Shear stress is the tangential force of the flowing blood on the endothelial surface of the blood vessel. Shear is described mathematically or ideal fluids, and in vitro models have enabled researchers to describe the effects of shear on endothelial cells. High shear stress, as found in laminar flow, promotes endothelial cell survival and quiescence, alignment in the direction of flow, and secretion of substances that promote vasodilation and anticoagulation. Low shear stress, or changing shear stress direction as found in turbulent flow, promotes endothelial proliferation and apoptosis, shape change, and secretion of substances that promote vasoconstriction, coagulation, and platelet aggregation. The precise pathways by which endothelial cells sense shear stress to promote their quiescent or activated pathways are currently unknown. Clinical applications include increasing shear stress via creation of an arteriovenous fistula or vein cuff to promote bypass graft flow and patency. Since an abnormal level of shear stress is implicated in the pathogenesis of atherosclerosis, neointimal hyperplasia, and aneurysmal disease, additional research to understand the effects of shear stress on the blood vessel may provide insight to prevent vascular disease.

Vascular smooth muscle cells exhibit varied responses after vessel injury and surgical interventions, including phenotypic switching, migration, proliferation, protein synthesis, and apoptosis. Although the source of the smooth muscle cells that accumulate in the vascular wall is controversial, possibly reflecting migration from the adventitia, from the circulating blood, or in situ differentiation, the intracellular signal transduction pathways that control these processes are being defined. Some of these pathways include the Ras-mitogen-activated protein kinase, phosphatidylinositol 3-kinase-Akt, Rho, death receptor-caspase, and nitric oxide pathways. Signal transduction pathways provide amplification, redundancy, and control points within the cell and culminate in biologic responses. We review some of the signaling pathways activated within smooth muscle cells that contribute to smooth muscle cell heterogeneity and development of pathology such as restenosis and neointimal hyperplasia.

SMC directly respond to oscillatory SS by increasing DNA synthesis, proliferation, and activation of the PI3K-Akt signal transduction pathway. These results suggest a mechanism of SMC survival and proliferation in response to endothelial-denuding arterial injury.

Orbital shear stress directly stimulates SMC proliferation in long-term culture in vitro and is mediated, at least partially, by the ERK1/2 pathway. The ERK1/2 pathway may also mediate the orbital shear-stress-stimulated switch from SMC contractile to synthetic phenotype. These results suggest that shear-stress-stimulated SMC proliferation after vascular injury is mediated by a pathway amenable to pharmacologic manipulation.

Both neointimal hyperplasia and inward remodeling contribute to restenosis and lumen loss. Nogo-B has been recently described as an inhibitor of vascular injury and neointimal hyperplasia. To determine whether Nogo-B expression may be a mediator of inward remodeling, we examine the localization of expression of Nogo-B in an in vivo model that examines both neointimal hyperplasia and inward remodeling. The rabbit carotid artery was subjected to balloon injury, outflow branch ligation to reduce flow, or both balloon injury and reduction in flow. In balloon injury-induced neointimal hyperplasia Nogo-B expression was reduced in the intima and media but stimulated in the adventitia. In low flow-induced inward remodeling medial Nogo-B expression was not reduced and adventitial Nogo-B expression was not stimulated. Low flow significantly augmented balloon injury-induced neointimal hyperplasia and was accompanied by reduced intimal and medial Nogo-B expression, and increased adventitial Nogo-B expression in both smooth muscle cells and macrophages. Low flow-induced inward remodeling is not associated with changes in medial Nogo-B expression and is distinct from injury-induced neointimal hyperplasia. Pharmacological strategies to inhibit neointimal hyperplasia and restenosis using normal flow models may only partially account for lumen loss and therefore may not accurately predict responses in patients with extensive outflow disease.

In 2003, the revised American Cancer Society guidelines recommended that breast self-examination (BSE) be optional. Of 822 women diagnosed with breast cancer in our hospital from 1994 to 2004, sixty four (7.7%) were 40 years of age or younger. Forty four (68.7%) of these young women discovered their breast cancers on BSE, 17 (18%) by mammography, and 3 (4.7%) by clinical breast examination by medical professionals. Of 758 women over 40 years of age diagnosed with breast cancer, 382 (49%) discovered their cancer by mammography, 278 (39%) by BSE, and 98 (14%) by a clinical breast examination. Lymph node metastases in the older women was one-half that in the younger women (21% versus 42%), and a higher percentage of younger women presented with more advanced disease. In response to increasing breast cancer in young women under 41 years of age, encouragement of proper breast self-examination is warranted and should be advocated.

Endometriosis is characterized by ectopic endometrial tissue, which responds to ovarian stimulation. Endometrioma is the term given to extra-pelvic endometriosis that forms a discrete mass surrounded by a connective tissue capsule. We present a retrospective review of five patients diagnosed with abdominal wall endometrioma in our institution within the last three years. We review symptoms, diagnostic methods, and surgical management, as well as current literature regarding this patient population. Endometrioma is an unusual disease process that must be included in the differential diagnosis of chronic abdominal pain associated with a mass in the incisional area of a patient with a previous Cesarean section. The development, cell biology, complex biochemical and endocrine features of its pathogenesis, and obvious intricate interaction with musculofascial elements relative to other abdominal wall layers are intriguing and merit further investigation.

No abstract