Relationship of Homocysteine level and Comorbidities in VA Patients: A Retrospective Chart Review

Introduction: Elevated serum homocysteine is known to be associated with endothelial dysfunction, which is seen in multiple chronic diseases which include, but is not limited to Alzheimer’s, Dementia, and cardiovascular disease. This necessitated our investigation into serum homocysteine levels in VA patients and their associated comorbid disorders. Our study aimed to investigate comorbidities associated with elevated homocysteine levels, defined by being greater than 15 micromole/liter. Methods: Informatics at the VA was used to obtain a list of 654 patients with homocysteine drawn during the period of the study (7/21/2009 through 12/31/2013) at the John D. Dingell VAMC. Subjects were adults over 18 years of age. Patient gender, BMI, vitals, vitamin supplementation, and associated comorbidities were retrospectively analyzed and documented in an Excel file. The data from the excel file were statistically analyzed using SPSS 25. For each comorbidity and patient characteristic, homocysteine levels were compared using Independent Samples Mann-Whitney U test. Results: After completing statistical analysis of comorbidities commonly found in our Veteran population, those with statistically significant elevated levels (P-value \u3c0.05) of homocysteine were found to be Hypertension (P-value 0.001), Chronic Kidney Disease (P-value \u3c0.001), Dementia (P-value 0.004), Alzheimer’s (P-value 0.018), Peripheral Vascular Disease (P-value 0.046), and male gender (P-value 0.037). Of note, psoriasis was not statistically significant (P-value 0.855). Conclusion: Elevated homocysteine levels are known to be pro-inflammatory, which likely plays a role in their elevation in hypertension, chronic kidney disease, dementia, Alzheimer’s, and Peripheral Vascular Disease, necessitating a need to reduce homocysteine levels to improve patient outcomes

CARMA Survey Toward Infrared-bright Nearby Galaxies (STING): Molecular Gas Star Formation Law in NGC4254

This study explores the effects of different assumptions and systematics on the determination of the local, spatially resolved star formation law. Using four star formation rate (SFR) tracers (H\alpha with azimuthally averaged extinction correction, mid-infrared 24 micron, combined H\alpha and mid-infrared 24 micron, and combined far-ultraviolet and mid-infrared 24 micron), several fitting procedures, and different sampling strategies we probe the relation between SFR and molecular gas at various spatial resolutions and surface densities within the central 6.5 kpc in the disk of NGC4254. We find that in the high surface brightness regions of NGC4254 the form of the molecular gas star formation law is robustly determined and approximately linear and independent of the assumed fraction of diffuse emission and the SFR tracer employed. When the low surface brightness regions are included, the slope of the star formation law depends primarily on the assumed fraction of diffuse emission. In such case, results range from linear when the fraction of diffuse emission in the SFR tracer is ~30% or less (or when diffuse emission is removed in both the star formation and the molecular gas tracer), to super-linear when the diffuse fraction is ~50% and above. We find that the tightness of the correlation between gas and star formation varies with the choice of star formation tracer. The 24 micron SFR tracer by itself shows the tightest correlation with the molecular gas surface density, whereas the H\alpha corrected for extinction using an azimuthally-averaged correction shows the highest dispersion. We find that for R<0.5R_25 the local star formation efficiency is constant and similar to that observed in other large spirals, with a molecular gas depletion time ~2 Gyr.Comment: accepted for publication in ApJ, vol 729, March 10 2011 issue; 30 pages; 14 figures; revised version includes referee's comments; results unchange

Modeling the Influence of Vitamin D Deficiency on Cigarette Smoke-Induced Emphysema

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. While the primary risk factor for COPD is cigarette smoke exposure, vitamin D deficiency has been epidemiologically implicated as a factor in the progressive development of COPD-associated emphysema. Because of difficulties inherent to studies involving multiple risk factors in the progression of COPD in humans, we developed a murine model in which to study the separate and combined effects of vitamin D deficiency and cigarette smoke exposure. During a 16-week period, mice were exposed to one of four conditions, control diet breathing room air (CD-NS), control diet with cigarette smoke exposure (CD-CSE), vitamin D deficient diet breathing room air (VDD-NS) or vitamin D deficient diet with cigarette smoke exposure (VDD-CSE). At the end of the exposure period, the lungs were examined by a pathologist and separately by morphometric analysis. In parallel experiments, mice were anesthetized for pulmonary function testing followed by sacrifice and analysis. Emphysema (determined by an increase in alveolar mean linear intercept length) was more severe in the VDD-CSE mice compared to control animals and animals exposed to VDD or CSE alone. The VDD-CSE and the CD-CSE mice had increased total lung capacity and increased static lung compliance. There was also a significant increase in the matrix metalloproteinase-9: tissue inhibitor of metalloproteinases-1 (TIMP-1) ratio in VDD-CSE mice compared with all controls. Alpha-1 antitrypsin (A1AT) expression was reduced in VDD-CSE mice as well. In summary, vitamin D deficiency, when combined with cigarette smoke exposure, seemed to accelerate the appearance of emphysemas, perhaps by virtue of an increased protease-antiprotease ratio in the combined VDD-CSE animals. These results support the value of our mouse model in the study of COPD

Habitat-Based Density Models for Three Cetacean Species off Southern California Illustrate Pronounced Seasonal Differences

Managing marine species effectively requires spatially and temporally explicit knowledge of their density and distribution. Habitat-based density models, a type of species distribution model (SDM) that uses habitat covariates to estimate species density and distribution patterns, are increasingly used for marine management and conservation because they provide a tool for assessing potential impacts (e.g., from fishery bycatch, ship strikes, anthropogenic sound) over a variety of spatial and temporal scales. The abundance and distribution of many pelagic species exhibit substantial seasonal variability, highlighting the importance of predicting density specific to the season of interest. This is particularly true in dynamic regions like the California Current, where significant seasonal shifts in cetacean distribution have been documented at coarse scales. Finer scale (10 km) habitat-based density models were previously developed for many cetacean species occurring in this region, but most models were limited to summer/fall. The objectives of our study were two-fold: (1) develop spatially-explicit density estimates for winter/spring to support management applications, and (2) compare model-predicted density and distribution patterns to previously developed summer/fall model results in the context of species ecology. We used a well-established Generalized Additive Modeling framework to develop cetacean SDMs based on 20 California Cooperative Oceanic Fisheries Investigations (CalCOFI) shipboard surveys conducted during winter and spring between 2005 and 2015. Models were fit for short-beaked common dolphin (Delphinus delphis delphis), Dall's porpoise (Phocoenoides dalli), and humpback whale (Megaptera novaeangliae). Model performance was evaluated based on a variety of established metrics, including the percentage of explained deviance, ratios of observed to predicted density, and visual inspection of predicted and observed distributions. Final models were used to produce spatial grids of average species density and spatially-explicit measures of uncertainty. Results provide the first fine scale (10 km) density predictions for these species during the cool seasons and reveal distribution patterns that are markedly different from summer/fall, thus providing novel insights into species ecology and quantitative data for the seasonal assessment of potential anthropogenic impacts

Modeling the influence of vitamin D deficiency on cigarette smoke-induced emphysema.

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. While the primary risk factor for COPD is cigarette smoke exposure, vitamin D deficiency has been epidemiologically implicated as a factor in the progressive development of COPD-associated emphysema. Because of difficulties inherent to studies involving multiple risk factors in the progression of COPD in humans, we developed a murine model in which to study the separate and combined effects of vitamin D deficiency and cigarette smoke exposure. During a 16 week period, mice were exposed to one of four conditions, control diet breathing room air (CD-NS), control diet with cigarette smoke exposure (CD-CSE), vitamin D deficient diet breathing room air (VDD-NS) or vitamin D deficient diet with cigarette smoke exposure (VDD-CSE). At the end of the exposure period, the lungs were examined by a pathologist and separately by morphometric analysis. In parallel experiments, mice were anesthetized for pulmonary function testing followed by sacrifice and analysis. Emphysema (determined by an increase in alveolar mean linear intercept length) was more severe in the VDD-CSE mice compared to control animals and animals exposed to VDD or CSE alone. The VDD-CSE and the CD-CSE mice had increased total lung capacity and increased static lung compliance. There was also a significant increase in the matrix metalloproteinase-9: tissue inhibitor of metalloproteinases-1 ratio in VDD-CSE mice compared with all controls. Alpha-1 antitrypsin expression was reduced in VDD-CSE mice as well. In summary, vitamin D deficiency, when combined with cigarette smoke exposure, seemed to accelerate the appearance of emphysemas, perhaps by virtue of an increased protease-antiprotease ratio in the combined VDD-CSE animals. These results support the value of our mouse model in the study of COPD