Integrating All Mobility Systems to Reduce Traffic Congestion

The problem of traffic congestion is common in most urban areas with associated negative impact on the social, economic, and ecological well-being of its residents. Traffic congestion is a common phenomenon in the city of Dubai with its large population and high rate of car ownership. To tackle the problem, this study looks at integrating all mobility systems in the city as a possible solution to the traffic congestion menace. The research methodology involves thematic analysis of secondary data on the subject derived from online databases and libraries. The thematic analysis revealed that Dubai had all the factors needed to integrate mobility system. The city has multiple public transport options, dedicated infrastructure, and mobility hubs close to populated areas. The integration would also offer smart solutions for reducing road accidents that are a major cause of congestion. Smart solutions identified include sharing real-time traffic information and the use of smart street signs to notify road users. The Road and Transport Authority (RTA) facilitates smart initiatives like the integration of all mobility systems through policy formulation. Currently, the body has projects like ‘Smart Traffic Systems’ that help in reducing congestion in the road. All efforts to integrate the mobility systems in Dubai are in line with the vision of Smart Dubai that seeks to improve the livability of the city by leveraging information, data, and available resources

Elevated serum leptin levels in patients with acute myocardial infarction; correlation with coronary angiographic and echocardiographic findings

BACKGROUND: To assess the relationship between serial serum leptin levels in patients with acute myocardial infarction (AMI) who received thrombolysis and the degree of coronary atherosclerosis, coronary reperfusion, echocardiographic findings, and clinical outcome. 51 consecutive patients presenting with AMI were studied. Clinical characteristics including age, sex, body mass index (BMI) and cardiovascular risk factors were recorded. Serial serum leptin levels at the time of admission and subsequently at 0, 6, 12, 24, 36, 60 hours afterwards were obtained. Coronary angiography was performed in 34 patients; the relation between serum leptin levels and evidence of coronary reperfusion as well as the extent of coronary atherosclerosis according to the coronary artery surgery study classification (CASS) were evaluated. Echocardiographic evaluation was performed in all patients. 36 matched patients were enrolled as control group who had serum leptin level 9.4 ± 6.5 ng/ml. RESULTS: The patients mean age was 50.5 ± 10.6 years. There were 47 males and 3 females. 37.1% were diabetics, 23.5% were hypertensive, 21.6% were dyslipidemic and 22.7% were obese (BMI ≥ 30). Leptin concentrations (ng/ml) increased and peaked at the 4th sample (36 hrs) after admission (mean ± SD) sample (1) =9.55 ± 7.4, sample (2) =12.9 ± 8.4, sample (3) =13.8 ± 10.4, sample (4) =18.9 ± 18.1, sample (5) =11.4 ± 6.5, sample (6) =10.8 ± 8.9 ng/ml. There was a significant correlation between serum leptin and BMI (r = 0.342; p = 0.03). Leptin levels correlated significantly to creatine kinase level on the second day (r = 0.43, p ≤ 0.01). Significant correlation of mean serum leptin with the ejection fraction (P < 0.05) was found. No difference in timing of peak serum leptin between patients who achieved coronary reperfusion vs. those who did not (p = 0.8). There was a trend for an increase in the mean serum leptin levels with increasing number of diseased vessels. There was no correlation between serum leptin levels and outcome neither during the hospitalization nor at 9 months follow up. CONCLUSION: Serum leptin levels increase after myocardial infarction. Serum leptin level may be a predictor of the left ventricular ejection fraction and the degree of atherosclerosis but not of coronary reperfusion

Lipidomics for the Prediction of the Unstable Coronary Plaque

Plaques that build up in the lining of the coronary arteries are made up of lipids, inflammatory cells, smooth muscle cells and connective tissue. Thormbosis of a not necessarily occlusive but unstable plaque most often causes episodes of unstable angina and myocardial infarction (MI). Preventing this sudden and adverse event seems to be the only effective startegy to reduce mortality and morbidity of coronary artery disease (CAD). Countries in the Middle East bear a heavy burden from cardiovascular disease. The population of Qatar is particularly prone to CAD with patients presenting with MI at a young age. The prevalence of CAD is in turn promoted by risk factors such as smoking, hypertension, dyslipidemia, diabetes and sedentary lifestyles. Metabolomics approaches to the identification of disease biomarkers rely principally on the comparitive analysis of metabolite expression in normal and disease patients, animal models or cell cultures to identify aberrantly expressed proteins or concentration changes in metabolites that may represent new biomarkers or elucidate a disease mechanism. Lipidomics is the global identification and quantification of a diverse range of lipids in biological systems and is a subset field in metabolomics. The eukaryotic lipidome might compise of 10,000 to 100,000 individual species of lipids originating from a few hundred lipid classes. These lipids are distributed as part of biological membranes, energy storage substances and sometimes function as signal transducers. Altered lipid metabolism and dyslipidemia in the context of inflammation and oxidative stress are driving forces in the transition from stable to unstable plaques. Therefore, a characteristic lipid signature within unstable human plaques and also in the circulating blood plasma could be a predictor of an oncoming cardiac event. This ongoing study was conducted on samples volunteered by acute coronary syndrome (ACS) patients at the Heart Hospital, Doha, Qatar. ACS is a term that describes any condition brought on by the sudden reduced blood flow to the heart due to thrombosis in the coronary arteries and encompasses unstable angina (UA) and both ST-segment elevation (STEMI) and non ST-segment elevation myocardial infarction (NSTEMI). A complete occlusive thrombi leads to extensive myocardial cell death and typically produces an elevated ST-segment in the electrocardiogram. In UA, ischemia occurs unpredictably and suddenly and is caused by the temporary formation of blood clots within the coronary arteries. Unstable angina often occurs before a MI. Distinguished from ACS are patients with stable angina (SA) who develop symptoms due to exertional ischemia. The aim of this study was to profile the global individual lipid levels of subjects in Qatar with unstable CAD, comparing global lipid levels between patients with unstable angina and ST-elevated myocardial infarction. We chose to discover the lipid biomarkers using a workflow utilizing tandem mass spectrometry with on-line ultra-high pressure liquid chromatography (UPLC-MS/MS). Mass spectrometry is a powerful technique that can be used to identify unknown compounds, to quantify known materials and to elucidate the structure and chemical properties of molecules. Recent advances in the accuracy and speed to the technology allow data acquisition for the global analysis of proteins, lipids and metabolites from complex samples such as blood plasma or serum. As we were trying to discover a new lipid biomarker, a technique that would maximise the number of compounds detected, identified and quantified them was favourable. Once the samples were analysed by tandem mass spectrometry, the ion intensity data from each sample was aligned with each other by retention time and lipid mass, normalised and deconvoluted. The signals were then attributed to a particular lipid species by utilising a lipid database and comparing the mass of the detected lipid and piecing together information gained from the fragment data of that lipid from the orbitrap. Statistical analyses of the signals for each individual lipid were then conducted by comparing within group percent coefficient of variation (?CV), fold change and analysis of variance (ANOVA) tests between sample groups and q-value and power calculations. Principal component analysis (PCA) was conducted in order to differentiate the samples under supervised conditions into STEMI and UA groups. A total of 1,663 and 874 lipid compounds were identified in positive and negative modes of mass spectrometry respectively. Of these, 7 compounds showed a significant change (ANOVA p-value < or equal to 0.001) between the STEMI and UA groups. The identities of these compounds are yet to be elucidated. Of the compounds with a significant change between sample groups of ANOVA p-value < or equal to 0.005, five compounds were able to be identified by mass and spectral matching with a lipid database. The PCA scores plot, which distributes samples in multi-dimensional space according to the variance seen in each principal component, showed very low evidence of discrimination between the sample groups with sample scores clustered in a single mixed pattern. This analysis suggests that the lipid abundance changes between the sample groups were difficult to find. This was most likely due to a combination of two reasons: (1) large within-group biological variance that needs to be overcome to detect the between-group variances and (2) the low differences in lipid concentrations between the sample groups. With a greater number of samples, this results is expected to change as the power of the study would increase. Successful results obtained from this study will aid healthcare professional in intervening with appropriate treatment in persons showing no symptoms but are under threat of developing angina or acute MI. The discovery of a lipid biomarker could assist healthcare professionals in prevention of an acute cardiac event thereby saving lives.qscienc

The Association between Serum LDL Cholesterol and Genetic Variation in Chromosomal Locus 1p13.3 among Coronary Artery Disease Patients

Background. Several polymorphisms of a locus on chromosome 1p13.3 have a significant effect on low-density lipoprotein cholesterol (LDL-C), atherosclerosis, and acute coronary syndrome (ACS). Methods. We aimed to investigate the association between rs599839, rs646776, and rs4970834 of locus 1p13.3 and serum LDL-C and severity of coronary artery stenosis in ACS patients. Genotyping of the rs599839, rs646776, and rs4970834 polymorphisms was performed on Arab patients undergoing coronary angiography for ACS. Patients were divided into group A (ACS with insignificant stenosis (<50%)) and group B (with significant stenosis (≥50%)). Results. Patients carrying the minor G allele in rs599839 had significantly lower mean of LDL-C (2.58 versus 3.44 mM, P=0.026) than homozygous A allele carriers (GG versus AA). Carriers of minor C allele in rs64776 had significantly higher mean of HDL-C (2.16 versus 1.36 mM, P=0.004) than carriers of the T alleles (AA versus GG). The odd ratio and 95% confidence interval for dominant model for G allele carriers of rs599839 were 0.51 (0.30–0.92), P=0.038, among patients with significant stenosis. Conclusions. Polymorphisms rs646776 and rs599839 of locus 1p13.3 were significantly associated with LDL-C and other lipid parameters. In addition, the G-allele carriers of variant rs599839 had a significant protective effect against the atherosclerosis.Qatar National Research Fund (a member of Qatar Foundation) under its Undergraduate Research Experience Program no. UREP: 07-091–3-020

Elevated serum leptin levels in patients with acute myocardial infarction; correlation with coronary angiographic and echocardiographic findings

Abstract Background To assess the relationship between serial serum leptin levels in patients with acute myocardial infarction (AMI) who received thrombolysis and the degree of coronary atherosclerosis, coronary reperfusion, echocardiographic findings, and clinical outcome. 51 consecutive patients presenting with AMI were studied. Clinical characteristics including age, sex, body mass index (BMI) and cardiovascular risk factors were recorded. Serial serum leptin levels at the time of admission and subsequently at 0, 6, 12, 24, 36, 60 hours afterwards were obtained. Coronary angiography was performed in 34 patients; the relation between serum leptin levels and evidence of coronary reperfusion as well as the extent of coronary atherosclerosis according to the coronary artery surgery study classification (CASS) were evaluated. Echocardiographic evaluation was performed in all patients. 36 matched patients were enrolled as control group who had serum leptin level 9.4 ± 6.5 ng/ml. Results The patients mean age was 50.5 ± 10.6 years. There were 47 males and 3 females. 37.1% were diabetics, 23.5% were hypertensive, 21.6% were dyslipidemic and 22.7% were obese (BMI ≥ 30). Leptin concentrations (ng/ml) increased and peaked at the 4th sample (36 hrs) after admission (mean ± SD) sample (1) =9.55 ± 7.4, sample (2) =12.9 ± 8.4, sample (3) =13.8 ± 10.4, sample (4) =18.9 ± 18.1, sample (5) =11.4 ± 6.5, sample (6) =10.8 ± 8.9 ng/ml. There was a significant correlation between serum leptin and BMI (r = 0.342; p = 0.03). Leptin levels correlated significantly to creatine kinase level on the second day (r = 0.43, p ≤ 0.01). Significant correlation of mean serum leptin with the ejection fraction (P p = 0.8). There was a trend for an increase in the mean serum leptin levels with increasing number of diseased vessels. There was no correlation between serum leptin levels and outcome neither during the hospitalization nor at 9 months follow up. Conclusion Serum leptin levels increase after myocardial infarction. Serum leptin level may be a predictor of the left ventricular ejection fraction and the degree of atherosclerosis but not of coronary reperfusion.</p

Association of β-Adrenergic Receptor Gene Polymorphisms With Acute Coronary Syndrome and Cardiovascular Risk Factors in an Arab Population

We evaluated the association between beta-adrenergic receptor genes (ADRB1 and ADRB2) polymorphism, cardiovascular risk, and acute coronary syndrome (ACS) in individuals from an Arab ethnicity. A total of 388 Qatari participants were assessed and genotyped for ADRB1 (rs1801252 & rs1801253) and ADRB2 (rs1042718 & rs1042713) polymorphisms using allele-specific PCR. Minor allele frequencies (MAF) in each single-nucleotide polymorphisms (SNPs) did not show statistically significant difference between cases and controls. A higher proportion of patients with ACS had homozygous minor alleles (GG) for rs1801253 (28.8% vs 17.1%; P =.019) compared with controls. Among cases with ACS, there was an association of minor allele frequency (G) for rs1801253 with severe coronary artery stenosis (0.485 vs 0.428; P =.04) than that of insignificant stenosis (<50% stenosis). There was a 3-fold increased risk of significant coronary stenosis in patients with diabetes mellitus (DM) and carrier of rs1801253 genotypes with dominant model (P =.01) and recessive model (P =.05). There is a possible synergic association between DM, carrier of ADRB1 (Arg389Gly) variants, and significant coronary artery stenosis among Arabs. Further prospective studies with larger sample sizes are warranted to support our findings. The Author(s) 2015.Scopu

The cardiovascular implication of single nucleotide polymorphisms of chromosome 9p21 locus among Arab population

Background: Based on several reports including genome-wide association studies, genetic variability has been linked with higher (nearly half) susceptibility toward coronary artery disease (CAD). We aimed to evaluate the association of chromosome 9p21 single nucleotide polymorphisms (SNPs): rs2383207, rs10757278, and rs10757274 with the risk and severity of CAD among Arab population. Materials and Methods: A prospective observational case-control study was conducted between 2011 and 2012, in which 236 patients with CAD were recruited from the Heart Hospital in Qatar. Patients were categorized according to their coronary angiographic findings. Also, 152 healthy volunteers were studied to determine if SNPs are associated with risk of CAD. All subjects were genotyped for SNPs (rs2383207, rs2383206, rs10757274 and rs10757278) using allele-specific real-time polymerase chain reaction. Results: Patients with CAD had a mean age of 57 ± 10; of them 77% were males, 54% diabetics, and 25% had family history of CAD. All SNPs were in Hardy-Weinberg equilibrium except rs2383206, with call rate >97%. After adjusting for age, sex and body mass index, the carriers of GG genotype for rs2383207 have increased the risk of having CAD with odds ratio (OR) of 1.52 (95% confidence interval [CI] = 1.01-2.961, P = 0.046). Also, rs2383207 contributed to CAD severity with adjusted OR 1.80 (95% CI = 1.04-3.12, P = 0.035) based on the dominant genetic model. The other SNPs (rs10757274 and rs10757278) showed no significant association with the risk of CAD or its severity. Conclusion: Among Arab population in Qatar, only G allele of rs2483207 SNP is significantly associated with risk of CAD and its severity

Chronic coronary syndromes without standard modifiable cardiovascular risk factors and outcomes: the CLARIFY registry

Background and Aims: It has been reported that patients without standard modifiable cardiovascular (CV) risk factors (SMuRFs—diabetes, dyslipidaemia, hypertension, and smoking) presenting with first myocardial infarction (MI), especially women, have a higher in-hospital mortality than patients with risk factors, and possibly a lower long-term risk provided they survive the post-infarct period. This study aims to explore the long-term outcomes of SMuRF-less patients with stable coronary artery disease (CAD). Methods: CLARIFY is an observational cohort of 32 703 outpatients with stable CAD enrolled between 2009 and 2010 in 45 countries. The baseline characteristics and clinical outcomes of patients with and without SMuRFs were compared. The primary outcome was a composite of 5-year CV death or non-fatal MI. Secondary outcomes were 5-year all-cause mortality and major adverse cardiovascular events (MACE—CV death, non-fatal MI, or non-fatal stroke). Results: Among 22 132 patients with complete risk factor and outcome information, 977 (4.4%) were SMuRF-less. Age, sex, and time since CAD diagnosis were similar across groups. SMuRF-less patients had a lower 5-year rate of CV death or non-fatal MI (5.43% [95% CI 4.08–7.19] vs. 7.68% [95% CI 7.30–8.08], P = 0.012), all-cause mortality, and MACE. Similar results were found after adjustments. Clinical event rates increased steadily with the number of SMuRFs. The benefit of SMuRF-less status was particularly pronounced in women. Conclusions: SMuRF-less patients with stable CAD have a substantial but significantly lower 5-year rate of CV death or non-fatal MI than patients with risk factors. The risk of CV outcomes increases steadily with the number of risk factors