Strategic Implications of Phobos as a Staging Point for Mars Surface Missions

As human exploration endeavors begin to set sights beyond low Earth orbit to the surface of the Moon, exploration of the surface of Mars continues to serve as the horizon destination to help focus development and research efforts. One Mars exploration strategy often discussed is the notion of utilizing the moons of Mars, namely Phobos, as an exploration destination prior to Mars surface missions. The premise behind this is that staging missions from Mars moons as well as exploring the moons themselves would be less costly and risky. However, understanding potential advantages of Phobos staging and exploration must be done in the context of the overall end-to-end Mars surface exploration needs, goals, objectives, campaign approach, and systems required. This paper examines the strategic implications of utilizing the moons of Mars as a potential location for exploration of Mars. Operational concepts utilizing both Phobos and Mars orbital strategies will be examined to understand the architectural impacts of this staging strategy. The strategic implications of each operational concept are assessed to determine the overall key challenges and strategic links to other exploration destinations. Results from this analysis indicate that, if the objective is to conduct Mars surface missions, utilizing Phobos as an exploration destination adds little benefit toward the goal of exploration of Mars

Requirement for a Uroplakin 3a-like protein in the development of zebrafish pronephric tubule epithelial cell function, morphogenesis, and polarity

Uroplakin (UP)3a is critical for urinary tract development and function; however, its role in these processes is unknown. We examined the function of the UP3a-like protein Upk3l, which was expressed at the apical surfaces of the epithelial cells that line the pronephric tubules (PTs) of the zebrafish pronephros. Embryos treated with upk3l-targeted morpholinos showed decreased pronephros function, which was attributed to defects in PT epithelial cell morphogenesis and polarization including: loss of an apical brush border and associated phospho-ERM proteins, apical redistribution of the basolateral Na+/K+-ATPase, and altered or diminished expression of the apical polarity complex proteins Prkcz (atypical protein kinase C zeta) and Pard3 (Par3). Upk3l missing its C-terminal cytoplasmic domain or containing mutations in conserved tyrosine or proline residues did not rescue, or only partially rescued the effects of Upk3l depletion. Our studies indicate that Upk3l promotes epithelial polarization and morphogenesis, likely by forming or stimulating interactions with cytoplasmic signaling or polarity proteins, and that defects in this process may underlie the pathology observed in UP3a knockout mice or patients with renal abnormalities that result from altered UP3a expression. © 2012 Mitra et al

Correlated defects, metal-insulator transition, and magnetic order in ferromagnetic semiconductors

The effect of disorder on transport and magnetization in ferromagnetic III-V semiconductors, in particular (Ga,Mn)As, is studied theoretically. We show that Coulomb-induced correlations of the defect positions are crucial for the transport and magnetic properties of these highly compensated materials. We employ Monte Carlo simulations to obtain the correlated defect distributions. Exact diagonalization gives reasonable results for the spectrum of valence-band holes and the metal-insulator transition only for correlated disorder. Finally, we show that the mean-field magnetization also depends crucially on defect correlations.Comment: 4 pages RevTeX4, 5 figures include

Impact of nutritional vitamin D supplementation on parathyroid hormone and 25-hydroxyvitamin D levels in non-dialysis chronic kidney disease : a meta-analysis

Background. Secondary hyperparathyroidism (SHPT) is a common and major complication in chronic kidney disease (CKD), reflecting the increase of parathyroid hormone (PTH) in response to reduced vitamin D signalling and hypocalcaemia. This meta-analysis evaluated the impact of nutritional vitamin D (NVD) (cholecalciferol or ergocalciferol) on SHPT-related biomarkers. Methods. A systematic literature search was performed in PubMed to identify relevant randomized control trials to be included in the meta-analysis. Fixed- and random-effects models were used to pool study-level results. Effects were studied within NVD study arms and relative to control groups (placebo/no treatment); the former in order to identify the effect of actively altering biomarkers levels. Results. Reductions in PTH from supplementation with NVD were small when observed within the NVD study arms (pooled reduction: 10.5 pg/mL) and larger when compared with placebo/no treatment (pooled reduction: 49.7 pg/mL). NVD supplementation increased levels of 25-hydroxyvitamin D [25(OH)D] in both analyses (increase within NVD study arm: 20.6 ng/mL, increase versus placebo/no treatment: 26.9 ng/mL). While small and statistically non-significant changes in phosphate and fibroblast growth factor 23 were observed, NVD supplementation caused calcium levels to increase when compared with placebo/no treatment (increase: 0.23 mg/dL). Conclusions. Our results suggest that supplementation with NVD can be used to increase 25(OH)D to a certain extent, while the potential of NVD to actively reduce PTH in non-dialysis-CKD patients with SHPT is limited

Vitamin B supplementation and nutritional intake of methyl donors in patients with chronic kidney disease: A critical review of the impact on epigenetic machinery

Cardiovascular morbidity and mortality are several-fold higher in patients with advanced chronic kidney disease (CKD) and end-stage renal disease (ESRD) than in the general population. Hyperhomocysteinemia has undoubtedly a central role in such a prominent cardiovascular burden. The levels of homocysteine are regulated by methyl donors (folate, methionine, choline, betaine), and cofactors (vitamin B6, vitamin B12,). Uremia-induced hyperhomocysteinemia has as its main targets DNA methyltransferases, and this leads to an altered epigenetic control of genes regulated through methylation. In renal patients, the epigenetic landscape is strictly correlated with the uremic phenotype and dependent on dietary intake of micronutrients, inflammation, gut microbiome, inflammatory status, oxidative stress, and lifestyle habits. All these factors are key contributors in methylome maintenance and in the modulation of gene transcription through DNA hypo-or hypermethylation in CKD. This is an overview of the epigenetic changes related to DNA methylation in patients with advanced CKD and ESRD. We explored the currently available data on the molecular dysregulations resulting from altered gene expression in uremia. Special attention was paid to the efficacy of B-vitamins supplementation and dietary intake of methyl donors on homocysteine lowering and cardiovascular protection

Current Therapy in CKD Patients Can Affect Vitamin K Status

Chronic kidney disease (CKD) patients have a higher risk of cardiovascular (CVD) morbidity and mortality compared to the general population. The links between CKD and CVD are not fully elucidated but encompass both traditional and uremic-related risk factors. The term CKD-mineral and bone disorder (CKD-MBD) indicates a systemic disorder characterized by abnormal levels of calcium, phosphate, PTH and FGF-23, along with vitamin D deficiency, decreased bone mineral density or altered bone turnover and vascular calcification. A growing body of evidence shows that CKD patients can be affected by subclinical vitamin K deficiency; this has led to identifying such a condition as a potential therapeutic target given the specific role of Vitamin K in metabolism of several proteins involved in bone and vascular health. In other words, we can hypothesize that vitamin K deficiency is the common pathogenetic link between impaired bone mineralization and vascular calcification. However, some of the most common approaches to CKD, such as (1) low vitamin K intake due to nutritional restrictions, (2) warfarin treatment, (3) VDRA and calcimimetics, and (4) phosphate binders, may instead have the opposite effects on vitamin K metabolism and storage in CKD patients

Vitamin D effects on bone homeostasis and cardiovascular system in patients with chronic kidney disease and renal transplant recipients

Poor vitamin D status is common in patients with impaired renal function and represents one main component of the complex scenario of chronic kidney disease–mineral and bone disorder (CKD–MBD). Therapeutic and dietary efforts to limit the consequences of uremia-associated vitamin D deficiency are a current hot topic for researchers and clinicians in the nephrology area. Evidence indicates that the low levels of vitamin D in patients with CKD stage above 4 (GFR < 15 mL/min) have a multifactorial origin, mainly related to uremic malnutrition, namely impaired gastrointestinal absorption, dietary restrictions (low-protein and low-phosphate diets), and proteinuria. This condi-tion is further worsened by the compromised response of CKD patients to high-dose cholecalciferol supplementation due to the defective activation of renal hydroxylation of vitamin D. Currently, the literature lacks large and interventional studies on the so-called non-calcemic activities of vitamin D and, above all, the modulation of renal and cardiovascular functions and immune response. Here, we review the current state of the art of the benefits of supplementation with native vitamin D in various clinical settings of nephrological interest: CKD, dialysis, and renal transplant, with a special focus on the effects on bone homeostasis and cardiovascular outcomes

A Summary of Experiments in Converting Copper Oxide Process Regenerator Off-Gases to Elemental Sulfur, CRADA 97-F006, Final Report

Sorbent Technologies Corporation (Sorbtech) of Twinsburg, Ohio has developed a new technology for converting SO{sub 2}-rich gas streams directly to elemental sulfur. Key to the technology is a special catalyst that promotes the reaction of SO{sub 2} with reformed natural gas. The technology evolved from earlier flue-gas desulfurization (FGD) work that Sorbtech engineers performed in the late 1980's. In 1995, with U.S. Department of Energy (DOE) support, Sorbtech designed and constructed a larger, skid-mounted pilot-test unit suitable for demonstrating the new technology in field tests. This Report summarizes months of preparation work and eight days of testing that were performed at FETC'S facilities during late September and early October, 1997. On the basis of the results of this phase of the project, the following conclusions were made: (1) The chemistry of the new technology was well proven and demonstrated at FETC. The overall S0{sub 2}-to-elemental sulfur yields were typically in the range of 93 to 98 percent. (The project goal was 95 percent, so the goal was exceeded). (2) Sulfur selectivity values, indicating the tendency of S0{sub 2} to be converted to elemental sulfur in preference to H{sub 2}S or COS, were typically in the range of 98 to 100 percent. (3) Bright yellow sulfur of high quality was produced at FETC. (4) The FETC regenerator exhaust gas presented no processing difficulties. Swings in the level of methane in the exhaust gas were handled with relative ease. (5) With the exception of the water condenser, all system components performed well. (6) Condensing of the sulfur after its production was a serious problem at FETC. Solid sulfur deposits built up in the process-gas lines at several locations in the system. Clogging of the lines necessitated terminating runs typically after 2 to 4 hours of operation. Clogging problems were most severe in the water condenser. Many planned parametric tests were not run because of the sulfur plugging problems. (7) Several suggestions were made by BP Oil Company for solving the sulfur pl ugging problems. Among the suggestions were to never allow the temperature of the process gas to fall below 118{degree}C, to increase the temperature of the sulfur condenser to 148{degree}C, and to eliminate the water condenser from the system entirely

Calcifying circulating cells: an uncharted area in the setting of vascular calcification in CKD patients

Vascular calcification, occurring during late-stage vascular and valvular disease, is highly associated with chronic kidney disease-mineral and bone disorders (CKD-MBD), representing a major risk factor for cardiovascular morbidity and mortality. The hallmark of vascular calcification, which involves both media and intima, is represented by the activation of cells committed to an osteogenic programme. Several studies have analysed the role of circulating calcifying cells (CCCs) in vascular calcification. CCCs are bone marrow (BM)-derived cells with an osteogenic phenotype, participating in intima calcification processes and defined by osteocalcin and bone alkaline phosphatase expression. The identification of CCCs in diabetes and atherosclerosis is the most recent, intriguing and yet uncharted chapter in the scenario of the bone-vascular axis. Whether osteogenic shift occurs in the BM, the bloodstream or both, is not known, and also the factors promoting CCC formation have not been identified. However, it is possible to recognize a common pathogenic commitment of inflammation in atherosclerosis and diabetes, in which metabolic control may also have a role. Currently available studies in patients without CKD did not find an association of CCCs with markers of bone metabolism. Preliminary data on CKD patients indicate an implication of mineral bone disease in vascular calcification, as a consequence of functional and anatomic integrity interruption of BM niches. Given the pivotal role that parathyroid hormone and osteoblasts play in regulating expansion, mobilization and homing of haematopoietic stem/progenitors cells, CKD-MBD could promote CCC formation

Testing the Resolving Power of 2-D K^+ K^+ Interferometry

Adopting a procedure previously proposed to quantitatively study two-dimensional pion interferometry, an equivalent 2-D chi^2 analysis was performed to test the resolving power of that method when applied to less favorable conditions, i.e., if no significant contribution from long lived resonances is expected, as in kaon interferometry. For that purpose, use is made of the preliminary E859 K^+ K^+ interferometry data from Si+Au collisions at 14.6 AGeV/c. As expected, less sensitivity is achieved in the present case, although it still is possible to distinguish two distinct decoupling geometries. The present analysis seems to favor scenarios with no resonance formation at the AGS energy range, if the preliminary K^+ K^+ data are confirmed. The possible compatibility of data with zero decoupling proper time interval, conjectured by the 3-D experimental analysis, is also investigated and is ruled out when considering more realistic dynamical models with expanding sources. These results, however, clearly evidence the important influence of the time emission interval on the source effective transverse dimensions. Furthermore, they strongly emphasize that the static Gaussian parameterization, commonly used to fit data, cannot be trusted under more realistic conditions, leading to distorted or even wrong interpretation of the source parameters!Comment: 11 pages, RevTeX, 4 Postscript figures include