ABSTRACT
Chronic venous insufficiency is an extensive progressive disease in need of public health attention. This insidious disease is a growing burden on patient quality of life and the health economy. Chronic venous insufficiency has become more pronounced in global populations, especially in regions exhibiting a higher rate of risk factors. It is critical for healthcare providers to recognise and intervene early to prevent ongoing and debilitating complications. This article provides a comprehensive review of chronic venous insufficiency outlining the anatomy, pathophysiology, clinical presentation, assessment and management options.
Subject(s)
Quality of Life , Venous Insufficiency , Chronic Disease , Humans , Risk Factors , Venous Insufficiency/complications , Venous Insufficiency/therapyABSTRACT
Aerobic exercise helps to maintain cardiovascular health in part by mitigating age-induced arterial stiffening. However, the long-term effects of exercise regimens on aortic stiffness remain unknown, especially in the intimal extracellular matrix layer known as the subendothelial matrix. To examine how the stiffness of the subendothelial matrix changes following exercise cessation, mice were exposed to an 8 week swimming regimen followed by an 8 week sedentary rest period. Whole vessel and subendothelial matrix stiffness were measured after both the exercise and rest periods. After swimming, whole vessel and subendothelial matrix stiffness decreased, and after 8 weeks of rest, these values returned to baseline. Within the same time frame, the collagen content in the intima layer and the presence of advanced glycation end products (AGEs) in the whole vessel were also affected by the exercise and the rest periods. Overall, our data indicate that consistent exercise is necessary for maintaining compliance in the subendothelial matrix.
Subject(s)
Endothelium, Vascular/metabolism , Mechanical Phenomena , Physical Conditioning, Animal , Animals , Aorta/cytology , Aorta/physiology , Biomechanical Phenomena , Collagen/metabolism , Glycation End Products, Advanced/metabolism , Male , Mice , Mice, Inbred C57BL , Pulse Wave Analysis , Rest , Stroke VolumeABSTRACT
Consumption of a high-fat, high-sugar diet and sedentary lifestyle are correlated with bulk arterial stiffening. While measurements of bulk arterial stiffening are used to assess cardiovascular health clinically, they cannot account for changes to the tissue occurring on the cellular scale. The compliance of the subendothelial matrix in the intima mediates vascular permeability, an initiating step in atherosclerosis. High-fat, high-sugar diet consumption and a sedentary lifestyle both cause micro-scale subendothelial matrix stiffening, but the impact of these factors in concert remains unknown. In this study, mice on a high-fat, high-sugar diet were treated with aerobic exercise or returned to a normal diet. We measured bulk arterial stiffness through pulse wave velocity and subendothelial matrix stiffness ex vivo through atomic force microscopy. Our data indicate that while diet reversal mitigates high-fat, high-sugar diet-induced macro- and micro-scale stiffening, exercise only significantly decreases micro-scale stiffness and not macro-scale stiffness, during the time-scale studied. These data underscore the need for both healthy diet and exercise to maintain vascular health. These data also indicate that exercise may serve as a key lifestyle modification to partially reverse the deleterious impacts of high-fat, high-sugar diet consumption, even while macro-scale stiffness indicators do not change.
Subject(s)
Aorta, Abdominal/pathology , Aorta, Abdominal/physiopathology , Diet, High-Fat , Dietary Sugars , Exercise Therapy/methods , Extracellular Matrix/pathology , Vascular Stiffness , Animals , Arterial Pressure , Diet, Healthy , Disease Models, Animal , Elastic Modulus , Male , Mice, Inbred C57BL , Microscopy, Atomic Force , Peripheral Arterial Disease/diagnosis , Peripheral Arterial Disease/etiology , Peripheral Arterial Disease/pathology , Peripheral Arterial Disease/physiopathology , Pulse Wave Analysis , Risk Reduction Behavior , Time FactorsABSTRACT
A recently published alternative hierarchy of coupled-cluster approximations is reformulated as a perturbative correction. A single variant, a model for the total electronic energy based on the perfect quadruples model, is explored in detail. The computational scaling of the method developed is the same as canonical second order Mo̸ller-Plesset perturbation theory (fifth order in the number of molecular orbitals), but its accuracy competes with the high-accuracy, high-cost standard CCSD(T), even when the latter is allowed to break spin-symmetry. The variation presented can be implemented without explicit calculation and storage of the most expensive energy contributions, thereby improving the range of systems which can be treated. The performance and scaling of the method are demonstrated with calculations on the water, fluorine, and oxirane molecules, and compared to the parent model.
ABSTRACT
We have identified and examined the excited state of the cluster-solvated, valence-bound acetonitrile anion dimer, consistent with recent experimental findings, determining that the cluster excited state is of predominantly single-excitation character. Potential energy surface scans in coordinates specific to a "dissociative" normal mode common between the excited and ground states of the valence anion as well as the ground-state neutral dimer species shed light on the proposed vibrational autodetachment mechanism, with calculated excited-state lifetime consistent with experiment.
