The relative contributions of microvascular inflammation and vasomotor dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been intensely studied. The present observational study was designed to examine the levels of circulating proinflammatory cytokines, anti-inflammatory cytokines, and vasoactive mediators during and after acute painful crisis. In symptomatic sickle cell patients, plasma levels of endothelin-1 and prostaglandin E2 were elevated during crises compared with healthy African-American controls. These levels had decreased, but not normalized, when patients were seen 1 to 3 weeks after discharge from hospital. Other mediators (tumor necrosis factor α [TNFα], interleukin-1β [IL-1β], IL-6, IL-8, and IL-10) were neither elevated in asymptomatic sickle cell disease nor in acute vaso-occlusive crisis. As a potent long-acting mediator of vasoconstriction and inflammation, endothelin-1 may play a key role in the cycle of ischemia and inflammation that initiates and sustains pain of crisis. The downregulatory effects of prostaglandin E2on immune cell function may contribute to the increased susceptibility to infection observed in patients with sickle cell disease.

Thyroglossal duct cysts (TDCs), the most common congenital cervical abnormality, originates from the medial anlage of the thyroid gland and presents as a painless asymptomatic midline suprahyoid mass. It does not represent a diagnostic challenge. The tract may persist as a fibrous cord or leave nests of cells anywhere along its embryonic path, and it gives rise to the development of TDC. The Sistrunk operation described in 1920 consists of en bloc cystectomy and central hyoidectomy, with tract excision up to the foramen cecum. This procedure remains an effective treatment for TDC. Malignant degeneration of TDC is rare (0.7%).

Engineering new tissues by transplanting cells on polymeric delivery devices is one approach to alleviate the vast shortage of donor tissue. However, it will be necessary to fabricate cell delivery devices that deliver cells to a given location and promote the formation of specific tissue structures from the transplanted cells and the host tissue. This report describes the design and fabrication of a polymeric device for guiding the development of tubular vascularized tissues, which may be useful for engineering a variety of tissues including intestine, blood vessels, tracheas, and ureters. Porous films of poly (D, L-lactic-co-glycolic acid) have been formed and fabricated into tubes capable of resisting compressional forces in vitro and in vivo. These devices promote the ingrowth of fibrovascular tissue following implantation into recipient animals, resulting in a vascularized, tubular tissue. To investigate the utility of these devices as cell delivery devices, enterocytes (intestinal epithelial cells) were seeded onto the devices in vitro. Enterocytes were found to attach to these devices and form an organized epithelial cell layer. These results suggest that these devices may be an appropriate delivery vehicle for transplanting cells and engineering new tubular tissues.

The relative contributions of microvascular inflammation and vasomotor dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been intensely studied. The present observational study was designed to examine the levels of circulating proinflammatory cytokines, anti-inflammatory cytokines, and vasoactive mediators during and after acute painful crisis. In symptomatic sickle cell patients, plasma levels of endothelin-1 and prostaglandin E2 were elevated during crises compared with healthy African-American controls. These levels had decreased, but not normalized, when patients were seen 1 to 3 weeks after discharge from hospital. Other mediators (tumor necrosis factor α [TNFα], interleukin-1β [IL-1β], IL-6, IL-8, and IL-10) were neither elevated in asymptomatic sickle cell disease nor in acute vaso-occlusive crisis. As a potent long-acting mediator of vasoconstriction and inflammation, endothelin-1 may play a key role in the cycle of ischemia and inflammation that initiates and sustains pain of crisis. The downregulatory effects of prostaglandin E2on immune cell function may contribute to the increased susceptibility to infection observed in patients with sickle cell disease.