37 research outputs found
Group Sum Chromatic Number of Graphs
We investigate the \textit{group sum chromatic number} (\gchi(G)) of
graphs, i.e. the smallest value such that taking any Abelian group \gr of
order , there exists a function f:E(G)\rightarrow \gr such that the sums
of edge labels properly colour the vertices. It is known that
\gchi(G)\in\{\chi(G),\chi(G)+1\} for any graph with no component of order
less than and we characterize the graphs for which \gchi(G)=\chi(G).Comment: Accepted for publication in European Journal of Combinatorics,
Elsevie
Group Irregularity Strength of Connected Graphs
We investigate the group irregularity strength () of graphs, i.e. the
smallest value of such that taking any Abelian group \gr of order ,
there exists a function f:E(G)\rightarrow \gr such that the sums of edge
labels at every vertex are distinct. We prove that for any connected graph
of order at least 3, if and otherwise,
except the case of some infinite family of stars
Automated Shack-Hartmann seeing measurements at the South Pole
The statistics and dynamics of the atmospheric seeing at the South Pole have been studied over a period of 101 days in winter. These measurements have been made with the first fully autonomous differential image motion monitor, the A-DIMM. The analysis shows an average seeing of 1.9ā³ with a standard deviation of 0.6ā³. The extensive set of data has allowed the study of the seeing time variations, showing that the seeing varies by a factor of two within a characteristic time of 2 hours
Progesterone induces expression of the prolactin receptor gene through cooperative action of Sp1 and C/EBP
Leaving Family for Work: Ambivalence and Mental Health Among Mexican Migrant Farmworker Men
Physical activity and glioma: A caseācontrol study with follow-up for survival
Purpose: High-grade disease accounts for ~ 70% of all glioma, and has a high mortality rate. Few modifiable exposures are known to be related to glioma risk or mortality. Methods: We examined associations between lifetime physical activity and physical activity at different ages (15ā18 years, 19ā29 years, 30ā39 years, last 10 years) with the risk of glioma diagnosis, using data from a hospital-based family caseācontrol study (495 cases; 371 controls). We followed up cases over a median of 25 months to examine whether physical activity was associated with all-cause mortality. Physical activity and potential confounders were assessed by self-administered questionnaire. We examined associations between physical activity (metabolic equivalent [MET]-h/wk) and glioma risk using unconditional logistic regression and with all-cause mortality in cases using Cox regression. Results: We noted a reduced risk of glioma for the highest ( ā„ 47 MET-h/wk) versus lowest ( \u3c 24 METh/wk) category of physical activity for lifetime activity (OR = 0.58, 95% CI: 0.38ā0.89) and at 15ā18 years (OR = 0.57, 95% CI: 0.39ā0.83). We did not observe any association between physical activity and all-cause mortality (HR for lifetime physical activity = 0.91, 95% CI: 0.64ā1.29). Conclusion: Our findings are consistent with previous research that suggested physical activity during adolescence might be protective against glioma. Engaging in physical activity during adolescence has many health benefits; this health behavior may also offer protection against glioma
Estrogen receptors ERĪ± and ERĪ² in proliferation in the rodent mammary gland
Most evidence supports the view that ERĪ± is responsible for estrogen (ovarian estradiol, E(2))-induced proliferation in the epithelial cells of the mammary gland, but despite this, proliferating epithelial cells do not express ERĪ±. We have examined this apparent paradox by studying the role of ERĪ± and ERĪ² in E(2)-induced proliferation in mammary glands (measured by BrdUrd incorporation into DNA) in mice with intact ERĪ² (WT mice) and those in which the ERĪ² gene has been inactivated (ERĪ²(-/-) mice). On treatment of ERĪ²(-/-) mice with E(2) or ovariectomized WT mice with E(2), tamoxifen, or a specific ERĪ² agonist (BAG), the number of BrdUrd-labeled cells in mammary glands increased from 3.4% in controls to 28-38% in the treated mice. This indicates that both ERĪ± and ERĪ² can mediate E(2)-induced proliferation independently of each other. With specific antibodies, ERĪ² was found in both epithelial and stromal cells, whereas ERĪ± was strictly epithelial. Within 4 h of a single dose of E(2), ERĪ± was lost from the nuclei of epithelial cells. In WT mice, ERĪ± reappeared by 24 h, but in ERĪ²(-/-) mice, return to the nucleus was delayed by 24 h. At 4 h after E(2), neither ERĪ± nor progesterone receptor was detectable in BrdUrd-labeled nuclei but by 48 h after E(2), 29% of the BrdUrd-labeled cells expressed ERĪ±, and 21-38% expressed progesterone receptor. During 3 weeks of continuous E(2) treatment, ERĪ² remained in the nucleus, but there was no detectable ERĪ±. With tamoxifen treatment, ERĪ± remained in the nucleus, but ERĪ² was lost. From these results, we conclude that ERĪ± receives the proliferation signal from E(2), initiates DNA synthesis, and is then lost from cells. The subsequent steps in proliferation can proceed in the absence of either ERĪ± or ERĪ². ERĪ² facilitates the return of ERĪ± to the nucleus and restores responsiveness to E(2). By down-regulating ERĪ², tamoxifen may prolong refractoriness to E(2) in mammary epithelium