Salvage of externally exposed ventricular assist devices.

Although externally exposed ventricular assist devices are associated with extremely high mortality rates, salvage may be accomplished by early aggressive wound debridement, transposition of a well-perfused autologous tissue (such as omentum), dead space obliteration, and adequate external coverage using vascularized tissue. The temporary suppression rather than the total eradication of the infection should be the goal of these procedures.

Muscle stapling technique for free muscle transfer to the face.

Free muscle transfer for facial reanimation can be facilitated by the use of a linear gastrointestinal stapler. This technique not only offers reliable muscle insertion at the recipient site but also helps to provide an adequate motor unit by facilitating safe muscle debulking, splitting, and tailoring.

Aneurysm of the radial artery following blunt trauma to the wrist.

Aneurysms involving the distal radial artery are rare lesions which are usually secondary to penetrating trauma or iatrogenic injury. Blunt trauma is an extremely uncommon cause. In the absence of a history of penetrating vascular injury, a radial artery aneurysm may easily be misdiagnosed as a nonvascular mass such as a synovial cyst. A diagnostic approach to these lesions is discussed emphasizing the role of noninvasive studies in uncomplicated cases. Excision of the aneurysm is recommended. The decision to ligate or reconstruct the radial artery remains controversial.

Extraarticular pigmented villonodular synovitis of the shoulder: a case report.

A rotator cuff tear was diagnosed in a 57-year-old woman based on physical examination and magnetic resonance imaging studies. At operation, an abnormal bursal lesion also was found. The lesion was completely extraarticular and was identified histologically as pigmented villonodular synovitis. The patient was treated with complete bursectomy and repair of the rotator cuff tear and remains asymptomatic 21 months after operation. Pigmented villonodular synovitis is a condition characterized by cell proliferation and deposition of hemosiderin into the lining tissues of joints, tendons, and bursae. The extraarticular form of pigmented villonodular synovitis is extremely rare and usually represents an extension of a primary intraarticular process. Only a few cases have been reported in which the lesion was found exclusively outside the joint with no intraarticular segment. In reviewing the literature, no case of exclusively extraarticular pigmented villonodular synovitis of the shoulder was found. The sequelae of extraarticular pigmented villonodular synovitis are poorly understood, but this lesion can be locally invasive, and if left untreated, may destroy surrounding tissues. Therefore, early diagnosis and treatment are important for optimal results.

The results of surgical treatment of trigger finger.

A three-part retrospective study was undertaken to review the long-term results of surgical treatment of trigger finger. Seventy-five patients were identified by chart review. Fifty-nine of these were assessed by a telephone survey, with a mean follow-up period of 48 months (range, 6-70 months). Forty-six patients (78%) underwent follow-up physical examination. Surgical treatment was successful in all patients. Ninety-seven percent of patients had complete resolution of triggering, and the rest had significant improvement of symptoms. The recurrence rate was 3%, with only a single patient requiring reoperation. Complications were infrequent and resulted in minimal morbidity. No nerve injuries, tendon bowstringing, or ulnar deviation of the digits were observed. There were no wound infections. Although steroid injections should remain the initial remedy for most trigger fingers, surgical intervention is highly successful for conservative treatment failures and should be considered for patients desiring quick and definitive relief from this disability.

Peptide YY selectively stimulates expression of the colonocytic phenotype.

Peptide YY (PYY) is produced by colonic mucosal endocrine cells and modulates gastrointestinal endocrine activity through specific Y-receptors. The direct effects of PYY on intestinal mucosal growth and differentiation remain uncharacterized. The abundance of PYY in colonic mucosa suggests that PYY acts locally to maintain colonocytic differentiation. We tested this hypothesis in human Caco-2 intestinal epithelial cells, which express alkaline phosphatase (AP) and dipeptidyl dipeptidase (DP), brush-border enzymes differentially concentrated in large and small intestinal mucosa, respectively. The effects of PYY on enzyme specific activity were compared with those of pancreatic polypeptide, neuropeptide-Y, vasoactive intestinal peptide, pentagastrin, bombesin, and selective Y1- and Y2-receptor agonists. Brush-border enzyme activity was assessed by AP and DP specific activity in cell lysates quantitated spectrophotometrically following synthetic substrate digestion. PYY, neuropeptide-Y, pancreatic polypeptide, and vasoactive intestinal peptide (10(-7) mol/L) stimulated AP activity. PYY brought about the greatest increase (38.0%+/-11.0%, n=48). Only PYY decreased DP specific activity (7.9%+/-2.2%, n=48). The Y2-agonist but not the Y1-agonist mimicked these PYY effects (increasing AP 28.3%+/-3.5% and decreasing DP 10.4%+/-3.6%). These data suggest that PYY promotes differentiation toward a colonocytic phenotype in Caco-2 intestinal epithelial cells and that this effect may be mediated through the Y2-receptor subtype.

Regulation of human colonic cell line proliferation and phenotype by sodium butyrate.

Colonic butyrate may maintain mucosal differentiation and oppose carcinogenesis. We characterized butyrate effects on differentiation, proliferation, and matrix interactions in Caco-2 and SW620 human colonic cells. Differentiation was assessed by brush border enzyme activity and doubling time by serial cell counts. Motility across matrix proteins was quantitated by monolayer expansion and correlated with adhesiveness to matrix. Integrin subunit surface pools were measured by immunoprecipitation. Butyrate-stimulated differentiation inhibited proliferation and was significantly more potent than acetate in this regard. Butyrate also inhibited motility across collagen I, collagen IV, and laminin, as well as decreasing adhesiveness to these matrices and beta 1, alpha 1, and alpha 2 integrin subunit surface expression. Butyrate acts in cultured cells at clinically relevant concentrations to oppose classical malignant behavior, inhibiting proliferation and motility while promoting differentiation. Since butyrate is derived from fermentation of dietary fiber, such mechanisms may contribute to the apparent protective action of fiber against colon carcinogenesis.

Restitution at the cellular level: regulation of the migrating phenotype.

Intestinal epithelial cells migrating across a mucosal defect are generally described as dedifferentiated, a term that suggests a loss of regulatory biology. Since cell biology may be more readily studied in established cell lines than in vivo, a model is developed using the human Caco-2 intestinal epithelial cell migrating across matrix proteins. This resembles in vivo models of mucosal healing in its sheet migration and loss of the brush border enzymes, which are conventional markers for intestinal epithelial differentiation. Immunohistochemical studies of migrating Caco-2 cells suggest, however, that the rearrangements of cytoskeletal, cell-cell and cell-matrix proteins during migration are not random but seem adapted to the migratory state. Indeed, Caco-2 migration may be substantially regulated by a variety of physiologic and pharmacologic stimuli and differentiation, measured by the specific activity of the intestinal epithelial brush border enzymes alkaline phosphatase and dipeptidyl dipeptidase, may be independently pharmacologically programmed during the stimulation or inhibition of cell motility.

Primary malignant lymphoma of the intestine.

Primary intestinal lymphoma is uncommon but not rare. Its pathology and potential therapy are complex. Its epidemiology has changed radically over the past century, reflecting a sharp surge in the incidence of intestinal lymphoma, particularly that associated with immunosuppression. Recent advances in diagnosis, a new approach to pathologic classification by immunotyping, and a new staging system have influenced therapy. New multimodal therapeutic protocols have improved the prognosis of this once deadly disease.

Glutamine modulates phenotype and stimulates proliferation in human colon cancer cell lines.

Glutamine supplementation has been advocated for patients requiring parenteral nutritional support. However, the direct effect of glutamine on neoplastic cells is poorly understood. We therefore investigated the effects of glutamine on the proliferation, differentiation, and cell-matrix interactions of two human colon carcinoma cell lines (Caco-2 and SW620) adapted to glutamine-free media. Doubling times were calculated by logarithmic transformation of serial cell counts. Alkaline phosphatase, cathepsin C (dipeptidyl peptidase), lactase, and isomaltase expression (markers of differentiation) were assayed by digestion of synthetic substrates. Adhesion to matrix proteins was assessed by colorimetric quantitation of toluidine blue staining of adherent cells. Surface expression of Caco-2 receptors for matrix proteins (integrins) was studied by biotinylation and immunoprecipitation with specific antibodies. Glutamine (1-10 mM) dose-dependently stimulated Caco-2 proliferation on all matrices studied with maximal effect at 7 mM. For instance, Caco-2 doubling time on collagen IV decreased by 57 +/- 0.2% (SE) (P < 0.001). Glutamine inhibited the expression of all four digestive enzymes with maximal inhibition ranging from 10 to 40% (P < 0.05 for all). Adhesion to matrix proteins was markedly diminished (51 +/- 1%, P < 0.01) by glutamine (5 mM) treatment, correlating with decreased alpha 2 and beta 1 integrin subunit surface expression. Glutamine had similar effects on SW620 cells, stimulating proliferation, inhibiting digestive enzyme expression, and diminishing both adhesion and integrin surface expression. Glutamine supplementation modulates the phenotype of at least two human colon carcinoma cell lines, increasing proliferation, decreasing differentiation, and decreasing adhesion to matrix proteins in association with decreased integrin expression. Although the mechanisms of these effects await elucidation, such characteristics would appear to predict more aggressive tumor behavior and raise the possibility that nutritional supplementation with glutamine may be deleterious in patients with cancer.