Background Obesity has been recognized as a worldwide growing problem, producing many pathologies including the promotion of “proinflammatory state.” The etiology of human obesity is still only partially understood; however, the genetic background has been proved. Its nature is complex, and currently, it appears that the combined effects of the interactions among multiple genes should receive more attention. Due to the fact that obesity promotes proinflammatory conditions, in this study, we investigated the genetic polymorphism of IL-1 family genes in healthy people with normal and elevated body mass index (BMI) and fat %. Results The single-nucleotide polymorphisms (SNPs) within the IL1A -889C > T (rs1800587), IL1B + 3954 T > C (rs1143634), and IL1RN -87G > A (rs2234677) genes alone were associated neither with BMI nor fat % values in tested group. The associations between SNP–SNP interaction and BMI for the IL1B × IL1RN interactions were significant for dominant model (p = 0.02) and codominant model (p = 0.03). The same SNP-SNP interaction (IL1B × IL1RN) was associated also with fat % for codominant (p = 0.01) and recessive (p = 0.002) models. Conclusions This study further confirmed that IL-1 family genes are involved in genetic background of obesity. It has been shown that interaction IL1B × IL1RN was associated with both BMI and fat % with rare T allele protecting form higher values. Thus, even if certain polymorphisms in single genes of IL-1 family cannot be defined as related to obesity in examined population, the genetic interrelationships should be analyzed.

Interleukin 6 (IL-6) is a cytokine with both pro- and anti-inflammatory actions, but is also considered as a “metabolic hormone” involved in immune responses, affecting glucose, protein and lipid metabolism. It has been proposed to be related to obesity, but various results have been presented. Thus, in this study, the very homogenous population of young, male military professionals, living in the same conditions involving high physical activity, has been selected to avoid the influence of environmental factors. The subjects were divided into groups depending on the obesity parameters BMI (body mass index) and fat percentage (fat%), and the following IL-6 SNPs (Single Nucleotide Polymorphisms) were analyzed: rs1800795, rs1800796 and rs13306435. No relation was found between obesity parameters and IL-6 polymorphisms rs1800795, rs1800796 and rs13306435. It may be postulated that even if a genetic predisposition involves IL-6 genes, this effect in individuals with obesity of a low grade is minor, or can be avoided or at least markedly reduced by changes in lifestyle.

Anticonvulsant and antilethal effects of imidazenil, a new imidazobenzodiazepine derivative, in fluostigmine (DFP; diisopropyl phosphorofluoridate) intoxications were studied and compared with the effects of diazepam on mice and rats. Special attention was payed to the myorelaxant effects of both drugs. It was stated that imidazenil (i) significantly decreased convulsion intensity in mice, (ii) quickly inhibited seizure patterns in bioelectrical activity in the rat's brain, (iii) significantly increased antilethal effectiveness of the standard therapy in mice intoxicated with DFP. These effects are comparable to those of diazepam. However, effects of imidazenil in the rota-rod test of the mouse were noted in doses 5-10 times higher than therapeutic ones, when effects of diazepam on motor co-ordination were seen in therapeutic dosage.

coupling of agonist binding to gating of the ion channel, indicating that agonist binding and subsequent ion channel opening are separate, but related processes. Phy differentially displaces [125 I]a-BGT from the chimeric nAChR, suggesting that the b subunit is not involved in Phy binding, and that Phy targets the insect agonist binding loop C. ACKNOWLEDGEMENTSWe would like to thank Dr B Schmitt (Max-PlanckInstitut fu È r Hirnforschung, Frankfurt, Germany) and Dr M Ballivet (University of Geneva, Switzerland) for kindly providing us with cDNA encoding the SAD and the chick b2 subunit, respectively.

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