16 research outputs found
Policy Matters: : EDI Evaluation of an Academic Library's Policies
Why does policy matter, and how can libraries reform their policies to create a more equitable library for library workers and library users? The authors discuss their experience in reviewing the policies of their library with an EDI (Equity, Diversity, and Inclusion) lens. The authors describe how they initiated and developed this project, the factors that they considered in forming their evaluation rubric, and what they learned from the process
Vascular Remodeling in Health and Disease
The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall
Chronic inflammation and oxidative stress in human carcinogenesis
A wide array of chronic inflammatory conditions predispose susceptible
cells to neoplastic transformation. In general, the longer
the inflammation persists, the higher the risk of cancer. A mutated
cell is a sine qua non for carcinogenesis. Inflammatory processes
may induce DNA mutations in cells via oxidative/nitrosative stress.
This condition occurs when the generation of free radicals and
active intermediates in a system exceeds the system’s ability to
neutralize and eliminate them. Inflammatory cells and cancer cells
themselves produce free radicals and soluble mediators such as
metabolites of arachidonic acid, cytokines and chemokines, which
act by further producing reactive species. These, in turn, strongly
recruit inflammatory cells in a vicious circle. Reactive intermediates
of oxygen and nitrogen may directly oxidize DNA, or may
interfere with mechanisms of DNA repair. These reactive substances
may also rapidly react with proteins, carbohydrates and lipids,
and the derivative products may induce a high perturbation in the
intracellular and intercellular homeostasis, until DNA mutation.
The main substances that link inflammation to cancer via oxidative/
nitrosative stress are prostaglandins and cytokines. The effectors
are represented by an imbalance between pro-oxidant and
antioxidant enzyme activities (lipoxygenase, cyclooxygenase and
phospholipid hydroperoxide glutathione-peroxidase), hydroperoxides
and lipoperoxides, aldehydes and peroxinitrite. This review
focalizes some of these intricate events by discussing the relationships
occurring among oxidative/nitrosative/metabolic stress,
inflammation and cancer