The social context of smoking: A qualitative study comparing smokers of high versus low socioeconomic position

Background: The reductions in smoking prevalence in a number of industrialised countries are accompanied by a strong social gap and associated health inequality. Groups such as the World Health Organisation emphasise the importance of exploring potential causal factors for smoking such as socio-economic context & position. There has been little effort to compare the social context of smoking for smokers of high versus lower socio-economic position (SEP) to consider how tobacco control efforts might reduce smoking-related health inequality. Method: Purposive sampling was used to recruit participants for eight focus groups. The groups were segregated by age, gender and SEP. Samples were selected from suburbs within the Sydney metropolitan area defined as either high or low SEP based on the Socio Economic Index for Areas. Emergent themes were analysed according to Poland's six dimensions of the social context of smoking. Differences according to SEP, age group and gender were explored. Results: While there was commonality in social experiences for smokers across groups, some important aspects of the social context of smoking varied. Smokers of high SEP appeared to be aware of particular social pressures not to smoke on five of the six social context dimensions (power, body, identity, consumption and place). Not only were some of those pressures absent for low SEP participants, there were additional influences within the social context which were pro-smoking. Conclusions: In order to narrow the health inequality gap associated with smoking, it is important to take account of the more pro-smoking social context experienced by low SEP smokers. Suggestions are made regarding social marketing campaigns, support for quit assistance and approaches to the regulation of smoking which may assist inminimising smoking-related health inequality

Probe dependence of allosteric enhancers on the binding affinity of adenosine A1‐receptor agonists at rat and human A1‐receptors measured using NanoBRET

Background and Purpose: Adenosine is a local mediator that regulates a number of physiological and pathological processes via activation of adenosine A1‐receptors. The activity of adenosine can be regulated at the level of its target receptor via drugs that bind to an allosteric site on the A1‐receptor. Here, we have investigated the species and probe dependence of two allosteric modulators on the binding characteristics of fluorescent and nonfluorescent A1‐receptor agonists. Experimental Approach: A Nano‐luciferase (Nluc) BRET (NanoBRET) methodology was used. This used N‐terminal Nluc‐tagged A1‐receptors expressed in HEK293T cells in conjunction with both fluorescent A1‐receptor agonists (adenosine and NECA analogues) and a fluorescent antagonist CA200645.Key Results: PD 81,723 and VCP171 elicited positive allosteric effects on the binding affinity of orthosteric agonists at both the rat and human A1‐receptors that showed clear probe dependence. Thus, the allosteric effect on the highly selective partial agonist capadenoson was much less marked than for the full agonists NECA, adenosine, and CCPA in both species. VCP171 and, to a lesser extent, PD 81,723, also increased the specific binding of three fluorescent A1‐receptor agonists in a species‐dependent manner that involved increases in Bmax and pKD.Conclusions and Implications: These results demonstrate the power of the NanoBRET ligand‐binding approach to study the effect of allosteric ligands on the binding of fluorescent agonists to the adenosine A1‐receptor in intact living cells. Furthermore, our studies suggest that VCP171 and PD 81,723 may switch a proportion of A1‐receptors to an active agonist conformation (R*)

The Effect of Work Rate on Oxygen Uptake Kinetics During Exhaustive Severe Intensity Cycling Exercise

The effect of work rate on oxygen uptake kinetics during exhaustive severe intensity cycling exercise Jennifer L. Sylvester, Samantha D. Burdette, Steven W. Cross, Nosa O. Idemudia, John, H. Curtis, Jakob L. Vingren, David W. Hill. Applied Physiology Laboratory, University of North Texas, Denton, TX During exhaustive severe intensity exercise, the oxygen uptake (VO2) increases exponentially, with a time constant of ~30 s. After ~1 to 2 min, a slow component emerges and drives the VO2 to its maximum. There are clear differences in the VO2 response profile across exercise intensity domains. These disparities might not be attributable to metabolic demand but, rather, to characteristics of the various intensity domains, such as the consequences of lactic acid production. PURPOSE: To investigate the role of exercise intensity on the VO2 response profile at intensities wholly within the severe domain. METHODS: Four women (mean ± SD: age 22 ± 2 years, height 167 ± 7 cm, mass 66 ± 5 kg) and eight men (age 23 ± 2 yr, height 179 ± 9 cm, mass 78 ± 10 kg) performed exhaustive constant-power cycle ergometer tests at two different severe intensity work rates (263 ± 78 W and 214 ± 64 W). Smoothed breath-by-breath VO2 data were fitted to a two-component (primary response and slow component) model using iterative regression. RESULTS: Times to exhaustion were 217 ± 27 s and 590 ± 82 s, respectively. The VO2max values were the same at the two different work rates (2973 ± 691 ml·min-1 and 3011 ± 728 ml·min-1). The amplitude of the primary response was greater (p \u3c 0.05) at the higher work rate (2095 ± 716 ml·min-1) than at the lower work rate (1857 ± 618 ml·min-1) and the amplitude of the slow component was smaller (367 ± 177 ml·min-1 vs 645 ± 347 ml·min-1). In addition, the time delay before the emergence of the slow component was shorter at the higher work rate (92 ± 22 s vs 116 ± 42 s). CONCLUSION: The results show that exercise intensity per se affects the VO2 response profile within the severe intensity domain and suggest that metabolic demand drives the primary response of VO2 kinetics within this domain. Category to be judged: Master\u27

The Effect of Pedaling Cadence on the Kinetics of Oxygen Uptake During Severe Intensity Exercise

During exhaustive severe intensity exercise, the oxygen uptake (VO2) increases exponentially, with a time constant of ~30 s. After ~1 to 2 min, a slow component emerges and drives the VO2 to its maximum. Pedaling cadence contributes to the metabolic demand at a given work rate and affects several responses to cycling exercise. PURPOSE: To determine the effect of pedaling cadence on parameters of the two-component VO2 response profile during severe intensity exercise. METHODS: Eight women (mean ± SD: age 22 ± 1 yr, height 161 ± 6 cm, and weight 58.8 ± 2.3 kg) and 10 men (age 23 ± 1 yr, height 180 ± 6 cm, and weight 82.9 ± 4.4 kg) performed exhaustive constant-power cycle ergometer tests using pedaling cadences of 60 rpm, 80 rpm, and 100 rpm. RESULTS: Times to exhaustion were smaller at higher cadences (220 ± 85 \u3c 299 ± 118 \u3c 368 ± 168 s), whereas VO2max values were the same at all cadences (2786 ± 729 = 2768 ± 749 = 2774 ± 732 ml/min). The mean response time of the primary response was faster at higher pedaling cadences (27 ± 5 \u3c 32 ± 5 \u3c 37 ± 5 s); the amplitude of the primary response was greater at the highest cadence (2045 ± 577 \u3e 1890 ± 493 = 1899 ± 515 ml/min); and the time delay before the slow component was smaller at higher cadences (85 ± 11 \u3c 105 ± 17 \u3c 118 ± 19 s). CONCLUSION: These results demonstrate that pedaling cadence affects the VO2 response profile. The higher cadences speed the primary or fundamental response and hasten the emergence of the slow component. This may have implications for the sport of cycling and should be considered when evaluating cardio-respiratory and metabolic responses to cycle ergometer exercise

The effect of two selective A1-receptor agonists and the bitopic ligand VCP746 on heart rate and regional vascular conductance in conscious rats

Background and purposeAdenosine is a local mediator that regulates physiological and pathological processes via activation of four G protein‐coupled receptors (A1, A2A, A2B, A3). We have investigated the effect of two A1‐receptor selective agonists and the novel A1‐receptor bitopic ligand VCP746 on the rat cardiovascular system.Experimental ApproachTo investigate the effect of these A1‐agonists on the cardiovascular system, we evaluated their regional haemodynamic responses in conscious rats. Male Sprague Dawley rats (350–450g) were chronically implanted with pulsed Doppler flow probes (positioned around the renal and mesenteric arteries, and the descending abdominal aorta) and catheters (jugular vein and caudal artery). Cardiovascular responses were measured following i.v. infusion (3 min each dose) of CCPA (120, 400, 1200 ng.kg‐1.min‐1), capadenoson or adenosine (30, 100, 300 μg.kg‐1.min‐1) or VCP746 (6, 20, 60 μg.kg‐1.min‐1) following pre‐dosing with DPCPX (0.1 mg.kg‐1 i.v.) or vehicle.Key ResultsCCPA produced a significant A1‐receptor‐mediated decrease (p less than 0.05) in heart rate that was accompanied by vasoconstrictions in the renal and mesenteric vascular beds but an increase in hindquarters vascular conductance. The partial agonist capadenoson also produced an A1‐receptor‐mediated bradycardia. In contrast, VCP746 produced increases in heart rate and renal and mesenteric vascular conductance that were not mediated by A1‐receptors. In vitro studies confirmed that VCP746 had potent agonist activity at both A2A and A2B receptors.Conclusions and ImplicationsThese results suggest VCP746 mediates its cardiovascular effects via activation of A2 rather than A1 adenosine receptors. This has implications for the design of future bitopic ligands that incorporate A1 allosteric ligand moieties

Widespread winners and narrow-ranged losers: land use homogenizes biodiversity in local assemblages worldwide

Human use of the land (for agriculture and settlements) has a substantial negative effect on biodiversity globally. However, not all species are adversely affected by land use, and indeed, some benefit from the creation of novel habitat. Geographically rare species may be more negatively affected by land use than widespread species, but data limitations have so far prevented global multi-clade assessments of land-use effects on narrow-ranged and widespread species. We analyse a large, global database to show consistent differences in assemblage composition. Compared with natural habitat, assemblages in disturbed habitats have more widespread species on average, especially in urban areas and the tropics. All else being equal, this result means that human land use is homogenizing assemblage composition across space. Disturbed habitats show both reduced abundances of narrow-ranged species and increased abundances of widespread species. Our results are very important for biodiversity conservation because narrow-ranged species are typically at higher risk of extinction than widespread species. Furthermore, the shift to more widespread species may also affect ecosystem functioning by reducing both the contribution of rare species and the diversity of species’ responses to environmental changes among local assemblages

Involvement of β-adrenoceptors in the cardiovascular responses induced by selective adenosine A2A and A2B receptor agonists

A2A and A2B adenosine receptors produce regionally selective regulation of vascular tone and elicit differing effects on mean arterial pressure (MAP), whilst inducing tachycardia. The tachycardia induced by the stimulation of A2A or A2B receptors has been suggested to be mediated by a reflex increase in sympathetic activity. Here, we have investigated the role of β1- and β2-adrenoceptors in mediating the different cardiovascular responses to selective A2A and A2B receptor stimulation. Hemodynamic variables were measured in conscious male Sprague-Dawley rats (350–450 g) via pulsed Doppler flowmetry. The effect of intravenous infusion (3 min per dose) of the A2A-selective agonist CGS 21680 (0.1, 0.3, 1.0 µg.kg−1.min−1) or the A2B-selective agonist BAY 60–6583 (4.0, 13.3, 40.0 µg.kg−1.min−1) in the absence or following pre-treatment with the non-selective β-antagonist propranolol (1.0 mg.kg−1), the selective β1-antagonist CGP 20712A (200 µg.kg−1), or the selective β2-antagonist ICI 118,551 (2.0 mg.kg−1) was investigated (maintenance doses also administered). CGP 20712A and propranolol significantly reduced the tachycardic response to CGS 21680, with no change in the effect on MAP. ICI 118,551 increased BAY 60–6583-mediated renal and mesenteric flows, but did not affect the heart rate response. CGP 20712A attenuated the BAY 60–6583-induced tachycardia. These data imply a direct stimulation of the sympathetic activity via cardiac β1-adrenoceptors as a mechanism for the A2A- and A2B-induced tachycardia. However, the regionally selective effects of A2B agonists on vascular conductance were independent of sympathetic activity and may be exploitable for the treatment of acute kidney injury and mesenteric ischemia

The Influence of Health Literacy on Reach, Retention, and Success in a Worksite Weight Loss Program

To examine if employee health literacy (HL) status moderated reach, retention, and weight outcomes in a worksite weight loss program

COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors

The clinical manifestations of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for coronavirus disease 2019 (COVID-19) commonly include dyspnoea and fatigue, and they primarily involve the lungs. However, extra-pulmonary organ dysfunctions, particularly affecting the cardiovascular system, have also been observed following COVID-19 infection. In this context, several cardiac complications have been reported, including hypertension, thromboembolism, arrythmia and heart failure, with myocardial injury and myocarditis being the most frequent. These secondary myocardial inflammatory responses appear to be associated with a poorer disease course and increased mortality in patients with severe COVID-19. In addition, numerous episodes of myocarditis have been reported as a complication of COVID-19 mRNA vaccinations, especially in young adult males. Changes in the cell surface expression of angiotensin-converting enzyme 2 (ACE2) and direct injury to cardiomyocytes resulting from exaggerated immune responses to COVID-19 are just some of the mechanisms that may explain the pathogenesis of COVID-19-induced myocarditis. Here, we review the pathophysiological mechanisms underlying myocarditis associated with COVID-19 infection, with a particular focus on the involvement of ACE2 and Toll-like receptors (TLRs)