Locally finite groups containing a 2 -element with Chernikov centralizer

Suppose that a locally finite group G has a 2-element g with Chernikov centralizer. It is proved that if the involution in ⟨g⟩ has nilpotent centralizer, then G has a soluble subgroup of finite index

Estimation of Effective Day Length at Any Light Intensity Using Solar Radiation Data

The influence of day length on living creatures differs with the photosensitivity of the creature; however, the possible sunshine duration (N0) might be an inadequate index of the photoperiod for creatures with low light sensitivity. To address this issue, the authors tried to estimate the effective day length, i.e., the duration of the photoperiod that exceeds a certain threshold of light intensity. Continual global solar radiation observation data were gathered from the baseline surface radiation network (BSRN) of 18 sites from 2004 to 2007 and were converted to illuminance data using a luminous efficiency model. The monthly average of daily photoperiods exceeding each defined intensity (1 lx, 300 lx, … 20,000 lx) were calculated [defined as Ne(lux)]. The relationships between the monthly average of global solar radiation (Rs), N0, and Ne(lux) were investigated. At low light intensity (<500 lx), Ne(lux) were almost the same as N0. At high light intensity (>10,000 lx), Ne(lux) and Rs showed a logarithmic relationship. Using these relationships, empirical models were derived to estimate the effective day length at different light intensities. According to the validation of the model, the effective day length for any light intensity could be estimated with an accuracy of less than 11% of the mean absolute percentage error (MAPE) in the estimation of the monthly base photoperiod. Recently, a number of studies have provided support for a link between day length and some diseases. Our results will be useful in further assessing the relationships between day length and these diseases

Z-permutable subgroups of finite groups

Let ℨ be a complete set of Sylow subgroups of a finite group G, that is, a set composed of a Sylow p-subgroup of G for each p dividing the order of G. A subgroup H of G is called ℨ-permutable if H permutes with all members of ℨ. The main goal of this paper is to study the embedding of the ℨ-permutable subgroups and the influence of ℨ-permutability on the group structure

The Wnt Receptor Ryk Reduces Neuronal and Cell Survival Capacity by Repressing FOXO Activity During the Early Phases of Mutant Huntingtin Pathogenicity

The Wnt receptor Ryk is an evolutionary-conserved protein important during neuronal differentiation through several mechanisms, including γ-secretase cleavage and nuclear translocation of its intracellular domain (Ryk-ICD). Although the Wnt pathway may be neuroprotective, the role of Ryk in neurodegenerative disease remains unknown. We found that Ryk is up-regulated in neurons expressing mutant huntingtin (HTT) in several models of Huntington's disease (HD). Further investigation in Caenorhabditis elegans and mouse striatal cell models of HD provided a model in which the early-stage increase of Ryk promotes neuronal dysfunction by repressing the neuroprotective activity of the longevity-promoting factor FOXO through a noncanonical mechanism that implicates the Ryk-ICD fragment and its binding to the FOXO co-factor β-catenin. The Ryk-ICD fragment suppressed neuroprotection by lin-18/Ryk loss-of-function in expanded-polyQ nematodes, repressed FOXO transcriptional activity, and abolished β-catenin protection of mutant htt striatal cells against cell death vulnerability. Additionally, Ryk-ICD was increased in the nucleus of mutant htt cells, and reducing γ-secretase PS1 levels compensated for the cytotoxicity of full-length Ryk in these cells. These findings reveal that the Ryk-ICD pathway may impair FOXO protective activity in mutant polyglutamine neurons, suggesting that neurons are unable to efficiently maintain function and resist disease from the earliest phases of the pathogenic process in HD. © 2014 Tourette et al

The SMC-5/6 Complex and the HIM-6 (BLM) Helicase Synergistically Promote Meiotic Recombination Intermediate Processing and Chromosome Maturation during<i> Caenorhabditis elegans</i> Meiosis

Meiotic recombination is essential for the repair of programmed double strand breaks (DSBs) to generate crossovers (COs) during meiosis. The efficient processing of meiotic recombination intermediates not only needs various resolvases but also requires proper meiotic chromosome structure. The Smc5/6 complex belongs to the structural maintenance of chromosome (SMC) family and is closely related to cohesin and condensin. Although the Smc5/6 complex has been implicated in the processing of recombination intermediates during meiosis, it is not known how Smc5/6 controls meiotic DSB repair. Here, using Caenorhabditis elegans we show that the SMC-5/6 complex acts synergistically with HIM-6, an ortholog of the human Bloom syndrome helicase (BLM) during meiotic recombination. The concerted action of the SMC-5/6 complex and HIM-6 is important for processing recombination intermediates, CO regulation and bivalent maturation. Careful examination of meiotic chromosomal morphology reveals an accumulation of inter-chromosomal bridges in smc-5; him-6 double mutants, leading to compromised chromosome segregation during meiotic cell divisions. Interestingly, we found that the lethality of smc-5; him-6 can be rescued by loss of the conserved BRCA1 ortholog BRC-1. Furthermore, the combined deletion of smc-5 and him-6 leads to an irregular distribution of condensin and to chromosome decondensation defects reminiscent of condensin depletion. Lethality conferred by condensin depletion can also be rescued by BRC-1 depletion. Our results suggest that SMC-5/6 and HIM-6 can synergistically regulate recombination intermediate metabolism and suppress ectopic recombination by controlling chromosome architecture during meiosis