426 research outputs found

    Treatment of natural fiber for application in concrete pavement

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    Concrete crack is one of the main problems observed in concrete technology due to drying shrinkage. Incorporating fibers in concrete production is one of the mechanisms implemented to mitigate cracks. Nowadays, investigators concentrate on different techniques to replace human-made fiber with existing natural fibers for fiber-reinforced composite material. Utilization of natural fiber has an initiation for the development of eco-friendly materials by reducing damages caused by human-made materials and saving nonrenewable resources. Natural fibers are readily and abundantly available, sustainable, and biodegradable, with low cost and low density, and have superior specific properties. Nevertheless, there are some limitations of natural fiber compared to human-made fiber. Consequently, significant energy was applied to alter natural fiber’s surface and morphology using physical, chemical, and biological treatment techniques to overcome the limitation. The primary intention of surface treatment is to modify the bond between the fiber surface and the polymer matrix. However, based on this literature review, there were no specific treatment techniques to be followed to select the best one from the others as criteria. It should include all parameters to consider starting from the stage from the cradle to the grave, cost of chemicals, transportation, and labors, including energy consumption and effluent energy. Additionally, their environmental effect also investigated in detail to compare each other

    Knowledge and perception towards net care and repair practice in Ethiopia.

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    BACKGROUND: Long-lasting insecticidal nets (LLINs) are a key malaria control intervention. Although LLINs are presumed to be effective for 3 years under field or programmatic conditions, net care and repair approaches by users influence the physical and chemical durability. Understanding how knowledge, perception and practices influence net care and repair practices could guide the development of targeted behavioural change communication interventions related to net care and repair in Ethiopia and elsewhere. METHODS: This population-based, household survey was conducted in four regions of Ethiopia [Amhara, Oromia, Tigray, Southern Nations Nationalities Peoples Region (SNNPR)] in June 2015. A total of 1839 households were selected using multi-stage sampling procedures. The household respondents were the heads of households. A questionnaire was administered and the data were captured electronically. STATA software version 12 was used to analyse the data. Survey commands were used to account for the multi-stage sampling approach. Household descriptive statistics related to characteristics and levels of knowledge and perception on net care and repair are presented. Ordinal logistic regression was used to identify factors associated with net care and repair perceptions. RESULTS: Less than a quarter of the respondents (22.3%: 95% CI 20.4-24.3%) reported adequate knowledge of net care and repair; 24.6% (95% CI 22.7-26.5%) of the respondents reported receiving information on net care and repair in the previous 6 months. Thirty-five per cent of the respondents (35.1%: 95% CI 32.9-37.4%) reported positive perceptions towards net care and repair. Respondents with adequate knowledge on net care and repair (AOR 1.58: 95% CI 1.2-2.02), and those who discussed net care and repair with their family (AOR 1.47: 95% CI 1.14-1.89) had higher odds of having positive perceptions towards net care and repair. CONCLUSIONS: The low level of reported knowledge on net care and repair, as well as the low level of reported positive perception towards net repair need to be addressed. Targeted behavioural change communication campaigns could be used to target specific groups; increased net care and repair would lead to longer lasting nets

    Significance of placental cord insertion site in twin pregnancy

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    Objective To investigate the association between abnormal cord insertion and the development of twin‐specific complications, including birth‐weight discordance, selective fetal growth restriction (sFGR) and twin‐to‐twin transfusion syndrome (TTTS). Methods This was a single center retrospective cohort study of twin pregnancies. Abnormal cord insertion was defined as either marginal (umbilical cord attachment site less than 2 cm to the nearest margin of the placental disc) or velamentous (cord attached to the membrane before reaching the placental disc with clear evidence of vessels traversing the membranes to connect with the placental disc), as described in placental pathology reports. Twins with major structural or chromosomal abnormalities and monochorionic monoamniotic twins were not included in the study. Information on the pregnancies, ultrasound findings, prenatal investigations and interventions was obtained from the electronic ultrasound database, while data on placental histopathological findings, pregnancy outcome, mode of delivery, birth weight, gestational age at delivery and admission to the neonatal intensive care unit were obtained from maternity records. Categorical variables were compared using the chi‐square or Fisher's exact test, while continuous variables were compared using the Student's t‐test, ANOVA for multiple comparisons and the Kruskal–Wallis test. Results Of the 497 twin pregnancies included in the analysis, 351 (70.6%) were dichorionic and 146 (29.4%) were monochorionic. The incidence of birth‐weight discordance of 25% or more was significantly higher in pregnancies with velamentous and those with marginal cord insertions compared to those with normal cord insertion (24.0%, 15.3% vs 7.6%, P < 0.001 and P = 0.020, respectively). In pregnancies with birth‐weight discordance of 25% or more, the smaller twins had significantly higher prevalence of velamentous (13.8%) and marginal (34.2%) cord insertions compared with the larger twins (1.8% and 18.5%, respectively, P < 0.001). The smaller twins of the monochorionic diamniotic pregnancies showed an even higher prevalence of velamentous (29.5%) and marginal (40.9%) cord insertions compared with the larger twins (2.3% and 31.5%, respectively, P < 0.001). Compared with the normal cord insertion group, only velamentous insertion was associated significantly with the risk of sFGR (odds ratio (OR), 9.24 (95% CI, 2.05–58.84), P < 0.001) and birth‐weight discordance of 20% or more (OR, 4.34 (95% CI, 1.36–14.61), P = 0.007) and 25% or more (OR, 6.81 (95% CI, 1.67–34.12), P = 0.003) in monochorionic twin pregnancies. There was no significant association between velamentous cord insertion and TTTS (P = 0.591), or between marginal cord insertion and the development of sFGR (P = 0.233), birth‐weight discordance of 25% or more (P = 0.114) or TTTS (P = 0.487). Subgroup analysis of dichorionic twins showed that abnormal cord insertion was not associated with the risk of birth‐weight discordance (P = 0.999), sFGR (P = 0.308), composite neonatal adverse outcome (P = 0.637) or intrauterine death (P = 0.349). Conclusion Monochorionic twins with velamentous cord insertion are at increased risk of birth‐weight discordance and sFGR. Sonographic delineation of placental cord insertion could be of value in the antenatal stratification of twin pregnancies. Prospective studies are required to assess the value and predictive accuracy of this potential screening marker

    Drug-gene interactions of antihypertensive medications and risk of incident cardiovascular disease: a pharmacogenomics study from the CHARGE consortium

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    Background Hypertension is a major risk factor for a spectrum of cardiovascular diseases (CVD), including myocardial infarction, sudden death, and stroke. In the US, over 65 million people have high blood pressure and a large proportion of these individuals are prescribed antihypertensive medications. Although large long-term clinical trials conducted in the last several decades have identified a number of effective antihypertensive treatments that reduce the risk of future clinical complications, responses to therapy and protection from cardiovascular events vary among individuals. Methods Using a genome-wide association study among 21,267 participants with pharmaceutically treated hypertension, we explored the hypothesis that genetic variants might influence or modify the effectiveness of common antihypertensive therapies on the risk of major cardiovascular outcomes. The classes of drug treatments included angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, each study performed array-based genome-wide genotyping, imputed to HapMap Phase II reference panels, and used additive genetic models in proportional hazards or logistic regression models to evaluate drug-gene interactions for each of four therapeutic drug classes. We used meta-analysis to combine study-specific interaction estimates for approximately 2 million single nucleotide polymorphisms (SNPs) in a discovery analysis among 15,375 European Ancestry participants (3,527 CVD cases) with targeted follow-up in a case-only study of 1,751 European Ancestry GenHAT participants as well as among 4,141 African-Americans (1,267 CVD cases). Results Although drug-SNP interactions were biologically plausible, exposures and outcomes were well measured, and power was sufficient to detect modest interactions, we did not identify any statistically significant interactions from the four antihypertensive therapy meta-analyses (Pinteraction &gt; 5.0×10−8). Similarly, findings were null for meta-analyses restricted to 66 SNPs with significant main effects on coronary artery disease or blood pressure from large published genome-wide association studies (Pinteraction ≥ 0.01). Our results suggest that there are no major pharmacogenetic influences of common SNPs on the relationship between blood pressure medications and the risk of incident CVD

    Telomere shortening may be associated with human keloids

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    <p>Abstract</p> <p>Background</p> <p>Keloids are benign skin tumors that are the effect of a dysregulated wound-healing process in genetically predisposed patients. They are inherited with an autosomal dominant mode with incomplete clinical penetrance and variable expression. Keloids are characterized by formation of excess scar tissue beyond the boundaries of the wound. The exact etiology is still unknown and there is currently no appropriate treatment for keloid disease.</p> <p>Methods</p> <p>We analyzed sample tissues were obtained from 20 patients with keloid skin lesions and normal skin was obtained from 20 healthy donors. The telomeres were measured by Terminal Restriction Fragment (TRF) analysis and Real-Time PCR assay. Quantitative Real-Time RT-PCR analysis of hTERT gene expression was performed and intracellular ROS generation was measured.</p> <p>Results</p> <p>In this study, we determined whether telomeric shortening and the expression of human telomerase reverse transcriptase (hTERT) occurs in keloid patients. Using Terminal Restriction Fragment (TRF) analysis and Real-Time PCR assay, we detected a significant telomere shortening of 30% in keloid specimens compared to normal skin. Using quantitative Real-Time RT-PCR, telomerase activity was found absent in the keloid tissues. Moreover, an increase in ROS generation was detected in fibroblasts cell cultures from keloid specimens as more time elapsed compared to fibroblasts from normal skin.</p> <p>Conclusion</p> <p>Telomere shortening has been reported in several metabolic and cardiovascular diseases. We found that telomere shortening can also be associated with human keloids. Chronic oxidative stress plays a major role in the pathophysiology of several chronic inflammatory diseases. Here we found increased ROS generation in fibroblasts from keloid fibroblasts cell cultures when compared to normal skin fibroblasts. Hence we conclude that oxidative stress might be an important modulator of telomere loss in keloid because of the absence of active telomerase that counteracts telomere shortening.</p

    Circulating Monocyte Chemoattractant Protein-1 and Risk of Stroke: A Meta-Analysis of Population-Based Studies Involving 17,180 Individuals.

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    RATIONALE: Pro-inflammatory cytokines have been identified as potential targets for lowering vascular risk. Experimental evidence and Mendelian randomization suggest a role of monocyte-chemoattractant protein-1 (MCP-1) in atherosclerosis and stroke. However, data from large-scale observational studies are lacking. OBJECTIVE: To determine whether circulating levels of MCP-1 are associated with risk of incident stroke in the general population. METHODS AND RESULTS: We used previously unpublished data on 17,180 stroke-free individuals (mean age 56.7{plus minus}8.1 years; 48.8% males) from six population-based prospective cohort studies and explored associations between baseline circulating MCP-1 levels and risk of any stroke, ischemic stroke, and hemorrhagic stroke over a mean follow-up interval of 16.3 years (280,522 person-years at risk; 1,435 incident stroke events). We applied Cox proportional hazard models and pooled hazard ratios (HR) using random-effects meta-analyses. Following adjustments for age, sex, race, and vascular risk factors, higher MCP-1 levels were associated with increased risk of any stroke (HR per 1 SD increment in ln-transformed MCP-1: 1.07, 95%CI: 1.01-1.14). Focusing on stroke subtypes, we found a significant association between baseline MCP-1 levels and higher risk of ischemic stroke (HR: 1.11, [1.02-1.21]), but not hemorrhagic stroke (HR: 1.02, [0.82-1.29]). The results followed a dose-response pattern with a higher risk of ischemic stroke among individuals in the upper quartiles of MCP-1 levels as compared to the 1st quartile (HRs: 2nd quartile: 1.19 [1.00-1.42]; 3rd quartile: 1.35, [1.14-1.59]; 4th quartile: 1.38, [1.07-1.77]). There was no indication for heterogeneity across studies and in a sub-sample of four studies (12,516 individuals) the risk estimates were stable after additional adjustments for circulating levels of interleukin-6 and high-sensitivity C-reactive protein. CONCLUSIONS: Higher circulating levels of MCP-1 are associated with increased long-term risk of stroke. Our findings along with genetic and experimental evidence suggest that MCP-1-signaling might represent a therapeutic target to lower stroke risk.M. Georgakis is funded by scholarships from the German Academic Exchange Service (DAAD) and Onassis Foundation. The ARIC study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under Contract nos. (HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700005I, HHSN268201700004I). The DHS study was funded by a grant from the Donald W. Reynolds Foundation. The EPIC-Norfolk study is funded by grants from the Medical Research Council UK (G9502233, G0401527) and Cancer Research UK (C864/A8257, C864/A2883). FHS is supported by the National Heart, Lung and Blood Institute’s Framingham Heart Study (Contract No. N01-HC-25195 and No. HHSN268201500001I and 75N92019D00031), received funding by grants from the National Institute of Aging (R01s AG054076, AG049607, AG059421, U01-AG049505, AG058589 and AG052409) and the National Institute of Neurological Disorders and Stroke (R01 NS017950, UH2 NS100605), as well as grants for the MCP-1 measurements by NIH (1RO1 HL64753, R01 HL076784, 1 R01 AG028321). The KORA study was initiated and financed by the Helmholtz Zentrum München – German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. Furthermore, KORA research was supported within the Munich Center of Health Sciences (MC-Health), Ludwig-Maximilians-Universität, as part of LMUinnovativ. The MDCS-CV study has been supported with funding from the Swedish Research Council, Swedish Heart and Lung Foundations, and the Swedish Foundation for Strategic Research. This project has received funding from the European Union’s Horizon 2020 research and innovation programme (No 666881), SVDs@target (to M. Dichgans) and No 667375, CoSTREAM (to M. Dichgans); the DFG as part of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy – ID 390857198) and the CRC 1123 (B3) (to M. Dichgans); the Corona Foundation (to M. Dichgans); the Fondation Leducq (Transatlantic Network of Excellence on the Pathogenesis of Small Vessel Disease of the Brain)(to M. Dichgans); the e:Med program (e:AtheroSysMed) (to M. Dichgans) and the FP7/2007-2103 European Union project CVgenes@target (grant agreement number Health-F2-2013-601456) (to M. Dichgans)
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