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  • 1
    Online Resource
    Online Resource
    Wiley ; 2006
    In:  The FASEB Journal Vol. 20, No. 10 ( 2006-08), p. 1715-1717
    In: The FASEB Journal, Wiley, Vol. 20, No. 10 ( 2006-08), p. 1715-1717
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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  • 2
    In: BMC Bioinformatics, Springer Science and Business Media LLC, Vol. 18, No. 1 ( 2017-12)
    Type of Medium: Online Resource
    ISSN: 1471-2105
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2041484-5
    SSG: 12
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  • 3
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 139, No. 19 ( 2019-05-07)
    Abstract: The advent of new tobacco products such as electronic cigarettes and the dramatic rise in their use, especially by adolescents and young adults, are significant public health concerns. Electronic cigarettes have become the most popular tobacco products for youth and adolescents in the United States and are attracting youth to new avenues for nicotine addiction. Although these products may have benefit by helping some smokers quit or to move to a less harmful product, the long-term health effects of these products and the net public health effect associated with their use remain unclear and widely debated. There is increasing concern that the use of newer tobacco products may catalyze transition to the use of other tobacco products or recreational drugs, particularly in young adults. Therefore, there is urgent need for robust US Food and Drug Administration regulation of all tobacco products to avoid the significant economic and population health consequences of continued tobacco use. Although the American Heart Association acknowledges that the ultimate endgame would be an end to all tobacco and nicotine addiction in the United States, it supports first minimizing the use of all combustible tobacco products while ensuring that other products do not addict the next generation of youth and adolescents. The endgame strategy needs to be coordinated with the long-standing, evidence-based tobacco control strategies that have significantly reduced tobacco use and initiation in the United States.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1466401-X
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  • 4
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 142, No. Suppl_3 ( 2020-11-17)
    Abstract: Background: E-cigarette (e-cig) use has rapidly increased, especially among youth. Vaping has been linked to adverse cardiopulmonary effects, but the full extent of effects remains unknown. Several constituents in e-cigs may increase cardiac risk partly by disturbing cardiac electrophysiology and the autonomic nervous system. Hypothesis: E-cig aerosols will differentially induce pro-arrhythmic changes in cardiac conduction and autonomic balance in mice depending on the presence of nicotine and flavors. Methods: Electrocardiograms (ECGs) were collected by telemetry in 5 healthy male mice (C57BL/6) exposed for 6 hours to clean air or e-cig aerosols (9-minute puff sessions every 18 minutes) from JUUL e-liquids (Va. Tobacco, Mango, or Menthol at ≈5% nicotine benzoate), or a nicotine-free mixture of propylene glycol and vegetable glycerin solvents (PG:VG, 30:70 ratio). ECG morphology, heart rate variability (HRV), and arrhythmias were analyzed by mixed models with P 〈 0.05 (vs. Air) for all effects. Results: PG:VG increased high grade supraventricular block arrhythmias (121±45 events/hour) relative to Air (0±0 events/hour) and decreased heart rate (HR, -25±8 beats/min), whereas aerosols from all nicotine-containing e-liquids increased HR and decreased HRV, suggesting sympatho-excitation. However, these effects were significantly attenuated for Mango relative to Menthol and Va. Tobacco. As well, only PG:VG and Mango increased ventricular premature beats (VPBs, 9.6±3.7 and 5.5±1.2 events/hour, ±SEM) relative to Air (1.1±0.24 events/hour). VPBs correlated with changes in standard deviation of RR and mean HR from pre-exposure (Spearman’s r : 0.51 and -0.27, P 〈 0.0001). Prolonged repolarization (QTc) correlated with VPBs during exposures to PG:VG ( r = 0.38, P = 0.046), but not nicotine-containing e-liquids ( r = 0.15, P = 0.38). Conclusions: E-cigs may increase risk for cardiac arrhythmia through e-liquid solvents, which when thermally aerosolized generate toxic aldehydes and particulates. Nicotine and flavor chemicals may modify the cardiac and autonomic impacts of e-cigs. Further studies are needed to determine how e-cig aerosols induce cardiac arrhythmia and whether these effects translate to cardiac morbidity and mortality in humans.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1466401-X
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Vol. 146, No. Suppl_1 ( 2022-11-08)
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Electronic cigarettes (e-cigarettes) are advertised as a healthier alternative for combustible cigarettes and have become the most commonly used smoking product. There is limited data regarding the association of e-cigarettes and risk of cardiovascular disease (CVD). We assessed the association of chest pain reports across tobacco product use groups. We used data from the Population Assessment of Tobacco and Health (PATH) study which is a nationally representative longitudinal study of tobacco use behavior and health effects. We categorized tobacco use patterns into 4 groups: cigarette use, dual use, e-cigarette use, and non-use. Participants were asked if they have ever had chest pain and if they have had chest pain in the past 30 days. Binominal regression models were used to examine the association between tobacco use categories and the 2 chest pain outcomes. We adjusted for covariates including age, sex, race, education, BMI, hypercholesterolemia, hypertension, current use of other combustible tobacco products, secondhand smoke exposure, marijuana use in the past 30 days, recreational drug use and history of respiratory diseases. The cohort included 9,284 participants after excluding those with established CVD and those with missing outcome or exposure data. The Mean age was 57 (SD±11) years and 54% of participants were female. Among the participants, 3,020 were exclusive cigarette users, 213 were dual users, 175 were exclusive e-cigarette users (94% were former smokers), and 5,876 were non-users. Compared to non-use, combustible cigarette use had 1.48 (95% CI, 1.27, 1.73) odds of ever having chest pain and 1.72 (95% CI, 1.4, 2.11) odds of having chest pain in the past 30 days. Dual use was associated with 1.52 (CI 95%, 1.05, 2.19) odds of chest pain ever and 1.82 (95% CI, 1.17, 2.83) odds of 30 days chest pain. Exclusive e-cigarette use had 0.78 (95% CI, 0.49, 1.26) odds of ever having chest pain and 0.75 (95% CI, 0.39, 1.42) odds of having chest pain in the past 30 days. Our findings suggest that compared to non-use, exclusive e-cigarette use has similar rates of chest pain; whereas dual use and combustible cigarette use have increased rates of chest pain outcomes.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 6
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 146, No. Suppl_1 ( 2022-11-08)
    Abstract: Background: Carnosine, a naturally occurring dipeptide found in highly metabolic tissues like skeletal muscles and brain can reduce oxidative stress caused by acrolein and particulate matter (PM) exposure. The role of carnosine and its acrolein-conjugates (propanol and propanal) maybe crucial in reducing the effects of PM2.5 air pollution on cardiovascular (CV) health. Methods: We analyzed data of 103 healthy participants from baseline (Visit # 2, before randomization) of the ongoing Nucleophilic Defense against Particulate Matter Toxicity (NEAT) clinical trial (NCT03314987) which investigates whether dietary supplementation of carnosine can protect against effects of PM2.5 air pollution. All participants underwent computerized cognitive test “Cognition”. The Cognition test includes 10 neurocognitive test batteries (Table 1) and assesses distinct domains of cognition. Tests scores were assessed in blinded fashion by the University of Pennsylvania team for individual batteries and a cumulative score. Two-tailed Spearman’s rho was used for correlation and Generalized Linear Models (GLM) with gamma distribution log-link was used for regression. Results: Cumulative cognition score showed a negative association with pulse pressure. Carnosine-propanol levels had a significant modifying effect (Figure 1). Stratified analysis showed that this relationship was significantly modified by low (B= -0.03, P=0.005) and medium (B= -0.016, P=0.046) carnosine-propanol levels. High levels of carnosine-propanol or carnosine-propanal did not show any effect on the cognition-pulse pressure. Indices of metabolic syndrome were also negatively associated with cumulative score (all P 〈 0.05). Conclusions: Carnosine readily reacts with acrolein to reduce in-vivo oxidative stress by producing propanol and propanal aldehyde conjugates. Decrease in propanol conjugates is associated with higher CV health and in-turn higher cognitive outcomes.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1466401-X
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  • 7
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. suppl_3 ( 2015-11-10)
    Abstract: Objective: Results from several randomized, controlled cell therapy trials suggest that the use of autologous bone marrow mononuclear cells (BMMNCs) results in only modest benefits in patients with ST-segment elevation myocardial infarction (STEMI). However, the patients in these trials had varying combinations of underlying cardiovascular risk factors (CVRFs) and comorbidities. The autologous BMMNC product administered to each patient was unique. Based on our previous findings, the purpose of this study was to identify potential associations between specific CVRFs and BMMNC subsets in patients with STEMI. Methods: This study evaluated a cohort of patients with STEMI who were enrolled in either the CCTRN TIME or LateTIME trials and underwent BMMNC or placebo treatment (N=139). Flow cytometric analysis targeting phenotypic markers (eg, CD45, CD14, CD11b, CD3, CD19, CD31, and CD34) was used to assess the frequency of BMMNC subsets at baseline. The GRACE ACS Risk Score 2.0 - 3 year death (GRS) was used to stratify patients according to cardiovascular risk (low: GRS 〈 12%, moderate: GRS 12-30%, high: GRS 〉 30%). Multivariable models were then applied to assess relationships between BMMNC subsets and CVRFs, including age, smoking, hypertension, hyperlipidemia, and sex. Results: Patients were grouped as low GRS (n=69, 49.6%), moderate GRS (n=49, 35.3%), and high GRS (n=21, 15.1%). Patients with a high GRS had significantly lower frequencies of CD45+CD31+ cells than those with a low GRS (35.6% vs 40.3%, respectively, P=0.041). In multivariable analyses, age was inversely associated with the frequencies of CD34+ (P=0.011) and CD45+CD31+ (P=0.001) cells, and smoking was associated with a decrease in CD45+CD31+ cells (P=0.022). In addition, higher frequencies of CD11b+ cells were associated with hypertension (P=0.010) and hyperlipidemia (P=0.029). In contrast, the CD11b+ cell frequency was less in females (P=0.005). Conclusions: This study identified associations between specific CVRFs and BMMNC subsets. These associations may contribute to the heterogeneity of the cell product received. Thus, differences in patients’ comorbidities should be considered when designing future autologous cell therapy trials.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1466401-X
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  • 8
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. Suppl_1 ( 2021-11-16)
    Abstract: Introduction: Cardiovascular disease (CVD) is the leading cause of death from environmental exposures. Although exposure to particulate matter ≤2.5μm (PM 2.5 ) is an established risk factor for CVD, the contribution of other hazardous pollutant exposure to CVD risk is less clear. Hypothesis: We assessed the hypothesis that volatile organic compounds (VOCs) are associated with blood pressure in 778 nonsmokers from the Jackson Heart Study (JHS), a large, community based observational study of CVD in African Americans from the tri-county Jackson, MS area. Methods: We measured urinary metabolites of 17 parent VOCs in spot urine samples collected at baseline using UPLC/MS. We tested the association between VOC metabolites and blood pressure in nonsmokers using generalized linear models adjusted for age, sex, body mass index (BMI), estimated glomerular filtration rate, cholesterol to high-density lipoprotein ratio, triglycerides, blood pressure medications, diabetes, and PM 2.5 . Two measurements of systolic and diastolic blood pressure (SBP, DBP) in the resting state were averaged using a Hawksley random zero sphygmomanometer. Results: Included participants had a BMI of 31.3 ± 7.1 kg/m 2 (mean ± SD), had triglycerides of 99.9 ± 57.9 mg/dL, and a less than 10% prevalence of CVD events. More than one-third were affluent (37.8%) and almost half used blood pressure medications (46%). We found that metabolites of acrolein (CEMA) and crotonaldehyde (HPMMA) were associated with a 1.5mmHg (CI: 0.5, 2.7; p=0.01), and a 1.1mmHg higher (CI: 0.1, 2.0; p=0.02) SBP per interquartile range (IQR) of VOC metabolite, respectively. Additionally, we found a 0.5mmHg higher (CI: 0.1, 0.8; p= 0.01) DBP per IQR of styrene metabolite, MA. In subgroup analysis, the association between CEMA and MA and blood pressure persisted only in men. Conclusions: In conclusion, these findings suggest that exposure to VOCs (acrolein, crotonaldehyde, and styrene) may be a significant contributor to risk of hypertension among African American nonsmokers.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 9
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. suppl_3 ( 2015-11-10)
    Abstract: We have previously shown that acute exposure to air pollutants including particulate matter or the volatile acrolein leads to reversible suppression of circulating angiogenic cells in humans and mice. Exposure to tobacco smoke, which contains both particles and aldehydes such as acrolein, also suppresses EPC number and function in association with an increase in cardiovascular disease risk. To assess whether acrolein alone worsened vascular pathogenesis, we exposed mice to acrolein (1 ppm * 6h/day) in a murine model of hind limb ischemia. Mice were exposed to acrolein for 4 days prior to permanent right femoral artery and vein ligation and bisection (distal to inguinal ligament) with continued exposure to filtered air (control) or acrolein for another 2 weeks. Blood flow recovery in the ischemic hind limb was measured via Laser Doppler Perfusion Imaging (LDPI) and normalized as a percentage of flow in the non-ischemic limb. Although acute exposure to acrolein reduced the number of circulating angiogenic cells it had only a modest effect blood flow recovery after 7 days (% Recovery: air, 86.2±21.4; acrolein, 68.3±21.6, n=8,8, p=0.12). Hence to determine whether chronic acrolein exposure worsened chronic vascular injury, we exposed C57BL/6J mice to 1 ppm acrolein for 12 weeks. This long-term exposure significantly depressed (by 51%) circulating levels of Flk-1+/Sca-1+ cells (as % of lymphocytic counts: air 0.15±0.09; acrolein 0.07±0.05; p 〈 0.02). To tested if cell changes were associated with changes in atherogenesis, apoE-null mice on normal chow or high-fat diet were exposed to chronic acrolein (1 ppm; 12 week). Acrolein accelerated aortic atherosclerosis by 1.6-fold (p 〈 0.001) but it did not affect coincident dyslipidemia (total cholesterol: air, 1224±189; acrolein, 1076±195 mg/dL) compared with air-exposed, HFD-fed mice. These results suggest that that chronic low level acrolein exposure suppresses circulating angiogenic cells and accelerates atherogenesis; hence the atherogenic effect of exposure to traffic pollutants, indoor smoke or cigarette smoke may be in part attributable to acrolein. These findings could inform exposure risk assessments and the development of new policies for regulating pollutant exposure and tobacco product use.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1466401-X
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  • 10
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 117, No. 9 ( 2008-03-04), p. 1172-1182
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 117, No. 9 ( 2008-03-04), p. 1172-1182
    Abstract: Background— The modification of proteins with O -linked β- N -acetylglucosamine ( O -GlcNAc) represents a key posttranslational modification that modulates cellular function. Previous data suggest that O -GlcNAc may act as an intracellular metabolic or stress sensor, linking glucose metabolism to cellular function. Considering this, we hypothesized that augmentation of O -GlcNAc levels represents an endogenously recruitable mechanism of cardioprotection. Methods and Results— In mouse hearts subjected to in vivo ischemic preconditioning, O -GlcNAc levels were significantly elevated. Pharmacological augmentation of O -GlcNAc levels in vivo was sufficient to reduce myocardial infarct size. We investigated the influence of O -GlcNAc levels on cardiac injury at the cellular level. Lethal oxidant stress of cardiac myocytes produced a time-dependent loss of cellular O -GlcNAc levels. This pathological response was largely reversible by pharmacological augmentation of O -GlcNAc levels and was associated with improved cardiac myocyte survival. The diminution of O -GlcNAc levels occurred synchronously with the loss of mitochondrial membrane potential in isolated cardiac myocytes. Pharmacological enhancement of O -GlcNAc levels attenuated the loss of mitochondrial membrane potential. Proteomic analysis identified voltage-dependent anion channel as a potential target of O -GlcNAc modification. Mitochondria isolated from adult mouse hearts with elevated O -GlcNAc levels had more O -GlcNAc–modified voltage-dependent anion channel and were more resistant to calcium-induced swelling than cardiac mitochondria from vehicle mice. Conclusions— O -GlcNAc signaling represents a unique endogenously recruitable mechanism of cardioprotection that may involve direct modification of mitochondrial proteins critical for survival such as voltage-dependent anion channel.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 1466401-X
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