Space solar power systems

Studies were done on the feasibility of placing a solar power station called POwersat, in space. A general description of the engineering features are given as well as a brief discussion of the economic considerations

Effects of No-Tillage Production Practices on Crop Yields as Influenced by Crop and Growing Environment Factors

This paper evaluated differences between yields of no-tillage compared to conventional or reduced tillage and their associated downside risk. Six crops were evaluated along with how those yields and risks differed by various environmental factors such geographic location, precipitation, soil type and how long the practice had been used.no-tillage, conservation, conventional tillage, downside-risk, yield, Agribusiness, Environmental Economics and Policy, Farm Management, Land Economics/Use, Production Economics, Risk and Uncertainty,

Barriers to Hepatitis C Antiviral Therapy in HIV/HCV Co-Infected Patients in the United States: A Review

This review synthesized the literature for barriers to HCV antiviral treatment in persons with HIV/HCV co-infection. Searches of PubMed, Embase, CINAHL, and Web of Science were conducted to identify relevant articles. Articles were excluded based on the following criteria: study conducted outside of the United States, not original research, pediatric study population, experimental study design, non-HIV or non-HCV study population, and article published in a language other than English. Sixteen studies met criteria and varied widely in terms of study setting and design. Hepatic decompensation was the most commonly documented absolute/nonmodifiable medical barrier. Substance use was widely reported as a relative/modifiable medical barrier. Patient-level barriers included nonadherence to medical care, refusal of therapy, and social circumstances. Provider-level barriers included provider inexperience with antiviral treatment and/or reluctance of providers to refer patients for treatment. There are many ongoing challenges that are unique to managing this patient population effectively. Documenting and evaluating these obstacles are critical steps to managing and caring for these individuals in the future. In order to improve uptake of HCV therapy in persons with HIV/HCV co-infection, it is essential that barriers, both new and ongoing, are addressed, otherwise, treatment is of little benefit

Differences in outpatient care and treatment utilization for patients with HIV/HCV coinfection, HIV, and HCV monoinfection, a cross-sectional study

Background Few studies have explored how utilization of outpatient services differ for HIV/HCV coinfected patients compared to HIV or HCV monoinfected patients. The objectives of this study were to (1) compare annual outpatient clinic visit rates between coinfected and monoinfected patients, (2) to compare utilization of HIV and HCV therapies between coinfected and monoinfected patients, and (3) to identify factors associated with therapy utilization. Methods Data were from the 2005–2010 U.S. National Hospital Ambulatory Medical Care Surveys. Clinic visits with a primary or secondary ICD-9-CM codes for HIV or HCV were included. Coinfection included visits with codes for both HIV and HCV. Monoinfection only included codes for HIV or HCV, exclusively. Patients <15 years of age at time of visit were excluded. Predictors of HIV and HCV therapy were determined by logistic regressions. Visits were computed using survey weights. Results 3,021 visits (11,352,000 weighted visits) met study criteria for patients with HIV/HCV (8%), HIV (70%), or HCV (22%). The HCV subgroup was older in age and had the highest proportion of females and whites as compared to the HIV/HCV and HIV subgroups. Comorbidities varied significantly across the three subgroups (HIV/HCV, HIV, HCV): current tobacco use (40%, 27%, 30%), depression (32%, 23%, 24%), diabetes (9%, 10%, 17%), and chronic renal failure (<1%, 3%, 5%), (p < 0.001 for all variables). Annual visit rates were highest in those with HIV, followed by HIV/HCV, but consistently lower in those with HCV. HIV therapy utilization increased for both HIV/HCV and HIV subgroups. HCV therapy utilization remained low for both HIV/HCV and HCV subgroups for all years. Coinfection was an independent predictor of HIV therapy, but not of HCV therapy. Conclusion There is a critical need for system-level interventions that reduce barriers to outpatient care and improve uptake of HCV therapy for patients with HIV/HCV coinfection

Dietary Selenium Deficiency Exacerbates DSS-Induced Epithelial Injury and AOM/DSS-Induced Tumorigenesis.

Selenium (Se) is an essential micronutrient that exerts its functions via selenoproteins. Little is known about the role of Se in inflammatory bowel disease (IBD). Epidemiological studies have inversely correlated nutritional Se status with IBD severity and colon cancer risk. Moreover, molecular studies have revealed that Se deficiency activates WNT signaling, a pathway essential to intestinal stem cell programs and pivotal to injury recovery processes in IBD that is also activated in inflammatory neoplastic transformation. In order to better understand the role of Se in epithelial injury and tumorigenesis resulting from inflammatory stimuli, we examined colonic phenotypes in Se-deficient or -sufficient mice in response to dextran sodium sulfate (DSS)-induced colitis, and azoxymethane (AOM) followed by cyclical administration of DSS, respectively. In response to DSS alone, Se-deficient mice demonstrated increased morbidity, weight loss, stool scores, and colonic injury with a concomitant increase in DNA damage and increases in inflammation-related cytokines. As there was an increase in DNA damage as well as expression of several EGF and TGF-β pathway genes in response to inflammatory injury, we sought to determine if tumorigenesis was altered in the setting of inflammatory carcinogenesis. Se-deficient mice subjected to AOM/DSS treatment to model colitis-associated cancer (CAC) had increased tumor number, though not size, as well as increased incidence of high grade dysplasia. This increase in tumor initiation was likely due to a general increase in colonic DNA damage, as increased 8-OHdG staining was seen in Se-deficient tumors and adjacent, non-tumor mucosa. Taken together, our results indicate that Se deficiency worsens experimental colitis and promotes tumor development and progression in inflammatory carcinogenesis

National trends in hospitalization and mortality rates for patients with HIV, HCV, or HIV/HCV coinfection from 1996–2010 in the United States: a cross-sectional study

Abstract Background The comparative impact of chronic viral monoinfection versus coinfection on inpatient outcomes and health care utilization is relatively unknown. This study examined trends, inpatient utilization, and hospital outcomes for patients with HIV, HCV, or HIV/HCV coinfection. Methods Data were from the 1996–2010 National Hospital Discharge Surveys. Hospitalizations with primary ICD-9-CM codes for HIV or HCV were included for HIV and HCV monoinfection, respectfully. Coinfection included both HIV and HCV codes. Demographic characteristics, select comorbidities, procedural interventions, average hospital length of stay (LOS), and discharge status were compared by infection status (HIV, HCV, HIV/HCV). Annual disease estimates and survey weights were used to generate hospitalization rates. Results ~6.6 million hospitalizations occurred in patients with HIV (39%), HCV (56%), or HIV/HCV (5%). The hospitalization rate (hospitalizations per 100 persons with infection) decreased in the HIV group (29.8 in 1996; 5.3 in 2010), decreased in the HIV/HCV group (2.0 in 1996; 1.5 in 2010), yet increased in the HCV group (0.2 in 1996; 0.9 in 2010). Median LOS from 1996 to 2010 (days, interquartile range) decreased in all groups: HIV, 6 (3–10) to 4 (3–8); HCV, 5 (3–9) to 4 (2–6); HIV/HCV, 6 (4–11) to 4 (2–7). Age-adjusted mortality rates decreased for all three groups. The rate of decline was least pronounced for those with HCV monoinfection. Conclusion Hospitalizations have declined more rapidly for patients with HIV infection (including HIV/HCV coinfection) than for patients with HCV infection. This growing disparity between HIV and HCV underscores the need to allocate more resources to HCV care in hopes that similar large-scale improvements can also be accomplished for patients with HCV

Selenoprotein P Influences Colitis-Induced Tumorigenesis by Mediating Stemness and Oxidative Damage.

Patients with inflammatory bowel disease are at increased risk for colon cancer due to augmented oxidative stress. These patients also have compromised antioxidant defenses as the result of nutritional deficiencies. The micronutrient selenium is essential for selenoprotein production and is transported from the liver to target tissues via selenoprotein P (SEPP1). Target tissues also produce SEPP1, which is thought to possess an endogenous antioxidant function. Here, we have shown that mice with Sepp1 haploinsufficiency or mutations that disrupt either the selenium transport or the enzymatic domain of SEPP1 exhibit increased colitis-associated carcinogenesis as the result of increased genomic instability and promotion of a protumorigenic microenvironment. Reduced SEPP1 function markedly increased M2-polarized macrophages, indicating a role for SEPP1 in macrophage polarization and immune function. Furthermore, compared with partial loss, complete loss of SEPP1 substantially reduced tumor burden, in part due to increased apoptosis. Using intestinal organoid cultures, we found that, compared with those from WT animals, Sepp1-null cultures display increased stem cell characteristics that are coupled with increased ROS production, DNA damage, proliferation, decreased cell survival, and modulation of WNT signaling in response to H2O2-mediated oxidative stress. Together, these data demonstrate that SEPP1 influences inflammatory tumorigenesis by affecting genomic stability, the inflammatory microenvironment, and epithelial stem cell functions

2nd Annual Computer & Technology Law Institute

Materials from the 2nd Annual Computer & Technology Law Institute held by UK/CLE in March 2000

Rule-Based Cell Systems Model of Aging using Feedback Loop Motifs Mediated by Stress Responses

Investigating the complex systems dynamics of the aging process requires integration of a broad range of cellular processes describing damage and functional decline co-existing with adaptive and protective regulatory mechanisms. We evolve an integrated generic cell network to represent the connectivity of key cellular mechanisms structured into positive and negative feedback loop motifs centrally important for aging. The conceptual network is casted into a fuzzy-logic, hybrid-intelligent framework based on interaction rules assembled from a priori knowledge. Based upon a classical homeostatic representation of cellular energy metabolism, we first demonstrate how positive-feedback loops accelerate damage and decline consistent with a vicious cycle. This model is iteratively extended towards an adaptive response model by incorporating protective negative-feedback loop circuits. Time-lapse simulations of the adaptive response model uncover how transcriptional and translational changes, mediated by stress sensors NF-κB and mTOR, counteract accumulating damage and dysfunction by modulating mitochondrial respiration, metabolic fluxes, biosynthesis, and autophagy, crucial for cellular survival. The model allows consideration of lifespan optimization scenarios with respect to fitness criteria using a sensitivity analysis. Our work establishes a novel extendable and scalable computational approach capable to connect tractable molecular mechanisms with cellular network dynamics underlying the emerging aging phenotype