North-South Distribution of Solar Flares during Cycle 23

In this paper, we investigate the spatial distribution of solar flares in the northern and southern hemisphere of the Sun that occurred during the period 1996 to 2003. This period of investigation includes the ascending phase, the maximum and part of descending phase of solar cycle 23. It is revealed that the flare activity during this cycle is low compared to previous solar cycle, indicating the violation of Gnevyshev-Ohl rule. The distribution of flares with respect to heliographic latitudes shows a significant asymmetry between northern and southern hemisphere which is maximum during the minimum phase of the solar cycle. The present study indicates that the activity dominates the northern hemisphere in general during the rising phase of the cycle (1997-2000). The dominance of northern hemisphere is shifted towards the southern hemisphere after the solar maximum in 2000 and remained there in the successive years. Although the annual variations in the asymmetry time series during cycle 23 are quite different from cycle 22, they are comparable to cycle 21.Comment: 6 pages, 2 figures, 1 table; Accepted for the publication in the proceedings of international solar workshop held at ARIES, Nainital, India on "Transient Phenomena on the Sun and Interplanetary Medium" in a special issue of "Journal of Astrophysics and Astronomy (JAA)

Photospheric Magnetic Field: Relationship Between North-South Asymmetry and Flux Imbalance

Photospheric magnetic fields were studied using the Kitt Peak synoptic maps for 1976-2003. Only strong magnetic fields (B>100 G) of the equatorial region were taken into account. The north-south asymmetry of the magnetic fluxes was considered as well as the imbalance between positive and negative fluxes. The north-south asymmetry displays a regular alternation of the dominant hemisphere during the solar cycle: the northern hemisphere dominated in the ascending phase, the southern one in the descending phase during Solar Cycles 21-23. The sign of the imbalance did not change during the 11 years from one polar-field reversal to the next and always coincided with the sign of the Sun's polar magnetic field in the northern hemisphere. The dominant sign of leading sunspots in one of the hemispheres determines the sign of the magnetic-flux imbalance. The sign of the north-south asymmetry of the magnetic fluxes and the sign of the imbalance of the positive and the negative fluxes are related to the quarter of the 22-year magnetic cycle where the magnetic configuration of the Sun remains constant (from the minimum where the sunspot sign changes according to Hale's law to the magnetic-field reversal and from the reversal to the minimum). The sign of the north-south asymmetry for the time interval considered was determined by the phase of the 11-year cycle (before or after the reversal); the sign of the imbalance of the positive and the negative fluxes depends on both the phase of the 11-year cycle and on the parity of the solar cycle. The results obtained demonstrate the connection of the magnetic fields in active regions with the Sun's polar magnetic field in the northern hemisphere.Comment: 24 pages, 12 figures, 2 table

pEPito: a significantly improved non-viral episomal expression vector for mammalian cells

<p>Abstract</p> <p>Background</p> <p>The episomal replication of the prototype vector pEPI-1 depends on a transcription unit starting from the constitutively expressed <it>Cytomegalovirus </it>immediate early promoter (CMV-IEP) and directed into a 2000 bp long <it>matrix attachment region sequence </it>(MARS) derived from the human β-interferon gene. The original pEPI-1 vector contains two mammalian transcription units and a total of 305 CpG islands, which are located predominantly within the vector elements necessary for bacterial propagation and known to be counterproductive for persistent long-term transgene expression.</p> <p>Results</p> <p>Here, we report the development of a novel vector pEPito, which is derived from the pEPI-1 plasmid replicon but has considerably improved efficacy both <it>in vitro </it>and <it>in vivo</it>. The pEPito vector is significantly reduced in size, contains only one transcription unit and 60% less CpG motives in comparison to pEPI-1. It exhibits major advantages compared to the original pEPI-1 plasmid, including higher transgene expression levels and increased colony-forming efficiencies <it>in vitro</it>, as well as more persistent transgene expression profiles <it>in vivo</it>. The performance of pEPito-based vectors was further improved by replacing the CMV-IEP with the <it>human CMV enhancer/human elongation factor 1 alpha promoter </it>(hCMV/EF1P) element that is known to be less affected by epigenetic silencing events.</p> <p>Conclusions</p> <p>The novel vector pEPito can be considered suitable as an improved vector for biotechnological applications <it>in vitro </it>and for non-viral gene delivery <it>in vivo</it>.</p

The Genotype Specific Competitive Ability Does Not Correlate with Infection in Natural Daphnia magna Populations

Different evolutionary hypotheses predict a correlation between the fitness of a genotype in the absence of infection and the likelihood to become infected. The cost of resistance hypothesis predicts that resistant genotypes pay a cost of being resistant and are less fit in the absence of parasites. The inbreeding-infection hypothesis predicts that the susceptible individuals are less fit due to inbreeding depression.Here we tested if a host's natural infection status was associated with its fitness. First, we experimentally confirmed that cured but formerly infected Daphnia magna are genetically more susceptible to reinfections with Octosporea bayeri than naturally uninfected D. magna. We then collected from each of 22 populations both uninfected and infected D. magna genotypes. All were treated against parasites and kept in their asexual phase. We estimated their relative fitness in an experiment against a tester genotype and in another experiment in direct competition. Consistently, we found no difference in competitive abilities between uninfected and cured but formerly infected genotypes. This was the case both in the presence as well as in the absence of sympatric parasites during the competition trials.Our data do not support the inbreeding-infection hypothesis. They also do not support a cost of resistance, however ignoring other parasite strains or parasite species. We suggest as a possible explanation for our results that resistance genes might segregate largely independently of other fitness associated genes in this system

A prognostic DNA methylation signature for stage I non-small-cell lung cancer

Purpose Non-small-cell lung cancer (NSCLC) is a tumor in which only small improvements in clinical outcome have been achieved. The issue is critical for stage I patients for whom there are no available biomarkers that indicate which high-risk patients should receive adjuvant chemotherapy. We aimed to find DNA methylation markers that could be helpful in this regard. Patients and Methods A DNA methylation microarray that analyzes 450,000 CpG sites was used to study tumoral DNA obtained from 444 patients with NSCLC that included 237 stage I tumors. The prognostic DNA methylation markers were validated by a single-methylation pyrosequencing assay in an independent cohort of 143 patients with stage I NSCLC. Results Unsupervised clustering of the 10,000 most variable DNA methylation sites in the discovery cohort identified patients with high-risk stage I NSCLC who had shorter relapse-free survival (RFS; hazard ratio [HR], 2.35; 95% CI, 1.29 to 4.28; P = .004). The study in the validation cohort of the significant methylated sites from the discovery cohort found that hypermethylation of five genes was significantly associated with shorter RFS in stage I NSCLC: HIST1H4F, PCDHGB6, NPBWR1, ALX1, and HOXA9. A signature based on the number of hypermethylated events distinguished patients with high-and low-risk stage I NSCLC (HR, 3.24; 95% CI, 1.61 to 6.54; P = .001). Conclusion The DNA methylation signature of NSCLC affects the outcome of stage I patients, and it can be practically determined by user-friendly polymerase chain reaction assays. The analysis of the best DNA methylation biomarkers improved prognostic accuracy beyond standard staging. (C) 2013 by American Society of Clinical Oncology

Regional socioeconomic indicators and ethnicity as predictors of regional infant mortality rate in Slovakia

OBJECTIVE: Exploring the associations of regional differences in infant mortality with selected socioeconomic indicators and ethnicity could offer important clues for designing public health policy measures. METHODS: Data included perinatal and infant mortality in the 79 districts of the Slovak population in 2004. Linear regression was used to analyse the contribution of education, unemployment, income and proportion of Roma population on regional differences in perinatal and infant mortality rates. RESULTS: All the explored socioeconomic indicators and ethnicity individually contributed significantly to both perinatal and infant mortality, with the exception of income. In the model exploring the influence of all these variables together on perinatal and infant mortality, only the effect of the proportion of Roma population remained significant. This model explained 34.9% of the variance for perinatal and 36.4% of the variance for infant mortality. CONCLUSIONS: Living in Roma settlements indicates an accumulation of socioeconomic disadvantage. Health literacy, health-related behaviour and many other factors might contribute to the explanation of the differences in infant mortality, and a better understanding of these processes might help us to design tailored interventions

Intrinsic genetic characteristics determine tumor-modifying capacity of fibroblasts: matrix metalloproteinase-3 5A/5A genotype enhances breast cancer cell invasion

Background Stromal fibroblasts can contribute to tumor invasion through the release of matrix metalloproteinases (MMPs). Population studies have suggested that single nucleotide polymorphisms (SNPs) in MMP genes influence levels of expression and may be associated with breast cancer risk and with disease progression. This study directly examined the impact of MMP SNP genotype on the ability of host fibroblasts to promote tumor cell invasion. Methods Primary breast fibroblasts were isolated from patients with (n = 13) or without (n = 19) breast cancer, and their ability to promote breast cancer cell invasion was measured in in vitro invasion assays. Fibroblast invasion-promoting capacity (IPC) was analyzed in relation to donor type (tumor or non-tumor patient), MMP-1, MMP-3, and MMP-9 SNP genotype and MMP activity using independent samples t test and analysis of variance. All statistical tests were two-sided. Results Tumor-derived fibroblasts promoted higher levels of invasion than normal fibroblasts (p = 0.041). When IPC was related to genotype, higher levels of IPC were generated by tumor fibroblasts with the high-expressing MMP-3 5A/5A genotype compared with the 5A/6A and 6A/6A genotypes (p = 0.05 and 0.07, respectively), and this was associated with enhanced MMP-3 release. The functional importance of MMP-3 was demonstrated by enhanced invasion in the presence of recombinant MMP-3, whereas reduction occurred in the presence of a specific MMP-3 inhibitor. An inverse relationship was demonstrated between fibroblast IPC and the high-expressing MMP-1 genotype (p = 0.031), but no relationship was seen with MMP-9 SNP status. In contrast, normal fibroblasts showed no variation in IPC in relation to MMP genotype, with MMP-3 5A/5A fibroblasts exhibiting significantly lower levels of IPC than their tumor-derived counterparts (p = 0.04). Conclusion This study has shown that tumor-derived fibroblasts exhibit higher levels of IPC than normal fibroblasts and that the MMP-3 5A/5A genotype contributes to this through enhanced MMP-3 release. Despite a high-expressing genotype, normal fibroblasts do not exhibit higher IPC or enhanced MMP release. This suggests that more complex changes occur in tumor-derived fibroblasts, enabling full expression of the MMP SNP genotype and these possibly are epigenetic in nature. The results do suggest that, in women with breast cancer, a high-expressing MMP-3 genotype may promote tumor progression more effectively