Changes in Cardiovascular Health in the United States, 2003–2011

Background Cardiovascular disease is the leading cause of death in the United States, making improving cardiovascular health a key population health goal. As part of efforts to achieve this, the American Heart Association has developed the first comprehensive cardiovascular health index (CVHI). Our objective was to investigate the changes in CVHI in US states from 2003 to 2011. Methods and Results CVHI was examined using Behavioral Risk Factor Surveillance System data between 2003 and 2011 (odd‐numbered years). Total CVHI decreased from 3.73±0.01 in 2003 to 3.65±0.01 in 2009. The majority of states (88%) experienced a decline in CVHI and an increase in the prevalence of “poor” CVHI between 2003 and 2009. Among CVHI components, the highest prevalence of “ideal” was observed for blood glucose followed by smoking, whereas the lowest prevalence of “ideal” was observed for physical activity and diet. Between 2003 and 2009, prevalence of “ideal” smoking and diet status increased, while “ideal” prevalence of blood pressure, cholesterol, blood glucose, body mass index, and physical activity status decreased. We observed statistically significant differences between 2009 and 2011, outside the scope of the 2003–2009 trend, which we hypothesize are partially attributable to differences in sample demographic characteristics related to changes in Behavioral Risk Factor Surveillance System methodology. Conclusions Overall, CVHI decreased, most likely due to decreases in “ideal” blood pressure, body mass index, and cholesterol status, which may stem from low prevalence of “ideal” physical activity and diet status. These findings can be used to inform state‐specific strategies and targets to improve cardiovascular health

Midwest Evaluation of the Adult Functioning of Former Foster Youth

The Midwest Evaluation of the Adult Functioning of Former Foster Youth (Midwest Study) is a prospective study that has been following a sample of young people from Iowa, Wisconsin, and Illinois as they transition out of foster care into adulthood. It is a collaborative effort involving Chapin Hall at the University of Chicago; Partners for Our Children at the University of Washington, Seattle; the University of Wisconsin Survey Center; and the public child welfare agencies in Illinois, Iowa, and Wisconsin.The Midwest Study provides a comprehensive picture of how foster youth are faring during this transition since the Foster Care Independence Act of 1999 became law. Foster youth in Iowa, Wisconsin, and Illinois were eligible to participate in the study if they had entered care before their 16th birthday, were still in care at age 17, and had been removed from home for reasons other than delinquency. Baseline survey data were collected from 732 study participants when they were 17 or 18 years old. Study participants were re-interviewed at ages 19 (n = 603), 21 (n = 591), and 23 or 24 (n = 602). A fifth wave of survey data will be collected when study participants are 25 or 26 years old.Because many of the questions Midwest Study participants were also asked as part of the National Longitudinal Study of Adolescent Health, it is possible to make comparisons between this sample of former foster youth and a nationally representative sample of young people in the general population. These comparisons indicate that young people who have aged out of foster care are faring poorly as a group relative to their peers across a variety of domains.The Midwest Study also presents a unique opportunity to compare the outcomes of young people from one state (i.e., Illinois) that allows foster youth to remain in care until their 21st birthday to the outcomes of young people from two other states (i.e., Iowa and Wisconsin) in which foster youth generally age out when they are 18 years old. The data suggest that extending foster care until age 21 may be associated with better outcomes, at least in some domains

Using Multiple-hierarchy Stratification and Life Course Approaches to Understand Health Inequalities: The Intersecting Consequences of Race, Gender, SES, and Age

This study examines how the intersecting consequences of race-ethnicity, gender, socioeconomics status (SES), and age influence health inequality. We draw on multiple-hierarchy stratification and life course perspectives to address two main research questions. First, does racial-ethnic stratification of health vary by gender and/or SES? More specifically, are the joint health consequences of racial-ethnic, gender, and socioeconomic stratification additive or multiplicative? Second, does this combined inequality in health decrease, remain stable, or increase between middle and late life? We use panel data from the Health and Retirement Study (N = 12,976) to investigate between- and within-group differences in in self-rated health among whites, blacks, and Mexican Americans. Findings indicate that the effects of racial-ethnic, gender, and SES stratification are interactive, resulting in the greatest racial-ethnic inequalities in health among women and those with higher levels of SES. Furthermore, racial-ethnic/gender/SES inequalities in health tend to decline with age. These results are broadly consistent with intersectionality and aging-as-leveler hypotheses

Attributable healthcare utilization and cost of pneumonia due to drug-resistant streptococcus pneumonia: a cost analysis

Background: The burden of disease due to S. pneumoniae (pneumococcus), particularly pneumonia, remains high despite the widespread use of vaccines. Drug resistant strains complicate clinical treatment and may increase costs. We estimated the annual burden and incremental costs attributable to antibiotic resistance in pneumococcal pneumonia. Methods: We derived estimates of healthcare utilization and cost (in 2012 dollars) attributable to penicillin, erythromycin and fluoroquinolone resistance by taking the estimate of disease burden from a previously described decision tree model of pneumococcal pneumonia in the U.S. We analyzed model outputs assuming only the existence of susceptible strains and calculating the resulting differences in cost and utilization. We modeled the cost of resistance from delayed resolution of illness and the resulting additional health services. Results: Our model estimated that non-susceptibility to penicillin, erythromycin and fluoroquinolones directly caused 32,398 additional outpatient visits and 19,336 hospitalizations for pneumococcal pneumonia. The incremental cost of antibiotic resistance was estimated to account for 4% ($91 million) of direct medical costs and 5$233 million) of total costs including work and productivity loss. Most of the incremental medical cost ($82 million) was related to hospitalizations resulting from erythromycin non-susceptibility. Among patients under age 18 years, erythromycin non-susceptibility was estimated to cause 17$38 million in costs, or 39% of pneumococcal pneumonia costs attributable to resistance. Conclusions: We estimate that antibiotic resistance in pneumococcal pneumonia leads to substantial healthcare utilization and cost, with more than one-third driven by macrolide resistance in children. With 5% of total pneumococcal costs directly attributable to resistance, strategies to reduce antibiotic resistance or improve antibiotic selection could lead to substantial savings

A functional bacteria-derived restriction modification system in the mitochondrion of a heterotrophic protist

The overarching trend in mitochondrial genome evolution is functional streamlining coupled with gene loss; therefore, gene acquisition by mitochondria is considered to be exceedingly rare. Selfish elements in the form of self-splicing introns occur in many organellar genomes, but the wider diversity of selfish elements, and how they persist in the DNA of organelles, has not been explored. In the mitochondrial genome of a marine heterotrophic katablepharid protist, we identify a functional type II restriction modification (RM) system originating from a horizontal gene transfer (HGT) event involving bacteria related to flavobacteria. This RM system consists of an HpaII-like endonuclease and a cognate cytosine methyltransferase (CM). We demonstrate that these proteins are functional by heterologous expression in both bacterial and eukaryotic cells. These results suggest that a mitochondrial-encoded RM system can function as a toxin-antitoxin selfish element and that such elements could be co-opted by eukaryotic genomes to drive biased organellar inheritance.Peer reviewe

Does the use of store-and-forward telehealth systems improve outcomes for clinicians managing diabetic foot ulcers? A pilot study

Diabetic foot ulcers are one of the most hospitalised diabetes complications and contribute to many leg amputations.\ud Trained diabetic foot teams and specialists managing diabetic foot ulcers have demonstrated reductions in amputations and hospitalisation by up to 90%. Few such teams exist in Australia. Thus, access is limited for all geographical populations and may somewhat explain the high rates of hospitalisation.\ud Aim: This pilot study aims to analyse if local clinicians managing diabetic foot complications report improved access to diabetic foot specialists and outcomes with the introduction of a telehealth store-and-forward system.\ud Method: A store-and-forward telehealth system was implemented in six different Queensland locations between August 2009 and February 2010. Sites were offered ad hoc and/or fortnightly telehealth access to a diabetic foot speciality service. A survey was sent six months following commencement of the trial to the 14 eligible clinicians involved in the trial to gauge clinical perception of the telehealth system.\ud Results: Eight participants returned the surveys. The majority of responding clinicians reported that the telehealth system was easy to use (100%), improved their access to diabetic foot speciality services (75%), improved upskilling of local diabetes service staff (100%), and improved patient outcomes (100%).\ud Conclusion: This pilot study suggests that clinicians found the use of a telehealth store-and-forward system very useful in improving access to speciality services, clinical skills and patient outcomes. This study supports the recommendation that telehealth systems should be made available for diabetic foot ulcer management

Osteocyte dysfunction promotes osteoarthritis through MMP13-dependent suppression of subchondral bone homeostasis.

Osteoarthritis (OA), long considered a primary disorder of articular cartilage, is commonly associated with subchondral bone sclerosis. However, the cellular mechanisms responsible for changes to subchondral bone in OA, and the extent to which these changes are drivers of or a secondary reaction to cartilage degeneration, remain unclear. In knee joints from human patients with end-stage OA, we found evidence of profound defects in osteocyte function. Suppression of osteocyte perilacunar/canalicular remodeling (PLR) was most severe in the medial compartment of OA subchondral bone, with lower protease expression, diminished canalicular networks, and disorganized and hypermineralized extracellular matrix. As a step toward evaluating the causality of PLR suppression in OA, we ablated the PLR enzyme MMP13 in osteocytes while leaving chondrocytic MMP13 intact, using Cre recombinase driven by the 9.6-kb DMP1 promoter. Not only did osteocytic MMP13 deficiency suppress PLR in cortical and subchondral bone, but it also compromised cartilage. Even in the absence of injury, osteocytic MMP13 deficiency was sufficient to reduce cartilage proteoglycan content, change chondrocyte production of collagen II, aggrecan, and MMP13, and increase the incidence of cartilage lesions, consistent with early OA. Thus, in humans and mice, defects in PLR coincide with cartilage defects. Osteocyte-derived MMP13 emerges as a critical regulator of cartilage homeostasis, likely via its effects on PLR. Together, these findings implicate osteocytes in bone-cartilage crosstalk in the joint and suggest a causal role for suppressed perilacunar/canalicular remodeling in osteoarthritis

The acyl-CoA Synthetase, pudgy, Promotes Sleep and Is Required for the Homeostatic Response to Sleep Deprivation

The regulation of sleep and the response to sleep deprivation rely on multiple biochemical pathways. A critical connection is the link between sleep and metabolism. Metabolic changes can disrupt sleep, and conversely decreased sleep can alter the metabolic environment. There is building evidence that lipid metabolism, in particular, is a critical part of mounting the homeostatic response to sleep deprivation. We have evaluated an acyl-CoA synthetase, pudgy (pdgy), for its role in sleep and response to sleep deprivation. When pdgy transcript levels are decreased through transposable element disruption of the gene, mutant flies showed lower total sleep times and increased sleep fragmentation at night compared to genetic controls. Consistent with disrupted sleep, mutant flies had a decreased lifespan compared to controls. pdgy disrupted fatty acid handling as pdgy mutants showed increased sensitivity to starvation and exhibited lower fat stores. Moreover, the response to sleep deprivation is reduced when compared to a control flies. When we decreased the transcript levels for pdgy using RNAi, the response to sleep deprivation was decreased compared to background controls. In addition, when the pdgy transcription is rescued throughout the fly, the response to sleep deprivation is restored. These data demonstrate that the regulation and function of acyl-CoA synthetase plays a critical role in regulating sleep and the response to sleep deprivation. Endocrine and metabolic signals that alter transcript levels of pdgy impact sleep regulation or interfere with the homeostatic response to sleep deprivation

Open questions in the social lives of viruses

Social interactions among viruses occur whenever multiple viral genomes infect the same cells, hosts, or populations of hosts. Viral social interactions range from cooperation to conflict, occur throughout the viral world, and affect every stage of the viral lifecycle. The ubiquity of these social interactions means that they can determine the population dynamics, evolutionary trajectory, and clinical progression of viral infections. At the same time, social interactions in viruses raise new questions for evolutionary theory, providing opportunities to test and extend existing frameworks within social evolution. Many opportunities exist at this interface: Insights into the evolution of viral social interactions have immediate implications for our understanding of the fundamental biology and clinical manifestation of viral diseases. However, these opportunities are currently limited because evolutionary biologists only rarely study social evolution in viruses. Here, we bridge this gap by (1) summarizing the ways in which viruses can interact socially, including consequences for social evolution and evolvability; (2) outlining some open questions raised by viruses that could challenge concepts within social evolution theory; and (3) providing some illustrative examples, data sources, and conceptual questions, for studying the natural history of social viruses

Relationship between Expression of the Family of M Proteins and Lipoteichoic Acid to Hydrophobicity and Biofilm Formation in Streptococcus pyogenes

Background: Hydrophobicity is an important attribute of bacteria that contributes to adhesion and biofilm formation. Hydrophobicity of Streptococcus pyogenes is primarily due to lipoteichoic acid (LTA) on the streptococcal surface but the mechanism(s) whereby LTA is retained on the surface is poorly understood. In this study, we sought to determine whether members of the M protein family consisting of Emm (M protein), Mrp (M-related protein), Enn (an M-like protein), and the streptococcal protective antigen (Spa) are involved in anchoring LTA in a manner that contributes to hydrophobicity of the streptococci and its ability to form biofilms. Methodology/Principal Findings: Isogenic mutants defective in expression of emm, mrp, enn, and/or spa genes of eight different serotypes and their parental strains were tested for differences in LTA bound to surface proteins, LTA released into the culture media, and membrane-bound LTA. The effect of these mutations on the ability of streptococci to form a hydrophobic surface and to generate biofilms was also investigated. A recombinant strain overexpressing Emm1 was also engineered and similarly tested. The serotypes tested ranged from those that express only a single M protein gene to those that express two or three members of the M protein family. Overexpression of Emm1 led to enhanced hydrophobicity an