treatment than after treatment. Contralateral pretreatment amplitudes were also significantly higher (p < 0.01 and p < 0.05, respectively) than amplitudes in both groups of healthy volunteers. The mean side-to-side ratio of precentral P22/N30 component amplitudes was significantly higher in patients before treatment compared with after treatment and also compared with both control groups. These changes in dystonic patients probably reflect the direction of head rotation, the muscle pattern of torticollis, and the change in force of dystonic contraction after the treatment. The changes presumably could be the result of higher excitability of the precentral cortex contralateral to head rotation in patients with cervical dystonia and its change after successful BTX-A treatment.

Our study supports the idea that CD14 gene variants may act as disease modifiers of IgE-mediated allergic diseases.

Sarcoidosis is a granulomatous disorder showing a clear association with MHC (HLA) class I and class II genes. In order to investigate whether polymorphisms of nearby pro-inflammatory genes located within the MHC class III region may also contribute to susceptibility to sarcoidosis or to its clinical manifestation, tumour necrosis factor-alpha (TNF-alpha) and lymphotoxin-alpha (LT-alpha) genes were chosen for analysis in a case-control association study. In order to evaluate the findings on the TNF-alpha and LT-alpha genes in connection with the closely linked MHC class II region, 'classical' HLA-DRB1 locus was also investigated. Polymerase chain reaction-based methodologies were used in order to characterize two single-nucleotide polymorphisms (TNF-308*G/A and LTAlpha+252*A/G) and HLA-DRB1 allele groups in 114 Czech patients with pulmonary sarcoidosis and 425 healthy controls. LTA+252*G and HLA-DRB1*13 allele carriers were more frequent in patients, compared to those in controls. By contrast, HLA-DRB1*07 carriers were less frequent among sarcoidosis patients. The overrepresentation of TNF-308*A, LTAlpha+252*G and HLA-DRB1*03 allele carriers was found in a subgroup of sarcoidosis patients presenting with Lofgren's syndrome (LS) by comparison with the subgroup of patients without LS (NLS; phenotype frequency LS vs NLS: 68.8 vs 37.1% for TNF-308*A, 93.8 vs 66.3% for LTA+252*G and 68.8 vs 21.3% for DRB1*03). The data suggest that the LTAlpha and HLA-DRB1 genes themselves or a gene located nearby contributes to the susceptibility to sarcoidosis and that TNF-308*A, LTA+252*G and HLA-DRB1*03 alleles are associated (directly or via linkage with unknown causative locus) with LS as a specific manifestation of the disease.

Our data suggest that combined genotypes composed of the TNF-alpha and LT-alpha gene polymorphisms may influence the susceptibility to chronic periodontitis. We also showed that, comparing the two genes, the 1/1 genotype of the NcoI polymorphism in the first intron of the LT-alpha gene is a more informative marker and it may be one of the protective genetic factors against chronic periodontitis in our population.