Heart rate recovery after constant-load exercise tests is decreased in proportion to the importance (severity and diffusion) of exercise-induced lower-limb ischaemia

BACKGROUND: Conditions that may influence heart rate recovery at 1 min of recovery from exercise (HRR1: end-exercise heart rate minus heart rate 1 min after exercise) are not fully understood. We hypothesized that the \u27importance\u27 (both local severity and regional diffusion) of peripheral skeletal muscle ischaemia is associated with low HRR1. DESIGN AND METHODS: In 529 patients with suspected or confirmed peripheral vascular disease not receiving beta-blockers (61.4 +/- 11.3 years old), we retrospectively studied the relationship of HRR1 to exercise-induced changes in transcutaneous oxygen DROP index (limb changes minus chest changes from rest). The sum of DROP indices observed on both calves and both buttocks (DROPtot) provides the unique opportunity to estimate both the severity and the diffusion of exercise-induced ischaemia on the right and left side simultaneously. It was used during a constant-load treadmill test (3.2 km h(-1) ; 10% grade) to classify patients in quartiles, the fourth quartile representing the more \u27important\u27 ischaemias.RESULTS: There was an inverse relationship between quartiles of DROPtot and HRR1, even after adjustment for heart rate reserve (Delta HR: end-exercise minus resting heart rate), age (60 years), gender, body mass index, treadmill maximal walking distance and ankle brachial index: adjusted R = 0.629; P<0.0001. CONCLUSIONS: During constant-load treadmill testing, DROPtot, an index of the \u27importance\u27 of exercise-induced lower-limb ischaemia, correlates with HRR1. Whether HRR1 is improved in proportion of DROPtot improvement in patients undergoing surgery or rehabilitation for peripheral artery disease is a fascinating issue for future studies

Effect of skin temperature on skin endothelial function assessment

PURPOSE: Microcirculatory dysfunction plays a key role in the development of sepsis during which core temperature is often disturbed. Skin microvascular assessment using laser techniques has been suggested to evaluate microvascular dysfunction during sepsis, but skin microcirculation is also a major effector of human thermoregulation. Therefore we aimed to study the effect of skin temperature on endothelial- and non-endothelial microvascular responses.METHODS: Fifteen healthy participants were studied at different randomized ambient temperatures leading to low (28.0+/-2.0 degrees C), intermediate (31.6+/-2.1 degrees C), and high (34.1+/-1.3 degrees C) skin temperatures. We measured skin blood flow using laser speckle contrast imaging on the forearm in response to vasodilator microvascular tests: acetylcholine (ACh) iontophoresis, sodium nitroprussiate (SNP) iontophoresis, and post-occlusive reactive hyperemia (PORH). The results are expressed as absolute (laser speckle perfusion units, LSPU) or normalized values (cutaneous vascular conductance, CVC in LSPU/mmHg and multiple of baseline). RESULTS: Maximal vasodilation induced by these tests is modified by skin temperature. A low skin temperature induced a significant lower vasodilation for all microvascular tests when results are expressed either in absolute values or in CVC. For example, ACh peak was 57.6+/-19.6 LSPU, 66.8+/-22.2 LSPU and 88.5+/-13.0 LSPU for low, intermediate and high skin temperature respectively (p<0.05). When results are expressed in multiple of baseline, statistical difference disappeared. CONCLUSIONS: These results suggest that skin temperature has to be well controlled when performing microvascular assessments in order to avoid any bias. The effect of skin temperature can be corrected by expressing the results in multiple of baseline

Objective determination of the predefined duration of a constant-load diagnostic tests in arterial claudication

OBJECTIVE: The predefined duration to arbitrarily stop the tests during constant-load treadmill exercise is a subject of debate and widely variable in the literature. We hypothesized that the upper and lower limits for predefined durations of constant-load 3.2 km/hour 10% grade tests could be derived from the distribution of walking distances observed on a treadmill in a population of subjects referred for claudication or from the optimal cutoff point distance on a treadmill to confirm a limitation self-reported by history.METHODS: We conducted a retrospective analysis using a referral center, institutional practice, and ambulatory patients. We studied 1290 patients (86% male), 62.1 +/- 11.2 years of age, 169 +/- 8 cm height, 75.7 +/- 14.2 kg weight. Patients performed a standard constant-load treadmill test: 3.2 km hour(-1), 10% slope, maximized to 1000 meters (approximately 20 minutes). We analyzed the maximal walking distance self-reported (MWD(SR)) by history and the maximal walking distance measured on the treadmill (MWD(TT)). Patients reporting MWD(SR) >or=1000 meters were considered unlimited by history. RESULTS: Only 197 patients (15.3%) completed the 20-minute treadmill test. Among the 504 patients who did not stop before 250 meters, 47.8% stopped within the next 250 meters (were unable to walk 500 meters). This proportion falls to 7.5% among the 213 patients who did not stop before 750 meters. When the final goal was to estimate whether the treadmill test can discriminate patients with or without limitation by history, area under the receiver operating characteristic (ROC) curve was 0.809 +/- 0.016 (95% confidence interval [CI], 0.778-0.841; P < .0001), the best diagnostic performance was attained for an MWD(TT) of 299 meters (approximately 6.15 minutes). CONCLUSION: In patients undergoing constant-load treadmill exercise with a protocol of 3.2 km hour(-1) and 10% slope: a predefined duration of 7 minutes could be proposed as a lower limit for the predefined duration of the tests specifically if one aims at confirming the limitation by history with treadmill testing. Owing to the low risk that patients that could walk 750 meters (approximately 15 minutes) will have to stop in the next 250 meters, 15 minutes seems a reasonable upper limit for the predefined test duration in clinical routine

Limitations of self-reported estimates of functional capacity using the Walking Impairment Questionnaire

OBJECTIVE: A potential issue with the Walking Impairment Questionnaire (WIQ) is that it is relatively complex. We estimated the number of errors made by patients when self-completing the WIQ, and assessed the benefit of correcting missing, duplicate or paradoxical (i.e., reported lower difficulty for a higher-intensity task) answers.DESIGN: Prospective non-interventional study. MATERIALS: All consecutive new patients with claudication over a 3-month period. METHODS: The WIQ was self-completed before patients performed a constant-load treadmill walking test (maximised to 750 m). MAIN OUTCOME MEASURE: We analysed the coefficient of determination of the linear relationship between overall WIQ score (mean of the available subscales when at least two subscales are available) and treadmill maximal walking distance (MWD), before and after correction of errors. RESULTS: We studied 73 patients. Thirty-seven questionnaires had to be corrected for one or more errors. The coefficient of determination between the overall WIQ score and MWD was R(2) = 0.391 (n = 56) and R(2) = 0.426 (n = 73) before and after correction, respectively. CONCLUSION: Supervision of self-completed WIQs detects errors in almost half of the questionnaires, resulting in a missing overall WIQ score in 23% of cases among uncorrected questionnaires. The overall WIQ score correlates only moderately with MWD, even after correction

On the Pierce-Birkhoff Conjecture

International audienceThis paper represents a step in our program towards the proof of the Pierce--Birkhoff conjecture. In the nineteen eighties J. Madden proved that the Pierce-Birkhoff conjecture for a ring A$is equivalent to a statement about an arbitrary pair of points$\alpha,\beta\in\sper\ A$and their separating ideal$$; we refer to this statement as the Local Pierce-Birkhoff conjecture at$\alpha,\beta$. In this paper, for each pair$(\alpha,\beta)$with$ht()=\dim A$, we define a natural number, called complexity of$(\alpha,\beta)$. Complexity 0 corresponds to the case when one of the points$\alpha,\beta$is monomial; this case was already settled in all dimensions in a preceding paper. Here we introduce a new conjecture, called the Strong Connectedness conjecture, and prove that the strong connectedness conjecture in dimension n-1 implies the connectedness conjecture in dimension n in the case when$ht()$is less than n-1. We prove the Strong Connectedness conjecture in dimension 2, which gives the Connectedness and the Pierce--Birkhoff conjectures in any dimension in the case when$ht()$less than 2. Finally, we prove the Connectedness (and hence also the Pierce--Birkhoff) conjecture in the case when dimension of A is equal to$ht()=3$, the pair$(\alpha,\beta)$is of complexity 1 and$A$ is excellent with residue field the field of real numbers

Fast GPGPU-Based Elliptic Curve Scalar Multiplication

This paper presents a fast implementation to compute the scalar multiplication of elliptic curve points based on a ``General-Purpose computing on Graphics Processing Units\u27\u27 (GPGPU) approach. A GPU implementation using Dan Bernstein\u27s Curve25519, an elliptic curve over a 255-bit prime field complying with the new 128-bit security level, computes the scalar multiplication in less than a microsecond on AMD\u27s R9 290X GPU. The presented methods and implementation considerations can be applied to any parallel architecture

Regulation of intestinal epithelial cells transcriptome by enteric glial cells: impact on intestinal epithelial barrier functions

<p>Abstract</p> <p>Background</p> <p>Emerging evidences suggest that enteric glial cells (EGC), a major constituent of the enteric nervous system (ENS), are key regulators of intestinal epithelial barrier (IEB) functions. Indeed EGC inhibit intestinal epithelial cells (IEC) proliferation and increase IEB paracellular permeability. However, the role of EGC on other important barrier functions and the signalling pathways involved in their effects are currently unknown. To achieve this goal, we aimed at identifying the impact of EGC upon IEC transcriptome by performing microarray studies.</p> <p>Results</p> <p>EGC induced significant changes in gene expression profiling of proliferating IEC after 24 hours of co-culture. 116 genes were identified as differentially expressed (70 up-regulated and 46 down-regulated) in IEC cultured with EGC compared to IEC cultured alone. By performing functional analysis of the 116 identified genes using Ingenuity Pathway Analysis, we showed that EGC induced a significant regulation of genes favoring both cell-to-cell and cell-to-matrix adhesion as well as cell differentiation. Consistently, functional studies showed that EGC induced a significant increase in cell adhesion. EGC also regulated genes involved in cell motility towards an enhancement of cell motility. In addition, EGC profoundly modulated expression of genes involved in cell proliferation and cell survival, although no clear functional trend could be identified. Finally, important genes involved in lipid and protein metabolism of epithelial cells were shown to be differentially regulated by EGC.</p> <p>Conclusion</p> <p>This study reinforces the emerging concept that EGC have major protective effects upon the IEB. EGC have a profound impact upon IEC transcriptome and induce a shift in IEC phenotype towards increased cell adhesion and cell differentiation. This concept needs to be further validated under both physiological and pathophysiological conditions.</p