Torsion-free crystallographic groups with indecomposable holonomy group II.

Let K be a principal ideal domain, G a finite group, and M a KG-module which is a free K-module of finite rank on which G acts faithfully. A generalized crystallographic group is a non-split extension C of M by G such that conjugation in C induces the G-module structure on M. ( When K = Z, these are just the classical crystallographic groups.) The dimension of C is the K-rank of M, the holonomy group of C is G, and C is indecomposable if M is an indecomposable KG-module. We study indecomposable torsion-free generalized crystallographic groups with holonomy group G when K is Z, or its localization Z((p)) at the prime p, or the ring Z(p) of p-adic integers. We prove that the dimensions of such groups with G non-cyclic of order p(2) are unbounded. For K = Z, we show that there are infinitely many non-isomorphic such groups with G the alternating group of degree 4 and we study the dimensions of such groups with G cyclic of certain orders

Torsion free groups with indecomposable holonomy group I

We study the torsion free generalized crystallographic groups with the indecomposable holonomy group which is isomorphic to either a cyclic group of order ${p^s}$ or a direct product of two cyclic groups of order ${p}$.Comment: 22 pages, AMS-Te

Kink-antikink vortex transfer in periodic-plus-random pinning potential: Theoretical analysis and numerical experiments

The influence of random pinning on the vortex dynamics in a periodic square potential under an external drive is investigated. Using theoretical approach and numerical experiments, we found several dynamical phases of vortex motion that are different from the ones for a regular pinning potential. Vortex transfer is controlled by kinks and antikinks, which either preexist in the system or appear spontaneously in pairs and then propagate in groups. When kinks and antikinks collide, they annihilate.Comment: 4 pages, 4 figure

HOST GENETICS OF SUSCEPTIBILITY Mutations in genes underlying atypical familial mycobacteriosis are not found in tuberculosis patients from Siberian populations

s u m m a r y Objectives: Atypical familial mycobacteriosis (AFM, OMIM #209950) is caused by mutations in genes regulating IL12/IFNG pathway. Some of the mutations exhibit incomplete penetrance, and they have been proposed to be involved in the common (polygenic) predisposition to tuberculosis (TB). We set out to test this hypothesis in two populations from Siberian region of Russia with high prevalence of TB. Material and methods: The prevalence of twelve mutations in IL12/IFNG pathway genes of were analysed in 331 Russians and 238 Tuvinians TB patients and in 279 healthy Russians and 265 healthy Tuvinians. A screening for new mutations and rare polymorphisms was carried out in 10 children with severe generalized TB and severe BCG-vaccine complications using Sanger's bidirectional sequencing. Results: Twelve mutations most commonly identified in AFM patients appeared to be "wild-type" monomorphic in the studied groups. No new mutations or rare polymorphisms were identified by sequencing. However, 15 common single nucleotide polymorphisms were found, none of which was associated with TB after correction for multiple testing. Conclusion: The results of the study contradict with a hypothesis that mutations underlying AFM syndrome are involved in the predisposition to TB

Стресс-индуцированная дисфункция тромбоцитов у крыс с фолат-зависимой гипергомоцистеинемией

A rat model of experimental hyperhomocysteinemia (HHC) caused by chronic folic acid deficiency was used to study the impact of swimming stress on the values of agonist-induced platelet aggregation and ATP release. At week 8 of HHC development, platelet aggregability and ATP levels in response to test inductors (ADP, thrombin, and collagen) moderately increased. After stress, the rate of platelet aggregation showed a more increase in rats with HHC; however, the increment was less pronounced than in the control group. The similar changes was observed in ATP, the release of which from dense platelet granules decreased in the experimental animals exposed to stress changes as compared to the controls. The experimental findings suggest that the stress potentiates platelet dysfunction in HHC. На модели экспериментальной гипергомоцистеинемии (ГГЦ) у крыс, вызванной хроническим дефицитом в организме фолиевой кислоты, изучалось влияние плавательного стресса на показатели агонист-индуцированной агрегации тромбоцитов и реакцию высвобождения из них АТФ. Показано, что на восьмой неделе развития ГГЦ агре-гационная способность тромбоцитов, как и уровень АТФ на все исследованные индукторы (АДФ, тромбин, коллаген), умеренно повышались. После стрессовой нагрузки интенсивность агрегации тромбоцитов у крыс с ГГЦ еще более возрастала, однако прирост ее был менее выраженным, чем в контрольной группе. Аналогичная динамика зарегистрирована со стороны АТФ, выброс которого из плотных тромбоцитарных гранул опытных животных, подвергнутых стрессу, уменьшался по сравнению с контролем. Результаты экспериментов свидетельствуют о потенцирующем влиянии стресса на дисфункцию тромбоцитов при ГГЦ.