An engineering analysis of a closed cycle plant growth module

The SOLGEM model is a numerical engineering model which solves the flow and energy balance equations for the air flowing through a growing environment, assuming quasi-steady state conditions within the system. SOLGEM provides a dynamic simulation of the controlled environment system in that the temperature and flow conditions of the growing environment are estimated on an hourly basis in response to the weather data and the plant growth parameters. The flow energy balance considers the incident solar flux; incoming air temperature, humidity, and flow rate; heat exchange with the roof and floor; and heat and moisture exchange with the plants. A plant transpiration subroutine was developed based plant growth research facility, intended for the study of bioregenerative life support theories. The results of a performance analysis of the plant growth module are given. The estimated energy requirements of the module components and the total energy are given

Analysis of enriched rare variants in JPH2-encoded junctophilin-2 among Greater Middle Eastern individuals reveals a novel homozygous variant associated with neonatal dilated cardiomyopathy.

Junctophilin-2 (JPH2) is a part of the junctional membrane complex that facilitates calcium-handling in the cardiomyocyte. Previously, missense variants in JPH2 have been linked to hypertrophic cardiomyopathy; however, pathogenic "loss of function" (LOF) variants have not been described. Family-based genetic analysis of GME individuals with cardiomyopathic disease identified an Iranian patient with dilated cardiomyopathy (DCM) as a carrier of a novel, homozygous single nucleotide insertion in JPH2 resulting in a stop codon (JPH2-p.E641*). A second Iranian family with consanguineous parents hosting an identical heterozygous variant had 2 children die in childhood from cardiac failure. To characterize ethnicity-dependent genetic variability in JPH2 and to identify homozygous JPH2 variants associated with cardiac disease, we identified variants in JPH2 in a worldwide control cohort (gnomAD) and 2 similar cohorts from the Greater Middle East (GME Variome, Iranome). These were compared against ethnicity-matched clinical whole exome sequencing (WES) referral tests and a case cohort of individuals with hypertrophic cardiomyopathy (HCM) based on comprehensive review of the literature. Worldwide, 1.45% of healthy individuals hosted a rare JPH2 variant with a significantly higher proportion among GME individuals (4.45%); LOF variants were rare overall (0.04%) yet were most prevalent in GME (0.21%). The increased prevalence of LOF variants in GME individuals was corroborated among region-specific, clinical WES cohorts. In conclusion, we report ethnic-specific differences in JPH2 rare variants, with GME individuals being at higher risk of hosting homozygous LOF variants. This conclusion is supported by the identification of a novel JPH2 LOF variant confirmed by segregation analysis resulting in autosomal recessive pediatric DCM due to presumptive JPH2 truncation

Dissemination of the nurse-administered Tobacco Tactics intervention versus usual care in six Trinity community hospitals: study protocol for a comparative effectiveness trial

Abstract Background The objectives of this smoking cessation study among hospitalized smokers are to: 1) determine provider and patient receptivity, barriers, and facilitators to implementing the nurse-administered, inpatient Tobacco Tactics intervention versus usual care using face-to-face feedback and surveys; 2) compare the effectiveness of the nurse-administered, inpatient Tobacco Tactics intervention versus usual care across hospitals, units, and patient characteristics using thirty-day point prevalence abstinence at thirty days and six months (primary outcome) post-recruitment; and 3) determine the cost-effectiveness of the nurse-administered, inpatient Tobacco Tactics intervention relative to usual care including cost per quitter, cost per life-year saved, and cost per quality-adjusted life-year saved. Methods/Design This effectiveness study will be a quasi-experimental design of six Michigan community hospitals of which three will get the nurse-administered Tobacco Tactics intervention and three will provide their usual care. In both the intervention and usual care sites, research assistants will collect data from patients on their smoking habits and related variables while in the hospital and at thirty days and six months post-recruitment. The intervention will be integrated into the experimental sites by a research nurse who will train Master Trainers at each intervention site. The Master Trainers, in turn, will teach the intervention to all staff nurses. Research nurses will also conduct formative evaluation with nurses to identify barriers and facilitators to dissemination. Descriptive statistics will be used to summarize the results of surveys administered to nurses, nurses’ participation rates, smokers’ receipt of specific cessation services, and satisfaction with services. General estimating equation analyses will be used to determine differences between intervention groups on satisfaction and quit rates, respectively, with adjustment for the clustering of patients within hospital units. Regression analyses will test the moderation of the effects of the interventions by patient characteristics. Cost-effectiveness will be assessed by constructing three ratios including cost per quitter, cost per life-year saved, and cost per quality-adjusted life-year saved. Discussion Given that nurses represent the largest group of front-line providers, this intervention, if proven effective, has the potential for having a wide reach and thus decrease smoking, morbidity and mortality among inpatient smokers. Trial registration Dissemination of Tobacco Tactics for Hospitalized Smokers NCT01309217http://deepblue.lib.umich.edu/bitstream/2027.42/109462/1/13063_2011_Article_1134.pd

Implementation of the Tobacco Tactics intervention versus usual care in Trinity Health community hospitals

Abstract Background Guided by the Reach, Effectiveness, Adoption, Implementation, and Maintenance (RE-AIM) implementation framework, a National Institutes of Health-sponsored study compared the nurse-administered Tobacco Tactics intervention to usual care. A prior paper describes the effectiveness of the Tobacco Tactics intervention. This subsequent paper provides data describing the remaining constructs of the RE-AIM framework. Methods This pragmatic study used a mixed methods, quasi-experimental design in five Michigan community hospitals of which three received the nurse-administered Tobacco Tactics intervention and two received usual care. Nurses and patients were surveyed pre- and post-intervention. Measures included reach (patient participation rates, characteristics, and receipt of services), adoption (nurse participation rates and characteristics), implementation (pre-to post-training changes in nurses' attitudes, delivery of services, barriers to implementation, opinions about training, documentation of services, and numbers of volunteer follow-up phone calls), and maintenance (continuation of the intervention once the study ended). Results Reach: Patient participation rates were 71.5 %. Compared to no change in the control sites, there were significant pre- to post-intervention increases in self-reported receipt of print materials in the intervention hospitals (n = 1370, p < 0.001). Adoption: In the intervention hospitals, all targeted units and several non-targeted units participated; 76.0 % (n = 1028) of targeted nurses and 317 additional staff participated in the training, and 92.4 % were extremely or somewhat satisfied with the training. Implementation: Nurses in the intervention hospitals reported increases in providing advice to quit, counseling, medications, handouts, and DVD (all p < 0.05) and reported decreased barriers to implementing smoking cessation services (p < 0.001). Qualitative comments were very positive (“user friendly,” “streamlined,” or “saves time”), although problems with showing patients the DVD and charting in the electronic medical record were noted. Maintenance: Nurses continued to provide the intervention after the study ended. Conclusions Given that nurses represent the largest group of front-line providers, this intervention, which meets Joint Commission guidelines for treating inpatient smokers, has the potential to have a wide reach and to decrease smoking, morbidity, and mortality among inpatient smokers. As we move toward more population-based interventions, the RE-AIM framework is a valuable guide for implementation. Trial registration ClinicalTrials.gov, NCT0130921

What factors affect patients' recall of general practitioners' advice?

<p>Abstract</p> <p>Background</p> <p>In order for patients to adhere to advice, provided by family doctors, they must be able to recall it afterwards. However, several studies have shown that most patients do not fully understand or memorize it. The aim of this study was to determine the influence of demographic characteristics, education, amount of given advice and the time between consultations on recalled advice.</p> <p>Methods</p> <p>A prospective survey, lasting 30 months, was conducted in an urban family practice in Slovenia. Logistic regression analysis was used to identify the risk factors for poorer recall.</p> <p>Results</p> <p>250 patients (87.7% response rate) received at least one and up to four pieces of advice (2.4 ± 0.8). A follow-up consultation took place at 47.4 ± 35.2 days. The determinants of better recall were high school (OR 0.4, 95% CI 0.15-0.99, p = 0.049) and college education (OR 0.3, 95% CI 0.10-1.00, p = 0.050), while worse recall was determined by number of given instructions three or four (OR 26.1, 95% CI 3.15-215.24, p = 0.002; OR 56.8, 95% CI 5.91-546.12, p < 0.001, respectively) and re-test interval: 15-30 days (OR 3.3, 95% CI 1.06-10.13, p = 0.040), 31-60 days (OR 3.2, 95% CI 1.28-8.07, p = 0.013) and more than 60 days (OR 2.5, 95% CI 1.05-6.02, p = 0.038).</p> <p>Conclusions</p> <p>Education was an important determinant factor and warrants further study. Patients should be given no more than one or two instructions in a consultation. When more is needed, the follow-up should be within the next 14 days, and would be of a greater benefit to higher educated patients.</p

The cardiac troponin C mutation Leu29Gln found in a patient with hypertrophic cardiomyopathy does not alter contractile parameters in skinned murine myocardium

The present study investigates the effects of the first mutation of troponin C (hcTnCL29Q) found in a patient with hypertrophic cardiomyopathy (HCM) on force–pCa relations and the interplay with phosphorylation of sarcomeric PKA substrates. In triton-skinned murine cardiac fibers, the endogenous mcTnC was extracted and the fibers were subsequently reconstituted with recombinant wild-type and mutant hcTnC. Force–pCa relations of preparations containing hcTnCL29Q or hcTnCWT were similar. Incubation of fibers reconstituted with the recombinant proteins with phosphatase to dephosphorylate sarcomeric PKA substrates induced an increase in Ca2+ sensitivity, slightly more pronounced (0.04 pCa units) in hcTnCL29Q-containing fibers. Incubation of the dephosphorylated fibers with PKA induced significant rightward shifts of force–pCa relations of similar magnitude with both, hcTnCL29Q and hcTnCWT. No significant effects of hcTnCL29Q on the velocity of unloaded shortening were observed. In conclusion, no major differences in contractile parameters of preparations containing hcTnCL29Q compared to hcTnCWT were observed. Therefore, it appears unlikely that hcTnCL29Q induces the development of HCM by affecting the regulation of Ca2+-activated force and interference with PKA-mediated modulation of the Ca2+ sensitivity of contraction

PI3Ks Maintain the Structural Integrity of T-Tubules in Cardiac Myocytes

Phosphoinositide 3-kinases (PI3Ks) regulate numerous physiological processes including some aspects of cardiac function. Although regulation of cardiac contraction by individual PI3K isoforms has been studied, little is known about the cardiac consequences of downregulating multiple PI3Ks concurrently.Genetic ablation of both p110α and p110β in cardiac myocytes throughout development or in adult mice caused heart failure and death. Ventricular myocytes from double knockout animals showed transverse tubule (T-tubule) loss and disorganization, misalignment of L-type Ca(2+) channels in the T-tubules with ryanodine receptors in the sarcoplasmic reticulum, and reduced Ca(2+) transients and contractility. Junctophilin-2, which is thought to tether T-tubules to the sarcoplasmic reticulum, was mislocalized in the double PI3K-null myocytes without a change in expression level.PI3K p110α and p110β are required to maintain the organized network of T-tubules that is vital for efficient Ca(2+)-induced Ca(2+) release and ventricular contraction. PI3Ks maintain T-tubule organization by regulating junctophilin-2 localization. These results could have important medical implications because several PI3K inhibitors that target both isoforms are being used to treat cancer patients in clinical trials

TRAF6 Promotes Myogenic Differentiation via the TAK1/p38 Mitogen-Activated Protein Kinase and Akt Pathways

p38 mitogen-activated protein kinase (MAPK) is an essential kinase involved in myogenic differentiation. Although many substrates of p38 MAPK have been identified, little is known about its upstream activators during myogenic differentiation. TRAF6 is known to function in cytokine signaling during inflammatory responses. However, not much is known about its role in myogenic differentiation and muscle regeneration. We showed here that TRAF6 and its intrinsic ubiquitin E3 ligase activity are required for myogenic differentiation. In mouse myoblasts, knockdown of TRAF6 compromised the p38 MAPK and Akt pathways, while deliberate activation of either pathway rescued the differentiation defect caused by TRAF6 knockdown. TAK1 acted as a key signal transducer downstream of TRAF6 in myogenic differentiation. In vivo, knockdown of TRAF6 in mouse muscles compromised the injury-induced muscle regeneration without impairing macrophage infiltration and myoblast proliferation. Collectively, we demonstrated that TRAF6 promotes myogenic differentiation and muscle regeneration via the TAK1/p38 MAPK and Akt pathways

Dunning rat prostate adenocarcinomas and alternative splicing reporters: powerful tools to study epithelial plasticity in prostate tumors in vivo

Using alternative splicing reporters we have previously observed mesenchymal epithelial transitions in Dunning AT3 rat prostate tumors. We demonstrate here that the Dunning DT and AT3 cells, which express epithelial and mesenchymal markers, respectively, represent an excellent model to study epithelial transitions since these cells recapitulate gene expression profiles observed during human prostate cancer progression. In this manuscript we also present the development of two new tools to study the epithelial transitions by imaging alternative splicing decisions: a bichromatic fluorescence reporter to evaluate epithelial transitions in culture and in vivo, and a luciferase reporter to visualize the distribution of mesenchymal epithelial transitions in vivo

Transverse tubule remodelling: a cellular pathology driven by both sides of the plasmalemma?

Transverse (t)-tubules are invaginations of the plasma membrane that form a complex network of ducts, 200–400 nm in diameter depending on the animal species, that penetrates deep within the cardiac myocyte, where they facilitate a fast and synchronous contraction across the entire cell volume. There is now a large body of evidence in animal models and humans demonstrating that pathological distortion of the t-tubule structure has a causative role in the loss of myocyte contractility that underpins many forms of heart failure. Investigations into the molecular mechanisms of pathological t-tubule remodelling to date have focused on proteins residing in the intracellular aspect of t-tubule membrane that form linkages between the membrane and myocyte cytoskeleton. In this review, we shed light on the mechanisms of t-tubule remodelling which are not limited to the intracellular side. Our recent data have demonstrated that collagen is an integral part of the t-tubule network and that it increases within the tubules in heart failure, suggesting that a fibrotic mechanism could drive cardiac junctional remodelling. We examine the evidence that the linkages between the extracellular matrix, t-tubule membrane and cellular cytoskeleton should be considered as a whole when investigating the mechanisms of t-tubule pathology in the failing heart