Metallicity Distribution Functions, Radial Velocities, and Alpha Element Abundances in Three Off-Axis Bulge Fields

We present radial velocities and chemical abundance ratios of [Fe/H], [O/Fe], [Si/Fe], and [Ca/Fe] for 264 red giant branch (RGB) stars in three Galactic bulge off-axis fields located near (l,b)=(-5.5,-7), (-4,-9), and (+8.5,+9). The results are based on equivalent width and spectrum synthesis analyses of moderate resolution (R~18,000), high signal-to-noise ratio (S/N~75-300) spectra obtained with the Hydra spectrographs on the Blanco 4m and WIYN 3.5m telescopes. The targets were selected from the blue side of the giant branch to avoid cool stars that would be strongly affected by CN and TiO; however, a comparison of the color-metallicity distribution in literature samples suggests our selection of bluer targets should not present a significant bias against metal-rich stars. We find a full range in metallicity that spans [Fe/H]\approx-1.5 to +0.5, and that, in accordance with the previously observed minor-axis vertical metallicity gradient, the median [Fe/H] also declines with increasing Galactic latitude in off-axis fields. The off-axis vertical [Fe/H] gradient in the southern bulge is estimated to be ~0.4 dex/kpc. The (+8.5,+9) field exhibits a higher than expected metallicity, with a median [Fe/H]=-0.23, that might be related to a stronger presence of the X--shaped bulge structure along that line-of-sight. All fields exhibit an identical, strong decrease in velocity dispersion with increasing metallicity that is consistent with observations in similar minor-axis outer bulge fields. Additionally, the [O/Fe], [Si/Fe], and [Ca/Fe] versus [Fe/H] trends are identical among our three fields, and are in good agreement with past bulge studies. [abridged]Comment: Accepted for Publication in the Astrophysical Journal; 120 pages (main text ends on page 24); 22 figures (figures end on page 46); 6 tables; electronic versions of the tables can be made available upon request to author C. Johnso

The metal-poor Knee in the Fornax Dwarf Spheroidal Galaxy

We present alpha-element abundances of Mg, Si, and Ti for a large sample of field stars in two outer fields of the Fornax dwarf spheroidal galaxy (dSph), obtained with VLT/GIRAFFE (R~16,000). Due to the large fraction of metal-poor stars in our sample, we are able to follow the alpha-element evolution from [Fe/H]=-2.5 continuously to [Fe/H]=-0.7 dex. For the first time we are able to resolve the turnover from the Type II supernovae (SNe) dominated, alpha-enhanced plateau down to subsolar [alpha/Fe] values due to the onset of SNe Ia, and thus to trace the chemical enrichment efficiency of the galaxy. Our data support the general concept of an alpha-enhanced plateau at early epochs, followed by a well-defined "knee", caused by the onset of SNe Ia, and finally a second plateau with sub-solar [alpha/Fe] values. We find the position of this knee to be at [Fe/H]=-1.9 and therefore significantly more metal-poor than expected from comparison with other dSphs and standard evolutionary models. Surprisingly, this value is rather comparable to the knee in Sculptor, a dSph about 10 times less luminous than Fornax. Using chemical evolution models, we find that both the position of the knee as well as the subsequent plateau at sub-solar level can hardly be explained unless the galaxy experienced several discrete star formation events with a drastic variation in star formation efficiency, while a uniform star formation can be ruled out. One possible evolutionary scenario is that Fornax experienced one or several major accretion events from gas-rich systems in the past, so that its current stellar mass is not indicative of the chemical evolution environment at ancient times. If Fornax is the product of several smaller building blocks, this may also have implications of the understanding on the formation process of dSphs in general.Comment: 10 pages, 6 Figures, accepted for publication in Ap

Interactions of the chemokines CXCL11 and CXCL12 in human tumor cells

BACKGROUND The chemokines, CXCL12 and CXCL11, are upregulated in tumors from many organs and control their progression. CXCL12 and CXCL11 affect tumor cell functions by either binding their prime receptors, CXCR4 and CXCR3, respectively, and/or CXCR7 as a common second chemokine receptor. In humans, CXCR3 exists in the functional splice variants, CXCR3A and CXCR3B, which either have pro- or anti-tumor activity, respectively. Despite the intimate crosstalk between the CXCL12- and CXCL11-system, the impact of a combination of CXCL12 and CXCL11 on tumor progression remains vague. METHODS In the present work, we have analyzed CXCL12 and CXCL11 for combined effects on migration, invasion, proliferation, and cytostatic-induced apoptosis of the human tumor cells, A549, A767, A772, DLD-1, and MDA-MB-231. RESULTS We demonstrate that the mode of interaction differs with respect to cell type and function and allows for either potentiation, attenuation or no changes of cellular responses. The divergent responses are not the result of the distinct use of different CXCL12- and CXCL11-receptors by the respective tumor cells, but in case of cell migration seem to be associated with the activation of p38 signaling pathways. CONCLUSIONS Our findings point to therapeutic limitations of ongoing efforts to selectively target CXCR3, CXCR4, or CXCR7 in cancer patients, and rather favor individualized targeting strategies

Does Vitamin D Deficiency Cause Hypertension? Current Evidence from Clinical Studies and Potential Mechanisms

Vitamin D deficiency is widely prevalent across all ages, races, geographical regions, and socioeconomic strata. In addition to its important role in skeletal development and calcium homeostasis, several recent studies suggest its association with diabetes, hypertension, cardiovascular disease, certain types of malignancy, and immunologic dysfunction. Here, we review the current evidence regarding an association between vitamin D deficiency and hypertension in clinical and epidemiological studies. We also look into plausible biological explanations for such an association with the renin-angiotensin-aldosterone system and insulin resistance playing potential roles. Taken together, it appears that more studies in more homogeneous study populations are needed before a firm conclusion can be reached as to whether vitamin D deficiency causes or aggravates hypertension and whether vitamin D supplementation is safe and exerts cardioprotective effects. The potential problems with bias and confounding factors present in previous epidemiological studies may be overcome or minimized by well designed randomized controlled trials in the future