Delayed reconstruction of the superior mesenteric vein with autogenous femoral vein.

A 38-year-old man underwent ligation of the superior mesenteric vein due to traumatic disruption. He developed severe bowel edema with large fluid losses through the open abdominal incision. On postoperative day 9, a superior mesenteric vein bypass was performed with autogenous femoral vein, and this resulted in prompt resolution of the bowel edema and allowed abdominal wound closure. He was able to resume a normal diet and was discharged on postinjury day 39. A magnetic resonance imaging scan performed 1 year later showed a patent graft.

Syndecan-1 displays a protective role in aortic aneurysm formation by modulating T cell-mediated responses.

OBJECTIVE: Chronic inflammation drives progressive and pathological remodeling inherent to formation of abdominal aortic aneurysm (AAA). Syndecan-1 (Sdc-1) is a cell surface heparan sulfate proteoglycan that displays the capacity to modulate inflammatory processes within the vascular wall. In the current investigation, the role of Sdc-1 in AAA formation was examined using 2 models of experimental aneurysm induction, angiotensin II infusion and elastase perfusion. METHODS AND RESULTS: Sdc-1 deficiency exacerbated AAA formation in both experimental models and was associated with increased degradation of elastin, greater protease activity, and enhanced inflammatory cell recruitment into the aortic wall. Bone marrow transplantation studies indicated that deficiency of Sdc-1 in marrow-derived cells significantly contributed to AAA severity. Immunostaining revealed augmented Sdc-1 expression in a subset of AAA localized macrophages. We specifically characterized a higher percentage of CD4(+) T cells in Sdc-1-deficient AAA, and antibody depletion studies established the active role of T cells in aneurysmal dilatation. Finally, we confirmed the ability of Sdc-1 macrophage to modulate the inflammatory chemokine environment. CONCLUSIONS: These investigations identify cross-talk between Sdc-1-expressing macrophages and AAA-localized CD4(+) T cells, with Sdc-1 providing an important counterbalance to T-cell-driven inflammation in the vascular wall.

Syndecans are differentially expressed during the course of aortic aneurysm formation.

BACKGROUND: The syndecan family of cell surface proteoglycans can bind and modulate the activity of a diverse group of soluble and insoluble ligands, which have been shown to modulate events relevant to acute tissue repair and chronic injury responses. The expression of members of the syndecan family of heparan sulfate proteoglycans during the course of aortic aneurysm formation has not been previously investigated. In this investigation, the spatiotemporal expression of syndecan-1, -2, and -4 was characterized in a murine model of aneurysm formation. METHODS: ApoE-deficient mice were maintained on an atherogenic diet for 8 weeks with concurrent infusion of angiotensin II (0.75 mg/kg/day SQ). The expression of syndecan-1, -2, and -4 at the site of aneurysm formation was characterized by immunohistochemical staining and colocalization determined by double fluorescent immunostaining. Correlative examination was performed on tissue specimens harvested from patients at the time of open aneurysm repair. RESULTS: In the aortic wall of age-matched, untreated mice, syndecan-4 was localized to the smooth muscle cells of the media. However, neither syndecan-1 nor syndecan-2 could be detected. Within 1 week of initiating a high fat diet and infusion of angiotensin II, syndecan-1 was abundantly expressed in infiltrating macrophages, predominantly localized to the periadventitial aorta. The expression of macrophage-associated syndecan-1 was accentuated during the course of aneurysm formation. As the aneurysm matured, syndecan-2 was abundantly expressed within the aortic thrombus and heterogeneous syndecan-4 staining noted within the aortic media. Significantly, abundant syndecan-1 positive macrophages were observed in explanted human specimens. CONCLUSIONS: Given the established functional properties of this family heparan sulfate proteoglycans, chronically accelerated macrophage syndecan-1 shedding could generate a sustained proinflammatory, proteolytic, growth-stimulating environment. As a component of a counterbalancing reparative process, cell surface syndecan-2 may assist in TGF-beta mediated responses to limit the growth of abdominal aortic aneurysms.

Conformational Study of trans-Cyclododecene by Dynamic NMR Spectroscopy and Computational Methods.

The (13)C spectrum of trans-cyclododecene (1) dissolved in propane showed seven peaks for the olefinic carbons at -164.5 degrees C, corresponding to three conformations of C(1) symmetry and a fourth conformation, with a population of 20.1%, of C(2) symmetry. The populations of the C(1) conformations were 57.0, 18.6, and 4.3%. Conformational space was searched for 1 using MM2. Free energies and populations were calculated by MM3, and the results of the low-temperature NMR study are discussed in terms of these calculations and the (13)C chemical shifts calculated for eight conformations by the GIAO method at the HF/6-311G level. The conformations of 1 and cyclododecane (2) are compared.