Dilatation Function Research Articles

Assessment of intracardiac flow and vorticity in the right heart of patients after repair of tetralogy of Fallot by flow-sensitive 4D MRI.

To comprehensively and quantitatively analyse flow and vorticity in the right heart of patients after repair of tetralogy of Fallot (rTOF) compared with healthy volunteers. Time-resolved flow-sensitive 4D MRI was acquired in 24 rTOF patients and 12 volunteers. Qualitative flow evaluation was based on consensus reading of two observers. Quantitative analysis included segmentation of the right atrium (RA) and ventricle (RV) in a four-chamber view to extract volumes and regional haemodynamic information for computation of regional mean and peak vorticity. Right heart intra-atrial, intraventricular and outflow tract flow patterns differed considerably between rTOF patients and volunteers. Peak RA and mean RV vorticity was significantly higher in patients (p = 0.02/0.05). Significant negative correlations were found between patients' maximum and mean RV and RA vorticity and ventricular volumes (p < 0.05). The main pulmonary artery (MPA) regurgitant flow was associated with higher RA and RV vorticity, which was significant for RA maximum and RV mean vorticity (p = 0.01/0.03). The calculation of vorticity based on 4D flow data is an alternative approach to assess intracardiac flow changes in rTOF patients compared with qualitative flow visualization. Alterations in intracardiac vorticity could be relevant with regard to the development of RV dilation and impaired function. • 4D flow MRI with vorticity calculation enables a novel approach to assess intracardiac flow. • Significantly higher intracardiac vorticity occurred in patients after repair of tetralogy of Fallot. • Regurgitant flow in the main pulmonary artery is associated with higher right heart vorticity.

A computational study on the superionic behaviour of ThO2.

This study reports the density functional theory (DFT) and classical molecular dynamics (MD) study of the lattice dynamical, mechanical and anionic transport behaviours of ThO2 in the superionic state. DFT calculations of phonon frequencies were performed at different levels of approximation as a function of isotropic dilation (ε) in the lattice parameter. With the expansion of the lattice parameter, there is a softening of B1u and Eu phonon modes at the X symmetry point of the Brillouin zone. As a result of the nonlinear decrease at the X point, the B1u and Eu phonon modes cross each other at ε = 0.03, which is associated with a sharp increase in the narrow peak of the phonon density of states, signifying a higher occupation and hence a higher coupling of these modes at high temperatures. The mode crossing also indicates anionic conductivity in the 〈001〉 direction leading to occupation of interstitial sites. Moreover, MD and nudged elastic band calculated diffusion barriers indicate that 〈001〉 is the easy direction for anion migration in the normal and superionic states. With a further increase in the lattice parameter, the B1u mode continues to soften and becomes imaginary at a strain (ε) of 0.036 corresponding to a temperature of 3430 K. The calculated temperature variation of single crystal elastic constants shows that the fluorite phase of ThO2 remains elastically stable up to the superionic regime, though the B1u phonon mode is imaginary in that state. This leads to anionic disorder at elevated temperatures. Tracking of anion positions in the superionic state as a function of time in MD simulations suggests a hopping model in which the oxygen ions migrate from one tetrahedral site to another via octahedral interstitial sites.

乳児期に診断し長期経過観察しているUhl病の一例

Uhl’s anomaly is a rare cardiac disease of unknown etiology characterized by a markedly distended right ventricle because of partial or complete absence of right ventricular myocardium, which consequently develops a parchment-like appearance. Patients usually present with symptoms in infancy and rarely survive to adulthood. We report the case of an 18-year-old patient with Uhl’s anomaly who was diagnosed in infancy and survived to adulthood without symptoms of heart failure. Angiocardiography at the age of 6-years showed a dilated right ventricle. Magnetic resonance imaging (MRI) at the age of 12-years showed an extremely dilated thin-walled right ventricle with almost complete absence of right ventricular myocardium. At the age of 15-years, his MRI images showed further dilatation of the right ventricle. Follow-up examinations revealed to manifestation of right heart failure, despite persistent right ventricular dilatation and impaired function. This case may be useful for understanding the natural history of Uhl’s anomaly.

Pulmonary Artery Dilation and Right Ventricular Function in Acute Kawasaki Disease.

Coronary artery inflammation and aneurysm formation are the most common complications of Kawasaki disease (KD). Valvulitis and myocarditis are also well described and may lead to valvar regurgitation and left ventricular dysfunction. However, functional changes in the right heart have rarely been reported. We noted several acute KD patients with dilated pulmonary arteries (PA) and thus sought to systematically characterize PA size and right-heart function in an unselected cohort of KD patients cared for at a single clinical center. Clinical, laboratory, and echocardiographic data from 143 acute KD subjects were analyzed. PA dilation was documented in 23 subjects (16.1 %); these subjects had higher median right ventricle myocardial performance index (RV MPI), higher ratio of early tricuspid inflow velocity to tricuspid annular early diastolic velocity (TV E/e'), and lower median TV e' velocity compared to the non-PA dilation group (0.50 vs 0.38 p < 0.01, 4.2 vs 3.6 p < 0.05, and 13.5 vs 15.2 cm/s p < 0.01, respectively). Almost all subjects with PA dilation had improved PA Z-score, RV MPI, and TV E/e' in the subacute phase (p < 0.01). There were no significant differences in indices of left ventricle function between PA dilation group and non-PA dilation group. In summary, PA dilation was documented in 16 % of acute KD subjects. These subjects were more likely to have echocardiographic indices consistent with isolated RV dysfunction that improved in the subacute phase. The long-term consequence of these findings will require longitudinal studies of this patient population.

An arithmetical approach to the convergence problem of series of dilated functions and its connection with the Riemann Zeta function

Given a periodic function f, we study the convergence almost everywhere and in norm of the series ∑kckf(kx). Let f(x)=∑m=1∞amsin⁡2πmx where ∑m=1∞am2d(m)<∞ and d(m)=∑d|m1, and let fn(x)=f(nx). We show by using a new decomposition of squared sums that for any K⊂N finite, ‖∑k∈Kckfk‖22≤(∑m=1∞am2d(m))∑k∈Kck2d(k2). If f(s)(x)=∑j=1∞sin⁡2πjxjs, s>1/2, by only using elementary Dirichlet convolution calculus, we show that for 0<ε≤2s−1, ζ(2s)−1‖∑k∈Kckfk(s)‖22≤1+εε(∑k∈K|ck|2σ1+ε−2s(k)), where σh(n)=∑d|ndh. From this we deduce that if f∈BV(T), 〈f,1〉=0 and∑kck2(log⁡log⁡k)4(log⁡log⁡log⁡k)2<∞, then the series ∑kckfk converges almost everywhere. This slightly improves a recent result, depending on a fine analysis on the polydisc [1, th. 3] (nk=k), where it was assumed that ∑kck2(log⁡log⁡k)γ converges for some γ>4. We further show that the same conclusion holds under the arithmetical condition∑kck2(log⁡log⁡k)2+bσ−1+1(log⁡log⁡k)b/3(k)<∞, for some b>0, or if ∑kck2d(k2)(log⁡log⁡k)2<∞. We also derive from a recent result of Hilberdink an Ω-result for the Riemann Zeta function involving factor closed sets. As an application we find that simple conditions on T and ν ensuring that for any σ>1/2, 0≤ε<σ, we havemax1≤t≤T⁡|ζ(σ+it)|≥C(σ)(1σ−2ε(ν)∑n|νσ−s+ε(n)2n2ε)1/2. We finally prove an important complementary result to Wintner's famous characterization of mean convergence of series ∑k=0∞ckfk.

Evidence of microvascular dysfunction in heart failure with preserved ejection fraction

ObjectiveWhile vascular dysfunction is well defined in patients with heart failure (HF) with reduced ejection fraction (HFrEF), disease-related alterations in the peripheral vasculature of patients with HF with preserved ejection...

Abstract 16027: Low-dose Clofibrate Protects the Heart and Kidney in the 5/6 NX Model of Chronic Kidney Disease

Cardiovascular related disease and/or events are the leading single cause of death in patients with chronic kidney disease (CKD), yet the pathological mechanisms involved are not well understood. We have previously reported that the 5/6 nephrectomy (5/6 NX) rat model of CKD exhibits left ventricle (LV) dilation, reduced function, and increased miR-21 levels 7 weeks post-surgery. Suppression of miR-21 prevented LV dilation and improved cardiac function, at least in part, by upregulation of target peroxisome proliferator-activated receptor alpha (PPARα). The focus of this study was to evaluate the therapeutic potential of clofibrate (CLO), a PPARα agonist, in the 5/6 NX model. We hypothesized that low-dose CLO treatment would reduce cardiac dysfunction in 5/6 NX rats. To test this, we performed 5/6 NX or sham surgery on 10 week old male Sprague Dawley rats. Left ventricular remodeling and function was evaluated by echocardiography prior to surgery and bi-weekly thereafter, throughout the 10 week study. Renal function was monitored by 24 hour urine and plasma creatinine measurements at those time points. We administered CLO (25 mg/kg/day i.p., roughly 1/10 the dose commonly used in rats) to a subset of animals (n=4-6/group) beginning 5 weeks post-5/6 NX. We found that 5/6 NX rats developed progressive LV dilation and impaired function over the 10 week study. Treatment with CLO completely prevented LV dilation and normalized wall thickness. Further, CLO treatment significantly increased % fractional shortening (47.9±6.0 CLO vs. 32.6±1.7 5/6 NX control, p&lt;0.05, ANOVA). With 10 weeks of 5/6 NX proximal convoluted tubules exhibited a loss of brush border, severe dilation of the tubules, and extensive epithelial shedding. Treatment of 5/6 NX rats with CLO largely prevented these changes. Despite this improvement in tubular morphology, plasma creatinine levels were not different than 5/6 NX controls. In conclusion, we find that low-dose CLO treatment initiated during progressive kidney disease is both cardio- and reno-protective. Our data suggest that PPARα agonists may be an effective therapeutic intervention in established CKD.

Abstract 18119: Structural and Functional Right Ventricular Remodelling is Related to Training Intensity in an Experimental Model of Endurance Training

Background: a deleterious, potentially arrhythmogenic right ventricle (RV) remodelling has been documented in response to regular training in athletes. However, it is unclear how exercise intensity contributes to RV adverse remodelling. Aim: Our aim was to evaluate the relationship between RV functional and structural remodelling,and the intensity of exercise in an animal model. Methods: Thirty-six Wistar rats were conditioned to run daily in a treadmill at a moderate (MOD, 45 min at 30cm/s; estimated 60% VO2max) or vigorous (VIG, 60 min at 60cm/s; estimated 85-90% VO2max) intensity for 16 weeks; Sedentary rats (SED) served as controls. An standard echocardiographic assessment of both ventricles and Tissue Doppler Imaging (TDI) of the RV were performed. Hemodynamics of both ventricles were evaluated with a sensor tip pressure catheter. Results: After MOD training, both ventricles similarly dilated (roughly 15%). RV function improved as shown by increased RV apical function assessed by TDI (Figure).With VIG training, though, RV disproportionately dilated (in comparison to MOD: 10±13% RV dilation vs 1±12% LV dilation, p&lt;0.05), RV systolic function declined, and RV diastolic function worsened (Figure).The hemodynamic experiments confirmed a decreased RV contractility and impaired relaxation with VIG training (Figure) in comparison to MOD. The LV systolic and diastolic function were unchanged in all groups. Conclusion: In this animal model we show that exercise intensity critically determines a dual response of the RV. A favourable adaptation of the RV after MOD training turned into disproportionate RV dilatation, decreased contractility and worse diastolic function in the VIG group. Our findings suggest the existence of an intensity threshold beyond which remodelling of the RV becomes maladaptive. Our work provides valuable data to identify athletes at risk of exercise related complications

Abstract 11691: Atorvastatin Reverses Impaired Voltage-gated K + Channels-mediated Coronary Vasodilation By Upregulating PPARγ In Diabetes (Best of Basic Science Abstract)

Aims: Voltage-gated K + (K v ) channels in vascular smooth muscle cells (VSMCs) play an important role in the regulation of coronary microcirculation. Atorvastatin (ATV) has shown some beneficial effects on vascular function, but the effect of ATV on K v channels-mediated coronary vasodilation remains unknown. The present study was designed to investigate the role of ATV in improving K v channels-mediated coronary dilator function in diabetes and the underlying mechanisms. Methods: Isolated VSMCs were incubated in normal or high glucose medium plus a different dose of ATV for 24 h at 37 o C. Patch-clamp recording and molecular biological techniques were used to assess the function and expression of K v channels. Control or type 2 diabetic rats were treated with ATV (50 mg/kg daily) by oral gavage for 10 weeks. Vasodilation of isolated rat coronary arteries was measured using a pressurized myograph. GW9662, the peroxisome proliferator-activated receptor gamma (PPARγ) antagonist, was used to determine whether the mechanism of ATV-improved K v channel function can be explained by upregulation of PPARγ pathway. Results: Patch-clamp analysis revealed that high glucose reduced K v current density by 58.7 ± 4.6%, which was accompanied by a downregulation of K v 1.2 and K v 1.5 expression. Treatment with ATV reversed the inhibitory effect of high glucose on K v current density in a dose-dependent manner (1 μmol/L, 15.0 ± 2.6%; 10 μmol/L, 49.1 ± 3.8%; 100 μmol/L, 69.9 ± 4.8%; P &lt; 0.05). In addition, ATV restored high glucose-induced downregulation of K v channel protein expression, and the difference was significant in both 10 μmol/L and 100 μmol/L groups. For in vivo study, K v channels-mediated coronary vasodilation was decreased in diabetic rats, compared with controls (9.1 ± 1.3 vs. 36.7 ± 1.4%, P &lt; 0.05), whereas this decrease was partly corrected by ATV (25.0 ± 2.8 vs. 9.1 ± 1.3%, P &lt; 0.05). Treatment with ATV prominently increased protein expression of PPARγ both in vitro and in vivo . The effect of ATV in regulating K v channels and K v channels-mediated vasodilation was markedly blunted by GW9662. Conclusions: In conclusion, treatment with ATV activates PPARγ pathway and preserves K v channel activity in VSMCs, thus providing improvement of coronary dilator function in diabetic rats.

A red orange extract modulates the vascular response to a recreational dive: a pilot study on the effect of anthocyanins on the physiological consequences of scuba diving

Nutritional antioxidants have been proposed as an expedient strategy to counter the potentially deleterious effects of scuba diving on endothelial function, flow-mediated dilation (FMD) and heart function. Sixteen volunteers performing a single standard dive (20 min at 33 m) according to US Navy diving procedures were randomly assigned to two groups: one was administered with two doses of 200 mg of an anthocyanins (AC)-rich extract from red oranges, 12 and 4 h before diving. Anthocyanins supplementation significantly modulated the effects of diving on haematocrit, body water distribution and FMD. AC administration significantly reduces the potentially harmful endothelial effects of a recreational single dive. The lack of any significant effect on the most common markers of plasma antioxidant capacity suggests that the mechanism underlying this protective activity is independent of the putative antioxidant effect of AC and possibly involves cellular signalling modulation of the response to high oxygen.

Pronephric tubule morphogenesis in zebrafish depends on Mnx mediated repression of irx1b within the intermediate mesoderm

Mutations in the homeobox transcription factor MNX1 are the major cause of dominantly inherited sacral agenesis. Studies in model organisms revealed conserved mnx gene requirements in neuronal and pancreatic development while Mnx activities that could explain the caudal mesoderm specific agenesis phenotype remain elusive. Here we use the zebrafish pronephros as a simple yet genetically conserved model for kidney formation to uncover a novel role of Mnx factors in nephron morphogenesis. Pronephros formation can formally be divided in four stages, the specification of nephric mesoderm from the intermediate mesoderm (IM), growth and epithelialisation, segmentation and formation of the glomerular capillary tuft. Two of the three mnx genes in zebrafish are dynamically transcribed in caudal IM in a time window that proceeds segmentation. We show that expression of one mnx gene, mnx2b, is restricted to the pronephric lineage and that mnx2b knock-down causes proximal pronephric tubule dilation and impaired pronephric excretion. Using expression profiling of embryos transgenic for conditional activation and repression of Mnx regulated genes, we further identified irx1b as a direct target of Mnx factors. Consistent with a repression of irx1b by Mnx factors, the transcripts of irx1b and mnx genes are found in mutual exclusive regions in the IM, and blocking of Mnx functions results in a caudal expansion of the IM-specific irx1b expression. Finally, we find that knock-down of irx1b is sufficient to rescue proximal pronephric tubule dilation and impaired nephron function in mnx-morpholino injected embryos. Our data revealed a first caudal mesoderm specific requirement of Mnx factors in a non-human system and they demonstrate that Mnx-dependent restriction of IM-specific irx1b activation is required for the morphogenesis and function of the zebrafish pronephros.

Progression of cervical dilatation in normal human labor is unpredictable.

The aim of this study was to analyze how the progression of cervical dilatation in active labor can be predicted by digital assessment in low-risk pregnant women, in spontaneous labor at term. This prospective observational study was performed on 328 women with singleton term gestations experiencing midwife-led labor according to local protocols, progressing to full dilatation and spontaneous delivery without any medical intervention. Mixed nonlinear models were adopted to (i) model individual cervical data into centile curves and (ii) calculate the time needed to gain 1 cm in cervical dilatation (TNG1cm ) modeled as a function of current dilatation. We correlated the first and the last TNG1cm on parturients with at least four cervical data points. TNG1cm showed large variations, both before and after 6 cm. This variability of natural progression of cervical curves described by the 10th and 90th centiles exceeded the differences observed in published curves from cohorts homogeneous for parity, weight and ethnicity. There was no significant correlation between the first and the last TNG1cm . Neonatal base excess was not significantly different in women with TNG1cm <10th centile and >90th centile. The rate of cervical dilatation, traced by parsimonious nonlinear mixed models, is largely unpredictable in the case of spontaneous naturally progressing labor, even when possible larger individual variability is excluded by prudent clinical rules. Future research in labor and delivery should be focused on the diagnosis of the causes that lie behind apparently erratic cervical changes.

On convergence almost everywhere of series of dilated functions

Let f(x)=∑ℓ∈Zaℓe2iπℓx, where ∑k≥1ak2d(k)<∞ and d(k)=∑d|k1 and let fn(x)=f(nx). We show by using a new decomposition of squared sums that, for any K⊂N finite, ‖∑k∈Kckfk‖22≤(∑m=1∞am2d(m))∑k∈Kck2d(k2). If fs(x)=∑j=1∞sin⁡2πjxjs, s>1/2, by only using elementary Dirichlet convolution calculus, we show that for 0<ε≤2s−1, ζ(2s)−1‖∑k∈Kckfks‖22≤1+εε(∑k∈K|ck|2σ1+ε−2s(k)), where σh(n)=∑d|ndh. From this, we deduce that if f∈BV(T), 〈f,1〉=0 and ∑k=1∞ck2(log⁡log⁡k)4(log⁡log⁡log⁡k)2<∞, then the series ∑kckfk converges almost everywhere. This slightly improves a recent result, depending on a fine analysis on the polydisc ([1], th. 3) (nk=k), where it was assumed that ∑k=1∞ck2(log⁡log⁡k)γ converges for some γ>4.

Probucol Protects Against Asymmetric Dimethylarginine-Induced Apoptosis in the Cultured Human Brain Microvascular Endothelial Cells.

Asymmetric dimethylarginine (ADMA) is emerging as a key contributor to endothelial dysfunction. The drug probucol was reported to have an anti-lipid peroxidation effect and improve endothelial dilation function. But little is known about the protective effect of probucol on ADMA-induced human brain microvascular endothelial cell (HBMEC) injury and its underlying mechanisms. Therefore, in this study, we investigated the effect of probucol on ADMA-induced HBMEC injury and its potential mechanisms. Results showed that probucol protected against ADMA-induced HBMEC injury in a dose-dependent manner; probucol pretreatment also significantly reduced the level of reactive oxygen species (ROS) and malondialdehyde (MDA), downregulated the expression of pro-apoptotic gene Bax and caspase-3 activity, as well as increased the brain-derived neurotrophic factor (BDNF) release and promoted anti-apoptotic gene Bcl-2 and eNOS expression in the cultured HBMECs. Furthermore, we found that ADMA significantly increased the phosphorylation of c-Jun NH2-terminal kinase (JNK) and p38, while probucol pretreatment effectively inhibited ADMA-induced JNK and p38 phosphorylation in HBMECs. In conclusion, our present results demonstrated that probucol protected against ADMA-induced HBMEC injury and suppressed oxidative stress through the JNK/p38 MAPK pathway, which was the potential underlying mechanism of HBMEC injury in ischemic cerebrovascular disease.

Laparoscopic treatment of ureteropelvic junction obstruction in five pediatric cases of pelvic kidneys

Ectopic kidney is a rare urologic condition and may be revealed by ureteropelvic junction obstruction (UPJO) in children, with pelvic kidney being the most common location. Our experience using a minimally invasive approach to treat UPJO by dismembered pyeloplasty led us to report five cases of UPJO with pelvic kidney operated on by transperitoneal laparoscopy, focusing on medium-term follow-up results and surgical technique. From 1999 to 2010, we reviewed all cases of UPJO managed in our center, a total of 391 patients. Among those, 125 patients were operated on via a minimal invasive approach, 104 by retroperitoneoscopy, and 21 by transperitoneal laparoscopy. Five patients presented ectopic pelvic kidney and were retrospectively reviewed. US-scan and uro-MRI were done preoperatively in all cases for anatomic and functional evaluation. Peri-operative data such as operative time, transfusion, and complications were reported. At last clinic, sonographic and functional evaluation was noted. Focusing on surgical technique, we reported the tips and tricks to successfully and easily perform the dismembered pyeloplasty: optimization of the trocars' location according to the kidney location and use of a transparietal stay stitch to stabilize the suture line of the pyeloplasty. All five patients underwent dismembered pyeloplasty, at a mean age of 8 years and a mean weight of 23.4kg. Mean operative time was 213min (min-max: 180-245). One case of giant hydronephrosis and megacalicosis required conversion at the beginning of the learning curve. None of the patients required blood transfusion. Mean hospital stay was 2.4 days (range: 1-4). All the patients had an uneventful postoperative recovery and good postoperative functional results, with either stable or improved pelvic dilatation and renal function at a mean follow-up of 3.3 years (range: 2-5.6). This small series of five ectopic kidneys reflects the surgical challenge for the pediatric surgeon to perform reconstructive surgery on an abnormal anatomy. However, increasing experience in robotics in urologic pediatric surgery may lead to shortening of operative time and facilitate both dissection and suturing. Dismembered pyeloplasty by transperitoneal laparoscopy is a feasible although technically demanding, safe and effective approach in the management of ureteropelvic junction obstruction in pelvic kidney in children.

Microvascular Dilator Function in Athletes: A Systematic Review and Meta-analysis.

Despite the growing research interest in vascular adaptations to exercise training over the last few decades, it remains unclear whether microvascular function in healthy subjects can be further improved by regular training. Herein, we sought to systematically review the literature and determine whether microvascular dilator function is greater in athletes compared to age-matched healthy untrained subjects. We conducted a systematic search of MEDLINE, Cochrane, EMBASE, and Web of Science since their inceptions until October 2013 for articles evaluating indices of primarily microvascular endothelium-dependent or endothelium-independent dilation (MVEDD and MVEID, respectively) in athletes. A meta-analysis was performed to determine the standardized mean difference (SMD) in MVEDD and MVEID between athletes and age-matched controls. Subgroup analyses were used to study potential moderating factors. Thirty-six studies were selected after systematic review, comprising 521 athletes (506 endurance-trained and 15 endurance- and strength-trained) and 496 age-matched control subjects. After data pooling, athletes presented higher MVEDD (31 studies; SMD, 0.47; P < 0.00001) and MVEID (14 studies; SMD, 0.51; P < 0.00001) compared with the control subjects. Similar results were observed in young (younger than 40 yr) and master (older than 55 yr) athletes when analyzed separately. Both young and master athletes present enhanced microvascular function compared with age-matched untrained but otherwise healthy subjects. These data provide evidence of a positive association between exercise training and microvascular function in the absence of known underlying cardiovascular disease.

Effects of overfeeding in breastfeeding period on blood pressure and vascular endothelial dilation function of rats

Objective To study the effects of postnatal overfeeding and high-fat diet on blood pressure of rats, and to explore the pathophysiological mechanism underlying hypertension induced by continuous early postnatal overfeeding. Methods Male Sprague-Dawley rats were randomly divided into normal feeding group (10/litter) and overfeeding group (3/litter) on postnatal day 3 with a random number table. After weaning at postnatal week 3, the rats were randomly given standard chow or high-fat (HF) diet until week 16. Hence four groups were analyzed, namely normal feeding group, breastfed overfeeding group, post-weaning overfeeding group, and continuous overfeeding group. Body weight was continuously monitored in each week. Visceral fat pad(retroperitoneal and perigenital), systolic pressure, and heart rate were observed at week 3 and week 16. Thoracic aorta was sampled for measurement of vascular endothelial dilation function. Histological morphology was observed with HE staining, nitric oxide content of thoracic aorta was detected with nitrate reductase method. The mRNA expression of endothelial nitric oxide synthase (eNOS) in thoracic aorta was determined by real-time polymerase chain reaction. The protein expressions of eNOS and phosphorylated eNOS were determined by Western blot. Results At week 3, breastfed overfeeding rats displayed significantly larger body weight [(77.80±0.57) g vs. (62.80±0.85)g, t=14.576, P<0.01] and visceral fat [retroperitoneal: (8.19±0.49)mg/g vs. (4.92±0.31)mg/g, t=5.629, P<0.01; perigenital: (3.50±0.29)mg/g vs. (2.08±0.13)mg/g, t=4.552, P<0.01] compared with normal feedindg rats, and the protein expression of phosphorylated eNOS in aortic tissues was significantly reduced to week 16 (F=15.215, P<0.01); high-fat diet feeding after weaning further increased the body weight and fat mass in breastfed overfeeding rats. At week 16, continuous overfeeding rats showed hypertension [(149±1.94)mmHg (1 mmHg=0.133 kPa), F=22.834, P<0.01], impaired vascular endothelial dilation function (F=7.648, P<0.05), and reduced protein expression of phosphorylated eNOS(F=15.215, P<0.01), while the post-weaning overfeeding group only had elevated blood pressure. Conclusions Overfeeding in breastfeeding period and high-fat diet after weaning leads to hypertension. The continuous decrease in phosphorylated eNOS in vascular tissues may be an important molecular process participating in the occurrence of vascular endothelial dysfunction in adults induced by postnatal overfeeding. Key words: Early postnatal overfeeding; Vascular endothelial dilation function; Hypertension; Nitric oxide; Phosphorylated endothelial nitric oxide synthase

Impact of prolonged sitting on lower and upper limb micro- and macrovascular dilator function.

What is the central question of this study? The prevalence of sedentary behaviour in the workplace and increased daily sitting time have been associated with the development of cardiovascular disease; however, studies investigating the impact of sitting on vascular function remain limited. What is the main finding and its importance? We demonstrate that there is a marked vulnerability of the vasculature in the lower and upper limbs to prolonged sitting and highlight the importance of physical activity in restoring vascular function in a limb-specific manner. Sedentary behaviour in the workplace and increased daily sitting time are on the rise; however, studies investigating the impact of sitting on vascular function remain limited. Herein, we hypothesized that 6 h of uninterrupted sitting would impair limb micro- and macrovascular dilator function and that this impairment could be improved with a bout of walking. Resting blood flow, reactive hyperaemia to 5 min cuff occlusion (microvascular reactivity) and associated flow-mediated dilatation (FMD; macrovascular reactivity) were assessed in popliteal and brachial arteries of young men at baseline (Pre Sit) and after 6 h of uninterrupted sitting (Post Sit). Measures were then repeated after a 10 min walk (~1000 steps). Sitting resulted in a marked reduction of resting popliteal artery mean blood flow and mean shear rate (6 h mean shear rate, -52 ± 8 s(-1) versus Pre Sit, P < 0.05). Interestingly, reductions were also found in the brachial artery (6 h mean shear rate, -169 ± 41 s(-1) versus Pre Sit, P < 0.05). Likewise, after 6 h of sitting, cuff-induced reactive hyperaemia was reduced in both the lower leg (-43 ± 7% versus Pre Sit, P < 0.05) and forearm (-31 ± 11% versus Pre Sit, P < 0.05). In contrast, popliteal but not brachial artery FMD was blunted with sitting. Notably, lower leg reactive hyperaemia and FMD were restored after walking. Collectively, these data suggest that prolonged sitting markedly reduces lower leg micro- and macrovascular dilator function, but these impairments can be fully normalized with a short bout of walking. In contrast, upper arm microvascular reactivity is selectively impaired with prolonged sitting, and walking does not influence this effect.

A transcendental invariant of pseudo-Anosov maps

For each pseudo-Anosov map ϕ : S → S , we associate it with a Q-vector space lying in R, and denote it by A ( S , ϕ ) . The invariant A ( S , ϕ ) is defined by an interaction between the Thurston norm and the dilatation of pseudo-Anosov maps. We develop a few nice properties of A ( S , ϕ ) and give a few examples to show that A ( S , ϕ ) is a nontrivial invariant. These nontrivial examples give an answer to a question asked by McMullen, and show that the minimal point of the restriction of the dilatation function on the fibered face need not be a rational point.

GCD sums from Poisson integrals and systems of dilated functions

Upper bounds for GCD sums of the form \sum_{k,{\ell}=1}^N\frac{(\mathrm {gcd}(n_k,n_{\ell}))^{2\alpha}}{(n_k n_{\ell})^\alpha} are established, where (n_k)_{1 \leq k \leq N} is any sequence of distinct positive integers and 0&lt;\alpha \le 1 ; the estimate for \alpha=1/2 solves in particular a problem of Dyer and Harman from 1986, and the estimates are optimal except possibly for \alpha=1/2 . The method of proof is based on identifying the sum as a certain Poisson integral on a polydisc; as a byproduct, estimates for the largest eigenvalues of the associated GCD matrices are also found. The bounds for such GCD sums are used to establish a Carleson–Hunt-type inequality for systems of dilated functions of bounded variation or belonging to \mathrm {Lip}_{1/2} , a result that in turn settles two longstanding problems on the a.e.\ behavior of systems of dilated functions: the a.e. growth of sums of the form \sum_{k=1}^N f(n_k x) and the a.e.\ convergence of \sum_{k=1}^\infty c_k f(n_kx) when f is 1 -periodic and of bounded variation or in \mathrm {Lip}_{1/2} .