From sneaker to bourgeois male: Long-term observations on recognized tompot blenny Parablennius gattorugine individuals reveal new information on their biology.

The behaviour of the tompot blenny Parablennius gattorugine was studied by underwater observation and photography on the south-west coast of the UK over an 11 year period, with >50 individuals identified at two locations by their distinctive skin markings. Observations showed males engaging in rapid swimming behaviour when approached by a female, and younger males using alternative 'sneaker' tactics before becoming 'bourgeois' territory-holders. The noninvasive recognition technique also facilitated detailed observations on territory retention (up to 7 years) and agonistic behaviours among both males and females.

Breaking up of prolonged sitting over three days sustains, but does not enhance, lowering of postprandial plasma glucose and insulin in overweight and obese adults.

To compare the cumulative (3-day) effect of prolonged sitting on metabolic responses during a mixed meal tolerance test (MTT), with sitting that is regularly interrupted with brief bouts of light-intensity walking. Overweight/obese adults (n=19) were recruited for a randomized, 3-day, outpatient, cross-over trial involving: (1) 7-h days of uninterrupted sitting (SIT); and (2) 7-h days of sitting with light-intensity activity breaks [BREAKS; 2-min of treadmill walking (3.2 km/h) every 20 min (total: 17 breaks/day)]. On days 1 and 3, participants underwent a MTT (75 g of carbohydrate, 50 g of fat) and the incremental area under the curve (iAUC) was calculated from hourly blood samples. Generalized estimating equation (GEE) models were adjusted for gender, body mass index (BMI), energy intake, treatment order and pre-prandial values to determine effects of time, condition and time × condition. The glucose iAUC was 1.3 ± 0.5 and 1.5 ± 0.5 mmol·h·l(-1) (mean differences ± S.E.M.) higher in SIT compared with BREAKS on days 1 and 3 respectively (condition effect: P=0.001), with no effect of time (P=0.48) or time × condition (P=0.8). The insulin iAUC was also higher on both days in SIT (day 1: ∆151 ± 73, day 3: ∆91 ± 73 pmol·h·l(-1), P=0.01), with no effect of time (P=0.52) or time × condition (P=0.71). There was no between-treatment difference in triglycerides (triacylglycerols) iAUC. There were significant between-condition effects but no temporal change in metabolic responses to MTT, indicating that breaking up of sitting over 3 days sustains, but does not enhance, the lowering of postprandial glucose and insulin.

Successful renal denervation decreases the platelet activation status in hypertensive patients.

AIMS: To determine whether renal denervation (RDN) in hypertensive patients affects the platelet activation status. METHODS AND RESULTS: We investigated the effect of RDN on the platelet activation status in 41 hypertensive patients undergoing RDN. Ambulatory blood pressure (BP), plasma sympathetic neurotransmitter Neuropeptide Y, and platelet activation markers were measured at baseline, at 3 months, and 6 months after RDN. RDN significantly decreased BP at 3 months (150.6 ± 11.3/80.9 ± 11.4 mmHg to 144.7 ± 12.0/77.1 ± 11.1 mmHg; P < 0.01) and at 6 months (144.3 ± 13.8/78.3 ± 11.1 mmHg; P < 0.01). Plasma levels of the sympathetic neurotransmitter Neuropeptide Y, an indicator of sympathetic nerve activity, were significantly decreased at 3 months (0.29 ± 0.11 ng/mL to 0.23 ± 0.11 ng/mL; P < 0.0001) and at 6 months (0.22 ± 0.12 ng/mL; P < 0.001) after RDN. This was associated with a reduction in platelet membrane P-selectin expression (3 months, P < 0.05; 6 months, P < 0.05), soluble P-selectin (6 months, P < 0.05), circulating numbers of platelet-derived extracellular vesicles (EVs) (3 months, P < 0.001; 6 months, P < 0.01), and phosphatidylserine expressing EVs (3 months, P < 0.001; 6 months, P < 0.0001), indicative of a reduction in platelet activation status and procoagulant activity. Only patients who responded to RDN with a BP reduction showed inhibition of P-selectin expression at 3 months (P < 0.05) and 6 months (P < 0.05) as well as reduction of glycoprotein IIb/IIIa activation at 3 months (P < 0.05). Notably, 13 patients who took aspirin did not show significant reduction in platelet P-selectin expression following RDN. CONCLUSION: Our results imply a connection between the sympathetic nervous system and the platelet activation status and provide a potential mechanistic explanation by which RDN can have favourable effects towards reducing cardiovascular complications.

Ambulatory arterial stiffness index as a predictor of blood pressure response to renal denervation.

BACKGROUND: Renal denervation (RDN) can reduce blood pressure (BP) in patients with resistant hypertension, but less so in patients with isolated systolic hypertension. A possible explanation is that patients with stiffer arteries may have lesser neural contribution to their hypertension. METHOD: We hypothesized that arterial stiffness predicts the response to RDN. From ambulatory BP monitoring (ABPM), ambulatory arterial stiffness index (AASI) was calculated as 1 - the regression slope of DBP versus SBP. RESULTS: In 111 patients with resistant hypertension, RDN reduced office and 24-h SBP after 3, 6, and 12 months (by -11 ±â€Š22, -11 ±â€Š25, -14 ±â€Š21 mmHg for office, and -4 ±â€Š11, -5 ±â€Š12, -5 ±â€Š15 mmHg for 24-h SBP, respectively, P < 0.01). Patients with baseline AASI above the median (>0.51) showed no change in 24-h SBP at 6 months after RDN (-0.4 ±â€Š12.3 mmHg, P > 0.05), whereas an AASI below 0.51was associated with a marked reduction (-9.3 ±â€Š11.0 mmHg, P < 0.01). Across AASI quartiles, patients in the highest quartile (AASI ≥ 0.60) had lower muscle sympathetic nerve activity than the other three quartiles (39 ±â€Š13 versus 49 ±â€Š13 bursts/min, P = 0.035). The responder rate, defined as a 24-h SBP reduction of at least 5% was 58% in the lowest AASI quartile (<0.45) and 16% in the highest quartile (≥0.60). After adjustment for age, sex, BMI, office and 24-h SBP, an AASI less than 0.51predicted those who respond to RDN (odds ratio 3.46, P = 0.04). CONCLUSION: We conclude that in patients with resistant hypertension, a lower AASI is an independent predictor of the BP response to RDN, possibly explained by a more pronounced neurogenic rather than biomechanical contribution to their BP elevation.

The Effect of Renal Denervation on Plasma Adipokine Profile in Patients with Treatment Resistant Hypertension.

Background: We previously demonstrated the effectiveness of renal denervation (RDN) to lower blood pressure (BP) at least partially via the reduction of sympathetic stimulation to the kidney. A number of adipocyte-derived factors are implicated in BP control in obesity. Aim: The aim of this study was to examine whether RDN may have salutary effects on the adipokine profile in patients with resistant hypertension (RH). Methods: Fifty seven patients with RH undergoing RDN program have been included in this study (65% males, age 60.8 ± 1.5 years, BMI 32.6 ± 0.7 kg/m2, mean ± SEM). Throughout the study, the patients were on an average of 4.5 ± 2.7 antihypertensive drugs. Automated seated office BP measurements and plasma concentrations of leptin, insulin, non-esterified fatty acids (NEFA), adiponectin and resistin were assessed at baseline and the 3 months after RDN. Results: There was a significant reduction in mean office systolic (168.75 ± 2.57 vs. 155.23 ± 3.17 mmHg, p < 0.001) and diastolic (90.68 ± 2.31 vs. 83.74 ± 2.36 mmHg, p < 0.001) BP 3 months after RDN. Body weight, plasma leptin and resistin levels and heart rate remained unchanged. Fasting insulin concentration significantly increased 3 months after the procedure (20.05 ± 1.46 vs. 29.70 ± 2.51 uU/ml, p = 0.002). There was a significant drop in circulating NEFA at follow up (1.01 ± 0.07 vs. 0.47 ± 0.04 mEq/l, p < 0.001). Adiponectin concentration was significantly higher after RDN (5,654 ± 800 vs. 6,644 ± 967 ng/ml, p = 0.024). Conclusions: This is the first study to demonstrate that RDN is associated with potentially beneficial effects on aspects of the adipokine profile. Increased adiponectin and reduced NEFA production may contribute to BP reduction via an effect on metabolic pathways. Clinical Trial Registration Number: NCT00483808, NCT00888433.

Renal Denervation Reduces Monocyte Activation and Monocyte-Platelet Aggregate Formation: An Anti-Inflammatory Effect Relevant for Cardiovascular Risk.

Overactivation of renal sympathetic nervous system and low-grade systemic inflammation are common features of hypertension. Renal denervation (RDN) reduces sympathetic activity in patients with resistant hypertension. However, its effect on systemic inflammation has not been examined. We prospectively investigated the effect of RDN on monocyte activation and inflammation in patients with uncontrolled hypertension scheduled for RDN. Ambulatory blood pressure, monocyte, and monocyte subset activation and inflammatory markers were assessed at baseline, 3 months, and 6 months after procedure in 42 patients. RDN significantly lowered blood pressure at 3 months (150.5±11.2/81.0±11.2 mm Hg to 144.7±11.8/77.9±11.0 mm Hg), which was sustained at 6 months (144.7±13.8/78.6±11.0 mm Hg). Activation status of monocytes significantly decreased at 3 months (P<0.01) and 6 months (P<0.01) after the procedure. In particular, classical monocyte activation was reduced at 6 months (P<0.05). Similarly, we observed a reduction of several inflammatory markers, including monocyte-platelet aggregates (3 months, P<0.01), plasma monocyte chemoattractant protein-1 levels (3 months, P<0.0001; 6 months, P<0.05), interleukin-1ß (3 months, P<0.05; 6 months, P<0.05), tumor necrosis factor-α (3 months, P<0.01; 6 months, P<0.05), and interleukin-12 (3 months, P<0.01; 6 months, P<0.05). A positive correlation was observed between muscle sympathetic nerve activity and monocyte activation before and after the procedure. These results indicate that inhibition of sympathetic activity via RDN is associated with a reduction of monocyte activation and other inflammatory markers in hypertensive patients. These findings point to a direct interaction between the inflammatory and sympathetic nervous system, which is of central relevance for the understanding of beneficial cardiovascular effects of RDN.

Alternating Sitting and Standing Increases the Workplace Energy Expenditure of Overweight Adults.

BACKGROUND: To determine whether alternating bouts of sitting and standing at work influences daily workplace energy expenditure (EE). METHODS: Twenty-three overweight/obese office workers (mean ± SD; age: 48.2 ± 7.9 y, body mass index: 29.6 ± 4.0 kg/m2) undertook two 5-day experimental conditions in an equal, randomized order. Participants wore a "metabolic armband" (SenseWear Armband Mini) to estimate daily workplace EE (KJ/8 h) while working (1) in a seated work posture (SIT condition) or (2) alternating between a standing and seated work posture every 30 minutes using a sit-stand workstation (STAND-SIT condition). To assess the validity of the metabolic armband, a criterion measure of acute EE (KJ/min; indirect calorimetry) was performed on day 4 of each condition. RESULTS: Standing to work acutely increased EE by 0.7 [95% CI 0.3-1.0] KJ/min (13%), relative to sitting (P = .002). Compared with indirect calorimetry, the metabolic armband provided a valid estimate of EE while standing to work (mean bias: 0.1 [-0.3 to 0.4] KJ/min) but modestly overestimated EE while sitting (P = .005). Daily workplace EE was greatest during the STAND-SIT condition (mean condition difference [95% CI]: 76 [8-144] KJ/8-h workday, P = .03). CONCLUSIONS: Intermittent standing at work can modestly increase daily workplace EE compared with seated work in overweight/obese office workers.

Reverse cardiac remodeling after renal denervation: Atrial electrophysiologic and structural changes associated with blood pressure lowering.

BACKGROUND: Hypertension is the most common modifiable risk factor associated with atrial fibrillation. OBJECTIVE: The purpose of this study was to determine the effects of blood pressure (BP) lowering after renal denervation on atrial electrophysiologic and structural remodeling in humans. METHODS: Fourteen patients (mean age 64 ± 9 years, duration of hypertension 16 ± 11 years, on 5 ± 2 antihypertensive medications) with treatment-resistant hypertension underwent baseline 24-hour ambulatory BP monitoring, echocardiography, cardiac magnetic resonance imaging, and electrophysiologic study. Electrophysiologic study included measurements of P-wave duration, effective refractory periods, and conduction times. Electroanatomic mapping of the right atrium was completed using CARTO3 to determine local and regional conduction velocity and tissue voltage. Bilateral renal denervation was performed, and all measurements repeated after 6 months. RESULTS: After renal denervation, mean 24-hour BP reduced from 152/84 mm Hg to 141/80 mm Hg at 6-month follow-up (P < .01). Global conduction velocity increased significantly (0.98 ± 0.13 m/s to 1.2 ± 0.16 m/s at 6 months, P < .01), conduction time shortened (32 ± 5 ms to 27 ± 6 ms, P < .01), and complex fractionated activity was reduced (37% ± 14% to 19% ± 12%, P = .02). Changes in conduction velocity correlated positively with changes in 24-hour mean systolic BP (R(2) = 0.55, P = .01). There was a significant reduction in left ventricular mass (139 ± 37 g to 120 ± 29 g, P < .01) and diffuse ventricular fibrosis (T1 partition coefficient 0.39 ± 0.07 to 0.31 ± 0.09, P = .01) on cardiac magnetic resonance imaging. CONCLUSION: BP reduction after renal denervation is associated with improvements in regional and global atrial conduction and reductions in ventricular mass and fibrosis. Whether changes in electrical and structural remodeling are solely due to BP lowering or are due in part to intrinsic effects of renal denervation remains to be determined.

Health-related quality of life and blood pressure 12 months after renal denervation.

AIM: To examine the effect of renal denervation (RDN) on blood pressure (BP) and health-related quality of life (QoL) in patients with resistant hypertension, pseudoresistant hypertension due to a white-coat effect and in patients with uncontrolled masked hypertension. METHODS: Using the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36), Beck Depression Inventory (BDI) and Spielberger's state and trait anxiety questionnaires, we examined QoL, symptoms of depression and anxiety prior to and 12 months following RDN. BP was assessed from clinic and ambulatory blood pressure monitoring (ABPM) recordings. RESULTS: Patients with uncontrolled masked hypertension had the highest BDI and anxiety scores among all groups at baseline. Twelve months following RDN clinic and ambulatory BP were reduced only in those patients with resistant hypertension (delta SBP: clinic -16 ±â€Š3 mmHg, ABPMday -8 ±â€Š2 mmHg, ABPMnight -8 ±â€Š2 mmHg, all P < 0.01). Clinic BP was reduced in the pseudoresistant group (-17 ±â€Š6 mmHg, P < 0.01) but was elevated in the uncontrolled masked group (+13 ±â€Š6 mmHg, P = 0.02). In all patients, trait anxiety (P < 0.05), BDI scores (P < 0.05) and the SF-36 mental component summary (MCS) score (P < 0.001) were improved. The improvement in the SF-36 MCS was confined to those patients with resistant hypertension (+4.0 ±â€Š1.1, P < 0.01). The change in clinic BP after RDN was related to the baseline clinic BP (systolic: r = 0.54, P < 0.001; diastolic r = 0.43, P < 0.001), the number of ablations delivered (both clinic and mean day ABPM systolic r = 0.24, P < 0.05) and to the change in SF-36 MCS score (systolic: r = 0.25, P = 0.01; diastolic r = 0.24, P = 0.02). CONCLUSION: These results indicate that in patients with confirmed resistant hypertension, RDN is associated with a reduction in BP and a sustained improvement in mental health-related aspects of QoL.

Alternating bouts of sitting and standing attenuate postprandial glucose responses.

PURPOSE: This study aimed to examine whether reductions in sitting time through alternating 30-min bouts of sitting and standing can reduce postprandial glucose, insulin, and triglyceride responses. METHODS: Twenty-three overweight/obese sedentary office workers (17 males and six females; mean ± SD: age, 48.2 ± 7.9 yr; body mass index, 29.6 ± 4.0 kg · m(-2)) undertook two short-term (5 d) experimental conditions in an equal, randomized (1:1) order. In a simulated office environment, participants performed typical occupational tasks for 8 h · d(-1) while in a 1) seated work posture (control condition) or 2) interchanging between a seated and standing work posture every 30 min using an electric, height-adjustable workstation (intervention condition). Fasting and postprandial blood samples after a mixed test drink were collected hourly for 4 h on days 1 and 5 of each condition to assess serum insulin, plasma glucose, and triglycerides. Dietary intake (kJ · d(-1)) and physical activity were standardized during each condition. The trial was registered with the Australian New Zealand Clinical Trials Registry (ACTRN12611000632998). RESULTS: After adjustment for time (days 1 and 5), incremental area under the analyte time curve differed significantly between conditions for plasma glucose (P = 0.007) but not for serum insulin or plasma triglycerides. Adjusted mean glucose incremental area under the analyte time curve was lowered by 11.1% after the intervention condition (6.38 mM · h(-1) (confidence interval, 5.04-7.71)) relative to the control condition (7.18 mM · h(-1) (confidence interval, 5.85-8.52)). No temporal changes (days 1 vs 5) between conditions were observed. CONCLUSIONS: Alternating standing and sitting in 30-min bouts results in modest beneficial effects on postprandial glucose responses in overweight/obese office workers.