Dark chocolate reduces endothelial dysfunction after successive breath-hold dives in cool water

Objective

The aim of this study is to observe the effects of dark chocolate on endothelial function after a series of successive apnea dives in non-thermoneutral water.

Methods

Twenty breath-hold divers were divided into two groups: a control group (8 males and 2 females) and a chocolate group (9 males and 1 female). The control group was asked to perform a series of dives to 20 m adding up to 20 min in the quiet diving pool of Conflans-Ste-Honorine (Paris, France), water temperature was 27 °C. The chocolate group performed the dives 1 h after ingestion of 30 g of dark chocolate. Flow-mediated dilatation (FMD), digital photoplethysmography, nitric oxide (NO), and peroxynitrite ONOO^?) levels were measured before and after each series of breath-hold dives.

Results

A significant decrease in FMD was observed in the control group after the dives (95.28 ± 2.9 % of pre-dive values, p < 0.001) while it was increased in the chocolate group (104.1 ± 2.9 % of pre-dive values, p < 0.01). A decrease in the NO level was observed in the control group (86.76 ± 15.57 %, p < 0.05) whereas no difference was shown in the chocolate group (98.44 ± 31.86 %, p > 0.05). No differences in digital photoplethysmography and peroxynitrites were observed between before and after the dives.

Conclusion

Antioxidants contained in dark chocolate scavenge free radicals produced during breath-hold diving. Ingestion of 30 g of dark chocolate 1 h before the dive can thus prevent endothelial dysfunction which can be observed after a series of breath-hold dives.     

Effect of a single, open-sea, air scuba dive on human micro- and macrovascular function

Purpose

Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function.

Methods

Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) microvascular function (laser Doppler flowmetry), as well as endothelial-dependent (flow-mediated dilation) and endothelial-independent (nitroglycerin-mediated dilation) function. Bubble grades were monitored with Doppler according to the Spencer grade.

Results

The mean KISS bubble score ranged from 21.10 ± 4.7 at rest to 55.03 ± 8.8 after knee flexion. The increase in cutaneous vascular conductance elicited by either acetylcholine (25.34 ± 6.71 to 7.63 ± 1.25 %, p = 0.021) or sodium nitroprusside (35.24 ± 8.75 to 7.61 ± 1.86 %, p = 0.017) was significantly reduced after diving. Similarly, both flow-mediated dilation (10.8 ± 0.9 to 5.4 ± 1.5 %, p = 0.002) and nitroglycerin-mediated dilation (15 ± 1.1 to 6.5 ± 1.6 %, p = 0.002) were also significantly decreased. There were no correlations between vascular parameters and bubble formation.

Conclusions

There appears to be a reduction in endothelium-dependent and endothelium-independent, macro- and microvascular function associated with diving. Our results suggest that in the process of vascular dysfunction during diving, functional changes in the vessel wall may not be limited to the endothelium and may be mediated by alterations in vascular smooth muscle.     

Relationship Between Peer Victimization and Posttraumatic Stress Among Primary School Children

Peer victimization is a common stressor experienced by children. Although peer victimization has been studied extensively, few studies have examined the potential link between peer victimization and posttraumatic stress disorder (PTSD), and no studies of which we are aware have examined this link among children in primary school. The paucity of studies examining the link between PTSD and peer victimization in primary school is surprising because peer victimization occurs more frequently and is more likely to be physical among 7‐ and 8‐year‐old children. This study assessed the relationship between peer victimization and PTSD in a sample of 358 elementary school children (ages 6–11 years). Results indicated that peer victimization accounted for 14.1% of PTSD symptom severity among boys and 10.1% among girls. Additionally, we found gender differences in the types of peer victimization that were most associated with PTSD symptom severity (d = 0.38). The long‐term developmental consequences that may be associated with peer victimization‐linked PTSD symptomatology are discussed.     

Non-invasive measurement of choroidal volume change and ocular rigidity through automated segmentation of high-speed OCT imaging

We have developed a novel optical approach to determine pulsatile ocular volume changes using automated segmentation of the choroid, which, together with Dynamic Contour Tonometry (DCT) measurements of intraocular pressure (IOP), allows estimation of the ocular rigidity (OR) coefficient. Spectral Domain Optical Coherence Tomography (OCT) videos were acquired with Enhanced Depth Imaging (EDI) at 7Hz during ~50 seconds at the fundus. A novel segmentation algorithm based on graph search with an edge-probability weighting scheme was developed to measure choroidal thickness (CT) at each frame. Global ocular volume fluctuations were derived from frame-to-frame CT variations using an approximate eye model. Immediately after imaging, IOP and ocular pulse amplitude (OPA) were measured using DCT. OR was calculated from these peak pressure and volume changes. Our automated segmentation algorithm provides the first non-invasive method for determining ocular volume change due to pulsatile choroidal filling, and the estimation of the OR constant. Future applications of this method offer an important avenue to understanding the biomechanical basis of ocular pathophysiology.OCIS codes: (170.3880) Medical and biological imaging, (170.4460) Ophthalmic optics and devices, (170.6935) Tissue characterization     

The p.A382T TARDBP gene mutation in Sardinian patients affected by Parkinson's disease and other degenerative parkinsonisms

Based on our previous finding of the p.A382T founder mutation in ALS patients with concomitant parkinsonism in the Sardinian population, we hypothesized that the same variant may underlie Parkinson's disease (PD) and/or other forms of degenerative parkinsonism on this Mediterranean island. We screened a cohort of 611 patients with PD (544 cases) and other forms of degenerative parkinsonism (67 cases) and 604 unrelated controls for the c.1144G > A (p.A382T) missense mutation of the TARDBP gene. The p.A382T mutation was identified in nine patients with parkinsonism. Of these, five (0.9 % of PD patients) presented a typical PD (two with familiar forms), while four patients (6.0 % of all other forms of parkinsonism) presented a peculiar clinical presentation quite different from classical atypical parkinsonism with an overlap of extrapyramidal–pyramidal–cognitive clinical signs. The mutation was found in eight Sardinian controls (1.3 %) consistent with a founder mutation in the island population. Our findings suggest that the clinical presentation of the p.A382T TARDBP gene mutation may include forms of parkinsonism in which the extrapyramidal signs are the crucial core of the disease at onset. These forms can present PSP or CBD-like clinical signs, with bulbar and/or extrabulbar pyramidal signs and cognitive impairment. No evidence of association has been found between TARDBP gene mutation and typical PD.     

When to perform bone scan in patients with newly diagnosed prostate cancer: external validation of a novel risk stratification tool

Purpose

To externally validate the performance characteristics of the Briganti’s risk stratification tool for baseline staging bone scan in patients with newly diagnosed prostate cancer (PCa).

Methods

From 2009 onwards, a consecutive series of patients with PCa were enrolled. All patients were staged to evaluate the presence of bone metastasis (BM) with a conventional total-body Tc 99 m MDP scintigraphy performed regardless of baseline PCa characteristics. The area under the curve (AUC) estimates were used to test the accuracy of the Briganti’s risk stratification tool that recommended staging baseline bone scan for patients with a biopsy Gleason score >7 or with a prostate-specific antigen (PSA) >10 ng/ml and palpable disease (cT2/T3). The new tool was compared to the European Association of Urology (EAU) guideline.

Results

A total of 313 patients were consecutively enrolled. Median age was 68 (range 49–95 years), and median PSA was 7 ng/ml (range 0.81–2,670). Twenty (6.4 %) patients presented BMs. Patients with BMs were significantly older, with higher PSA and a higher Gleason score (p = 0.001). The novel Briganti’s model was significantly (p = 0.001) more accurate (AUC: 0.75; CI: 0.632–0.859) than the EAU guideline (AUC: 0.64; CI: 0.52–0.761) for the prediction of BMs.

Conclusions

Our study validated in a group of patients with PCa the novel risk stratification tool proposed by Briganti, which presented a higher accuracy for baseline staging bone scan when compared with the EAU guideline. In our experience, this approach would further reduce (about 60 %) the use of staging baseline bone scan without compromising the ability to detect BMs in patients with PCa.     

Prostaglandin E2 type 1 receptors contribute to neuronal apoptosis after transient forebrain ischemia

Cyclooxygenase-2-derived prostaglandin E₂ (PGE₂) contributes to excitotoxic and ischemic neuronal cell death by engaging neuronal PGE₂ type 1 receptors (EP1R). Our previous studies have shown that EP1R signaling resulted in disturbances of intracellular Ca²⁺ homeostasis and suppression of the pro-survival protein kinase AKT. The aim of this study was to investigate whether these pathophysiological mechanism have a role in the neuronal cell death after transient forebrain ischemia. Mice were subjected to ischemia/reperfusion by bilateral common carotid artery occlusion. Hippocampal cornu ammonis area 1 (CA1) neuronal cell death was determined 5 days after reperfusion. Animals treated with the EP1R antagonist SC51089 or EP1R-deficient mice (EP1^−/−) showed significantly less neuronal injury as compared to vehicle-treated wild-type controls. Benefits of EP1R blockage were still evident 14 days after injury. Better neuronal survival was correlated with reduced neuronal caspase-3 activity and decreased nuclear translocation of the apoptosis-inducing factor . Neuroprotection could be reverted by intracerebroventricular administration of the phosphoinositide 3-kinase inhibitor {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002 and was not further increased by the calcineurin inhibitor FK506. These data implicate EP1R in postischemic neuronal apoptosis possibly by facilitating AKT inhibition.