Acute immune-inflammatory responses to a single bout of aerobic exercise in smokers; The effect of smoking history and status

© 2015 Kastelein, Duffield and Marino. This study examined the acute immune and inflammatory responses to exercise in smokers compared to non-smokers, and further, the effect of smoking history on these immune-inflammatory responses. Fifty-four recreationally active males who were either smokers (SM; n = 27) or non-smokers (NS; n = 27) were allocated into either young (YSM, YNS) or middle-aged groups (MSM, MNS) based on smoking status. Participants were matched for fitness and smoking habits and following familiarization and baseline testing, undertook an exercise protocol that involved 40 min of cycle ergometry at 50% of VO2peak. Venous blood was obtained pre- and post- (0 min, 1, and 4 h) exercise to measure circulating leukocytes and inflammatory markers interleukin (IL)-6, IL-1β, IL-1ra, and monocyte chemoattractant protein-1 (MCP-1). Compared to MNS, MSM showed elevated basal concentrations of MCP-1, which were increased with a longer smoking history (P < 0.05). In response to exercise, YSM demonstrated an amplified IL-6 response from immediately- to 1 h-post compared to YNS. Furthermore, IL-1ra in YSM was elevated above that of YNS across all time points (P < 0.05). The MSM group had higher IL-1β at baseline when compared to YSM, although IL-1ra was greater for YSM at baseline (P < 0.05). Finally, the post-exercise leukocyte response was greater in MSM compared to YSM and non-smokers (P < 0.05). In conclusion, smoker's exhibit elevated MCP-1 and IL-1β that seem to be evident with a longer smoking history (~15 years). Furthermore, the differences in exercise-induced inflammatory responses noted in YSM may be indicative tobacco smoke exposure priming circulating leukocytes to amplify inflammatory responses

The effect of high-intensity aerobic interval training on markers of systemic inflammation in sedentary populations

© 2017, Springer-Verlag Berlin Heidelberg. Purpose: This study examined the effects of high-intensity interval training (HIIT; 30 s sprint, 4–5 min passive recovery) and prolonged intermittent sprint training (PIST; 10 s sprint, 2–3 min moderate exercise) on the systemic inflammatory markers C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α), aerobic capacity, and anthropometry in a middle-aged, sedentary population. Methods: Fifty-five sedentary adults (age 49.2 ± 6.1 years) were randomised into HIIT (n = 20), PIST (n = 21), or a sedentary control group (CTRL n = 14). HIIT and PIST performed three training sessions per week for 9 weeks on a cycle ergometer, matched for total high-intensity time, while CTRL continued normal sedentary behaviours. Pre- and post-intervention testing involved measures of anthropometry, peak oxygen consumption (VO2peak), and venous blood collection for analyses of CRP and TNF-α. Results: HIIT and PIST increased VO2peak compared to CTRL (+3.66 ± 2.23 and 3.74 ± 2.62 mL kg min−1). A group × time interaction (p = 0.042) and main effect of time (p = 0.026) were evident for waist girth, with only HIIT showing a significant reduction compared to CTRL (−2.1 ± 2.8 cm). TNF-α and CRP showed no group × time interaction or time effect (p > 0.05). Conclusions: In sedentary individuals, 9 weeks of HIIT or PIST were effective to improve aerobic capacity; however, only HIIT significantly reduced waist girth and WHR compared to CTRL. Markers of systemic inflammation remained unchanged across all groups. Accordingly, for inflammation and VO2peak, the distribution of sprints and the active or passive recovery periods are inconsequential provided that total duration of high-intensity efforts is similar

Human in situ cytokine and leukocyte responses to acute smoking

© 2017 The Author(s). This study examined immune/inflammatory parameters following an acute tobacco smoking episode in smokers with varying smoking histories. Twenty-eight male habitual smokers were categorized according to smoking history, e.g. younger smoker (YSM) or middle-aged smoker (MSM). Participants were matched for fitness and smoking habits and following baseline testing, undertook a smoking protocol involving consumption of two cigarettes within 15 min. Venous blood was collected pre- and immediately, 1 h, and 4 h post-protocol to permit analyses of circulating levels of interleukin (IL)-6, IL-1β, IL-1ra, monocyte chemoattractant protein-1 (MCP-1), C-reactive protein (CRP), and leukocytes. No baseline differences were observed between groups for IL-1ra, IL-1β, or leukocytes. MCP-1 and IL-6 levels were significantly (p<0.05) elevated at baseline in YSM. Both groups showed an increase in MCP-1 levels from pre- to immediately post-cigarette consumption. The MSM also displayed an increase in IL-6 post-smoking, followed by a decline over the period from 1 to 4 h thereafter. A significant decline in circulating lymphocyte and eosinophil levels from immediately post-cigarette consumption to 1 h later was observed in both groups. Monocyte levels in the YSM followed a similar profile but no significant effects on this cell type were evident in the MSM. From these results, a 10-year difference in smoking history induces mild leukopenia. Altered responses due to smoking were also evident with respect to levels of circulating biomarkers, which may be indicative of an effect of differences in cumulative smoking history

Prevention of cardiovascular disease in patients with familial hypercholesterolaemia: the role of PCSK9 inhibitors

Familial hypercholesterolaemia is an autosomal dominant inherited disorder characterised by elevated low-density lipoprotein cholesterol levels and consequently an increased risk of atherosclerotic cardiovascular disease (ASCVD). Familial hypercholesterolaemia is relatively common, but is often underdiagnosed and undertreated. Cardiologists are likely to encounter many individuals with familial hypercholesterolaemia; however, patients presenting with premature ASCVD are rarely screened for familial hypercholesterolaemia and fasting lipid levels are infrequently documented. Given that individuals with familial hypercholesterolaemia and ASCVD are at a particularly high risk of subsequent cardiac events, this is a missed opportunity for preventive therapy. Furthermore, because there is a 50% chance that first-degree relatives of individuals with familial hypercholesterolaemia will also be affected by the disorder, the underdiagnosis of familial hypercholesterolaemia among patients with ASCVD is a barrier to cascade screening and the prevention of ASCVD in affected relatives. Targeted screening of patients with ASCVD is an effective strategy to identify new familial hypercholesterolaemia index cases. Statins are the standard treatment for individuals with familial hypercholesterolaemia; however, low-density lipoprotein cholesterol targets are not achieved in a large proportion of patients despite treatment. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have been shown to reduce low-density lipoprotein cholesterol levels considerably in individuals with familial hypercholesterolaemia who are concurrently receiving the maximal tolerated statin dose. The clinical benefit of PCSK9 inhibitors must, however, also be considered in terms of their cost-effectiveness. Increased awareness of familial hypercholesterolaemia is required among healthcare professionals, particularly cardiologists and primary care physicians, in order to start early preventive measures and to reduce the mortality and morbidity associated with familial hypercholesterolaemia and ASCVD

Cerebral oxygenation and sympathetic responses to smoking in young and middle-aged smokers

© The Author(s) 2016. This study examined the effects of acute tobacco smoking on cerebral oxygenation and autonomic function in 28 male, habitual smokers of shorter young smokers (YSM) or longer middle-aged smokers (MSM) smoking history. Following baseline testing, participants undertook a smoking protocol involving the consumption of two cigarettes within 15 min. Measures of cerebral oxygenation and autonomic function were collected before, during, and 0 min, 30 min, 1 h, and 4 h post-smoking. Tissue saturation index (TSI) for MSM was greater than YSM during cigarette consumption (p < 0.05). Moreover, MSM observed significant within-group changes for TSI during and post-cigarette consumption (p < 0.05). Further, MSM observed an increase in low frequency (LF) band from 30 min to 1 h post-consumption, followed by a decline, whereas elevations above MSM were observed in YSM at 4 h (p < 0.05). Both MSM and YSM showed a decrease in high-frequency (HF) band post-cigarette, while increased LF/HF ratio post-consumption was observed in YSM. A decline in the standard deviation of RR intervals, post-cigarette consumption was evident in MSM (p < 0.05). Moreover, the root mean square of RR interval in both groups similarly decreased following cigarette consumption (p < 0.05). Acute smoking affects heart rate variability, suggestive of vagal withdrawal, and maybe indicate an effect of smoking history. Additionally, prolonged smoking history alters cerebral microcirculatory responses to acute tobacco exposure in MSM

Infektionsabwehr und lymphatischer Rachenring

Foraging behaviours used by two female Australian fur seals (Arctocephalus pusillus doriferus) were documented during controlled feeding trials. During these trials the seals were presented with prey either free-floating in open water or concealed within a mobile ball or a static box feeding device. When targeting free-floating prey both subjects primarily used raptorial biting in combination with suction, which was used to draw prey to within range of the teeth. When targeting prey concealed within either the mobile or static feeding device, the seals were able to use suction to draw out prey items that could not be reached by biting. Suction was followed by lateral water expulsion, where water drawn into the mouth along with the prey item was purged via the sides of the mouth. Vibrissae were used to explore the surface of the feeding devices, especially when locating the openings in which the prey items had been hidden. The mobile ball device was also manipulated by pushing it with the muzzle to knock out concealed prey, which was not possible when using the static feeding device. To knock prey out of this static device one seal used targeted bubble blowing, where a focused stream of bubbles was blown out of the nose into the openings in the device. Once captured in the jaws, prey items were manipulated and re-oriented using further mouth movements or chews so that they could be swallowed head first. While most items were swallowed whole underwater, some were instead taken to the surface and held in the teeth, while being vigorously shaken to break them into smaller pieces before swallowing. The behavioural flexibility displayed by Australian fur seals likely assists in capturing and consuming the extremely wide range of prey types that are targeted in the wild, during both benthic and epipelagic foraging

Random variables with completely independent subcollections

AbstractWe investigate the algebra and geometry of the independence conditions on discrete random variables in which we consider a collection of random variables and study the condition of independence of some subcollections. We interpret independence conditions as an ideal of algebraic relations. After a change of variables, this ideal is generated by generalized 2×2 minors of multi-way tables and linear forms. In particular, let Δ be a simplicial complex on some random variables and A be the table corresponding to the product of those random variables. If A is Δ-independent table then A can be written as the entrywise sum AI+A0 where AI is a completely independent table and A0 is identically 0 in its Δ-margins.We compute the isolated components of the original ideal, showing that there is only one component that could correspond to probability distributions, and relate the algebra and geometry of the main component to that of the Segre embedding. If Δ has fewer than three facets, we are able to compute generators for the main component, show that it is Cohen–Macaulay, and give a full primary decomposition of the original ideal