943 research outputs found

    Non-pharmacological interventions to reduce psychological distress in patients undergoing diagnostic cardiac catheterization: a rapid review

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    Abstract Background: Cardiac catheterization is the standard procedure for the diagnosis of coronary heart disease. The threat physically and emotionally from this procedure can effect the patient’s perception of their health. The heightened psychological distress associated with this diagnostic procedure can cause adverse patient outcomes. Non-pharmacologic interventions have been implemented to reduce psychological distress associated with cardiac catheterization. Aims: The objective of this rapid review is to assess the efficacy of non-pharmacologic interventions (procedural education, relaxation techniques, psychological preparation) on psychological distress experienced by patients as they undergo a cardiac catheterization. Methods: Published, peer-reviewed, English-language intervention studies from 1981 to 2014 were identified in a search of CINAHL, Medline, and Cochrane Library. Eligible studies included adults undergoing cardiac catheterization. Studies included in this review used experimental and quasi-experimental designs and assessed at least one primary outcome: anxiety, depression, and pain to test non-pharmacologic interventions pre and post-cardiac catheterization. Researchers independently extracted data from included studies and completed a quality assessment using a published tool. Data was synthesised as a narrative. Results: There were 29 eligible experimental and quasi-experimental studies that tested the 3 interventions (n=2504). Findings suggest that non-pharmacologic interventions were able to effectively reduce psychological distress in some patients undergoing cardiac catheterization. Conclusion: Evidence is stronger in recent studies that non-pharmacologic interventions of procedural education and psychological preparation can reduce psychological distress in patients undergoing cardiac catheterization. Further research is needed to define the various relaxation techniques that can be effectively implemented for patients undergoing cardiac catheterization

    Merozoite surface protein-3α is a reliable marker for population genetic analysis of Plasmodium vivax

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    BACKGROUND: The knowledge on population structure of the parasite isolates has contributed greatly to understanding the dynamics of the disease transmission for designing and evaluating malaria vaccines as well as for drug applications. msp-1 and msp-3α genes have been used as a genetic marker in population studies of Plasmodium vivax isolates. In this study, msp-3α was compared and assessed with msp-1 marker in order to find whether msp-3α is a reliable genetic marker for P. vivax population studies. METHODS: This comparative study was designed and carried out as the first assessment of diversity in Pvmsp-3α gene by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in the 50 northern and 94 southern P. vivax isolates from Iran, which had been analysed before for msp-1 gene. RESULTS: Three allele size as, Type A (1.8 kb), Type B (1.5 kb) and Type C (1.2 kb) have been detected among both northern and southern isolates based on PCR results. Type C (70%) and Type A (68.7%) were the predominant fragments among northern and southern parasites, respectively. 99 distinct Pvmsp-3α fragments defined by the size were detected in the 94 southern samples by PCR analysis. However, no mixed genotype infections have been detected among northern isolates. Based on restriction pattern from digestion with Hha I and Alu I 12 and 49 distinct allelic variants have been detected among 50 northern and 94 southern isolates. However, based on msp-1 gene, 30 distinct variants identified in all 146-sequenced Iranian P. vivax isolate. CONCLUSION: The results suggested that PCR-RFLP on msp-3α gene is an adequate, applicable and easily used technique for molecular epidemiology studies of P. vivax isolates without the need for further sequencing analysis

    Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015

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    SummaryBackground The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context. Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI). Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa. Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Funding Bill & Melinda Gates Foundation

    How do nutrient conditions and species identity influence the impact of mesograzers in eelgrass-epiphyte systems?

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    Coastal eutrophication is thought to cause excessive growth of epiphytes in eelgrass beds, threatening the health and survival of these ecologically and economically valuable ecosystems worldwide. Mesograzers, small crustacean and gastropod grazers, have the potential to prevent seagrass loss by grazing preferentially and efficiently on epiphytes. We tested the impact of three mesograzers on epiphyte biomass and eelgrass productivity under threefold enriched nutrient concentrations in experimental indoor mesocosm systems under summer conditions. We compared the results with earlier identical experiments that were performed under ambient nutrient supply. The isopod Idotea baltica, the periwinkle Littorina littorea, and the small gastropod Rissoa membranacea significantly reduced epiphyte load under high nutrient supply with Rissoa being the most efficient grazer, but only high densities of Littorina and Rissoa had a significant positive effect on eelgrass productivity. Although all mesograzers increased epiphyte ingestion with higher nutrient load, most likely as a functional response to the quantitatively and qualitatively better food supply, the promotion of eelgrass growth by Idotea and Rissoa was diminished compared to the study performed under ambient nutrient supply. Littorina maintained the level of its positive impact on eelgrass productivity regardless of nutrient concentrations

    CCR2 and CXCR3 agonistic chemokines are differently expressed and regulated in human alveolar epithelial cells type II

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    The attraction of leukocytes from circulation to inflamed lungs depends on the activation of both the leukocytes and the resident cells within the lung. In this study we determined gene expression and secretion patterns for monocyte chemoattractant protein-1 (MCP-1/CCL2) and T-cell specific CXCR3 agonistic chemokines (Mig/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11) in TNF-α-, IFN-γ-, and IL-1β-stimulated human alveolar epithelial cells type II (AEC-II). AEC-II constitutively expressed high level of CCL2 mRNA in vitro and in situ , and released CCL2 protein in vitro . Treatment of AEC-II with proinflammatory cytokines up-regulated both CCL2 mRNA expression and release of immunoreactive CCL2, whereas IFN-γ had no effect on CCL2 release. In contrast, CXCR3 agonistic chemokines were not detected in freshly isolated AEC-II or in non-stimulated epithelial like cell line A549. IFN-γ, alone or in combination with IL-1β and TNF-α resulted in an increase in CXCL10, CXCL11, and CXCL9 mRNA expression and generation of CXCL10 protein by AEC-II or A549 cells. CXCL10 gene expression and secretion were induced in dose-dependent manner after cytokine-stimulation of AEC-II with an order of potency IFN-γ>>IL-1β ≥ TNF-α. Additionally, we localized the CCL2 and CXCL10 mRNAs in human lung tissue explants by in situ hybridization, and demonstrated the selective effects of cytokines and dexamethasone on CCL2 and CXCL10 expression. These data suggest that the regulation of the CCL2 and CXCL10 expression exhibit significant differences in their mechanisms, and also demonstrate that the alveolar epithelium contributes to the cytokine milieu of the lung, with the ability to respond to locally generated cytokines and to produce potent mediators of the local inflammatory response

    Diagnosis and treatment delay among pulmonary tuberculosis patients identified using the Taiwan reporting enquiry system, 2002–2006

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    <p>Abstract</p> <p>Background</p> <p>The tuberculosis reporting enquiry system was launched in Taiwan in 2001. Tuberculosis has been categorized as the third most important notifiable disease in Taiwan and the time required for reporting has been shortened to 7 days.</p> <p>Methods</p> <p>A total of 114,827 cases were reported using the Taiwan enquiry system between 2002 and 2006; of these, 26,027 (22.7%) were finally diagnosed as not being tuberculosis, 7,005 (8.2%) were diagnosed as extra-pulmonary tuberculosis and 3,677 (3.2%) were not a first-time diagnosis of tuberculosis, and these cases were hence excluded. Diagnosis time was defined as the length of time between the first medical examination (including chest radiography, sputum smear or sputum culture) to the diagnosis of PTB; treatment time was defined as the period from the diagnosis of PTB to the initiation of treatment. Using the cut-off at the 75<sup>th </sup>percentile, a period of longer than 9 days was defined as a <it>diagnosis delay </it>and a period of longer than 2 days as a <it>treatment delay</it>. Multiple logistic regression analysis was applied to analyze the risk factors associated with these delays.</p> <p>Results</p> <p>During the five-year study period, among the 78,118 new PTB patients reported in Taiwan, the mean diagnosis and treatment times were 12 and 5 days and the median times 1 day and 0 days, respectively. In total, 24.9% of the new PTB patients' diagnosis time delays were longer than 9 days and 20.3% of the patients' treatment time delays were longer than 2 days. The main factors associated with diagnosis delay included age, reporting year, living with family and a positive sputum culture (<it>p </it>< 0.0001); the risk factors significantly associated with treatment delay were increased age, an aboriginal ethnic background, a positive sputum culture and diagnosis at a non-medical center (<it>p </it>< 0.0001).</p> <p>Conclusion</p> <p>The Taiwan TB reporting enquiry system has successfully increased the confirmed PTB reporting rate from 64.4% to 71.5%. Greater age and a positive sputum culture were both found to significantly increase both diagnosis and treatment delays; treatment delay is also significantly affected by the patient having an aboriginal ethnic background and being diagnosed at a non-medical center.</p

    Degradation of Host Sphingomyelin Is Essential for Leishmania Virulence

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    In eukaryotes, sphingolipids (SLs) are important membrane components and powerful signaling molecules. In Leishmania, the major group of SLs is inositol phosphorylceramide (IPC), which is common in yeast and Trypanosomatids but absent in mammals. In contrast, sphingomyelin is not synthesized by Leishmania but is abundant in mammals. In the promastigote stage in vitro, Leishmania use SL metabolism as a major pathway to produce ethanolamine (EtN), a metabolite essential for survival and differentiation from non-virulent procyclics to highly virulent metacyclics. To further probe SL metabolism, we identified a gene encoding a putative neutral sphingomyelinase (SMase) and/or IPC hydrolase (IPCase), designated ISCL (Inositol phosphoSphingolipid phospholipase C-Like). Despite the lack of sphingomyelin synthesis, L. major promastigotes exhibited a potent SMase activity which was abolished upon deletion of ISCL, and increased following over-expression by episomal complementation. ISCL-dependent activity with sphingomyelin was about 20 fold greater than that seen with IPC. Null mutants of ISCL (iscl−) showed modest accumulation of IPC, but grew and differentiated normally in vitro. Interestingly, iscl− mutants did not induce lesion pathology in the susceptible BALB/c mice, yet persisted indefinitely at low levels at the site of infection. Notably, the acute virulence of iscl− was completely restored by the expression of ISCL or heterologous mammalian or fungal SMases, but not by fungal proteins exhibiting only IPCase activity. Together, these findings strongly suggest that degradation of host-derived sphingomyelin plays a pivotal role in the proliferation of Leishmania in mammalian hosts and the manifestation of acute disease pathology
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