Tortuous arteries and veins are commonly observed in humans and animals. While mild tortuosity is asymptomatic, severe tortuosity can lead to ischemic attack in distal organs. Clinical observations have linked tortuous arteries and veins with aging, atherosclerosis, hypertension, genetic defects and diabetes mellitus. However, the mechanisms of their formation and development are poorly understood. This review summarizes the current clinical and biomechanical studies on the initiation, development and treatment of tortuous blood vessels. We submit a new hypothesis that mechanical instability and remodeling could be mechanisms for the initiation and development of these tortuous vessels.

Ontology is increasingly seen as a key factor for enabling interoperability across heterogeneous systems and semantic web applications. Ontology mapping is required for combining distributed and heterogeneous ontologies. Developing such ontology mapping has been a core issue of recent ontology research. This paper presents ontology mapping categories, describes the characteristics of each category, compares these characteristics, and surveys tools, systems, and related work based on each category of ontology mapping. We believe this paper provides readers with a comprehensive understanding of ontology mapping and points to various research topics about the specific roles of ontology mapping.

BackgroundCadence (steps/min) may be a reasonable proxy-indicator of ambulatory intensity. A summary of current evidence is needed for cadence-based metrics supporting benchmark (standard or point of reference) and threshold (minimums associated with desired outcomes) values that are informed by a systematic process.ObjectiveTo review how fast, in terms of cadence, is enough, with reference to crafting public health recommendations in adults.MethodsA comprehensive search strategy was conducted to identify relevant studies focused on walking cadence and intensity for adults. Identified studies (n=38) included controlled (n=11), free-living observational (n=18) and intervention (n=9) designs.ResultsThere was a strong relationship between cadence (as measured by direct observation and objective assessments) and intensity (indirect calorimetry). Despite acknowledged interindividual variability, ≥100 steps/min is a consistent heuristic (e.g, evidence-based, rounded) value associated with absolutely defined moderate intensity (3 metabolic equivalents (METs)). Epidemiological studies report notably low mean daily cadences (ie, 7.7 steps/min), shaped primarily by the very large proportion of time (13.5 hours/day) spent between zero and purposeful cadences (<60 steps/min) at the population level. Published values for peak 1-min and 30-min cadences in healthy free-living adults are >100 and >70 steps/min, respectively. Peak cadence indicators are negatively associated with increased age and body mass index. Identified intervention studies used cadence to either prescribe and/or quantify ambulatory intensity but the evidence is best described as preliminary.ConclusionsA cadence value of ≥100 steps/min in adults appears to be a consistent and reasonable heuristic answer to ’How fast is fast enough?' during sustained and rhythmic ambulatory behaviour.Trial registration numberNCT02650258

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Rationale Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix (ECM) responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI) have not been explored. Objective To determine the impact of MMP-28 deletion on post-MI remodeling of the left ventricle (LV) Methods and Results Adult C57BL/6J wild type (WT, n=76) and MMP null (MMP-28−/−, n=86) mice of both sexes were subjected to permanent coronary artery ligation to create MI. MMP-28 expression decreased post-MI, and its cell source shifted from myocytes to macrophages. MMP-28 deletion increased day 7 mortality as a result of increased cardiac rupture post-MI. MMP-28−/− mice exhibited larger LV volumes, worse LV dysfunction, a worse LV remodeling index, and increased lung edema. Plasma MMP-9 levels were unchanged in the MMP-28−/− mice but increased in WT mice at day 7 post-MI. The mRNA levels of inflammatory and ECM proteins were attenuated in the infarct regions of MMP-28−/− mice, indicating reduced inflammatory and ECM responses. M2 macrophage activation was impaired when MMP-28 was absent. MMP-28 deletion also led to decreased collagen deposition and fewer myofibroblasts. Collagen cross-linking was impaired, due to decreased expression and activation of lysyl oxidase in the infarcts of MMP-28−/− mice. The LV tensile strength at day 3 post-MI, however, was similar between the two genotypes Conclusions MMP-28 deletion aggravated MI induced LV dysfunction and rupture, due to defective inflammatory response and scar formation by suppressing M2 macrophage activation.

BackgroundPrevious studies have reported that walking cadence (steps/min) is associated with absolutely-defined intensity (metabolic equivalents; METs), such that cadence-based thresholds could serve as reasonable proxy values for ambulatory intensities.PurposeTo establish definitive heuristic (i.e., evidence-based, practical, rounded) thresholds linking cadence with absolutely-defined moderate (3 METs) and vigorous (6 METs) intensity.MethodsIn this laboratory-based cross-sectional study, 76 healthy adults (10 men and 10 women representing each 5-year age-group category between 21 and 40 years, BMI = 24.8 ± 3.4 kg/m2) performed a series of 5-min treadmill bouts separated by 2-min rests. Bouts began at 0.5 mph and increased in 0.5 mph increments until participants: 1) chose to run, 2) achieved 75% of their predicted maximum heart rate, or 3) reported a Borg rating of perceived exertion > 13. Cadence was hand-tallied, and intensity (METs) was measured using a portable indirect calorimeter. Optimal cadence thresholds for moderate and vigorous ambulatory intensities were identified using a segmented regression model with random coefficients, as well as Receiver Operating Characteristic (ROC) models. Positive predictive values (PPV) of candidate heuristic thresholds were assessed to determine final heuristic values.ResultsOptimal cadence thresholds for 3 METs and 6 METs were 102 and 129 steps/min, respectively, using the regression model, and 96 and 120 steps/min, respectively, using ROC models. Heuristic values were set at 100 steps/min (PPV of 91.4%), and 130 steps/min (PPV of 70.7%), respectively.ConclusionsCadence thresholds of 100 and 130 steps/min can serve as reasonable heuristic thresholds representative of absolutely-defined moderate and vigorous ambulatory intensity, respectively, in 21–40 year olds. These values represent useful proxy values for recommending and modulating the intensity of ambulatory behavior and/or as measurement thresholds for processing accelerometer data.Trial registrationClinicaltrials.gov (NCT02650258).Electronic supplementary materialThe online version of this article (10.1186/s12966-019-0769-6) contains supplementary material, which is available to authorized users.

The stability of arteries under blood pressure load is essential to the maintenance of normal arterial function and the loss of stability can lead to tortuosity and kinking that are associated with significant clinical complications. However, mechanical analysis of arterial bent buckling is lacking. To address this issue, this paper presents a biomechanical model of arterial buckling. Using an elastic cylindrical arterial model, the mechanical equations for arterial buckling were developed and the critical buckling pressure was found to be a function of the wall stiffness (Young's modulus), arterial radius, length, wall thickness, and the axial strain. Both the model equations and experimental results demonstrated that the critical pressure is related to the axial strain. Arteries may buckle and become tortuous due to reduced (subphysiological) axial strain, hypertensive pressure, and a weakened wall. These results are in accordance with, and provide a possible explanation to the clinical observations that hypertension and aging are the risk factors for arterial tortuosity and kinking. The current model is also applicable to veins and ureters.

Tortuous arteries are often associated with aging, hypertension, atherosclerosis, and degenerative vascular diseases, but the mechanisms are poorly understood. Our recent theoretical analysis suggested that mechanical instability (buckling) may lead to tortuous blood vessels. The objectives of this study were to determine the critical pressure of artery buckling and the effects of elastin degradation and surrounding matrix support on the mechanical stability of arteries. The mechanical properties and critical buckling pressures, at which arteries become unstable and deform into tortuous shapes, were determined for a group of five normal arteries using pressurized inflation and buckling tests. Another group of nine porcine arteries were treated with elastase (8 U/ml), and the mechanical stiffness and critical pressure were obtained before and after treatment. The effect of surrounding tissue support was simulated using a gelatin gel. The critical pressures of the five normal arteries were 9.52 kPa (SD 1.53) and 17.10 kPa (SD 5.11) at axial stretch ratios of 1.3 and 1.5, respectively, while model predicted critical pressures were 10.11 kPa (SD 3.12) and 17.86 kPa (SD 5.21), respectively. Elastase treatment significantly reduced the critical buckling pressure (P < 0.01). Arteries with surrounding matrix support buckled into multiple waves at a higher critical pressure. We concluded that artery buckling under luminal pressure can be predicted by a buckling equation. Elastin degradation weakens the arterial wall and reduces the critical pressure, which thus leads to tortuous vessels. These results shed light on the mechanisms of the development of tortuous vessels due to elastin deficiency.