39 research outputs found
Complications and reoperations of the SB CharitƩ lumbar disc prosthesis: experience in 75 patients
Artificial disc prosthesis show fair to good short- and mid-term results. Long-term results are becoming apparent now, however, the incidence of late complications with this procedure remain poorly understood. In this report we will analyse late complications and discuss our experiences with salvage operations in patients with persistent pain after SB CharitĆ© disc prosthesis implantation. Seventy-five patients with persistent leg and back pain after insertion of an artificial disc prosthesis were enrolled in the study. In this negative selection frequently occurring late-complications were subsidence, wear, adjacent disc degeneration, facet joint degeneration and migration. In 15 patients we performed a posterior fusion without disc removal, and in 22 patients we removed 26 prostheses and performed a posterior and anterior fusion. The visual analogue scale (VAS) and Oswestry were examined before the salvage operation and after a follow-up period of at least 1Ā year, which is not yet available in all patients. The VAS and Oswestry decreased in the posterior group (nĀ =Ā 10) respectively from 8.0 (SD 0.9) to 6.3 (SD 2.1) and from 57.0 (SD 17.0) to 44.6 (SD 20.4); and in the disc removal group (nĀ =Ā 14) respectively from 8.0 (SD 0.9) to 5.6 (SD 2.7) and from 56.3 (SD 14.0) to 43.0 (SD 20.7). Serious late complications may occur following total disc replacement. Removal of the SB CharitĆ© artificial disc is feasible but with inherent risks. Removal of the disc prosthesis gives slightly better results than posterior fusion alone after a follow-up of at least 1Ā year
Half-integer Higher Spin Fields in (A)dS from Spinning Particle Models
We make use of O(2r+1) spinning particle models to construct linearized
higher-spin curvatures in (A)dS spaces for fields of arbitrary half-integer
spin propagating in a space of arbitrary (even) dimension: the field
potentials, whose curvatures are computed with the present models, are
spinor-tensors of mixed symmetry corresponding to Young tableaux with D/2 - 1
rows and r columns, thus reducing to totally symmetric spinor-tensors in four
dimensions. The paper generalizes similar results obtained in the context of
integer spins in (A)dS.Comment: 1+18 pages; minor changes in the notation, references updated.
Published versio
Induction of G1 and G2/M cell cycle arrests by the dietary compound 3,3'-diindolylmethane in HT-29 human colon cancer cells
<p>Abstract</p> <p>Background</p> <p>3,3'-Diindolylmethane (DIM), an indole derivative produced in the stomach after the consumption of broccoli and other cruciferous vegetables, has been demonstrated to exert anti-cancer effects in both <it>in vivo </it>and <it>in vitro </it>models. We have previously determined that DIM (0 ā 30 Ī¼mol/L) inhibited the growth of HT-29 human colon cancer cells in a concentration-dependent fashion. In this study, we evaluated the effects of DIM on cell cycle progression in HT-29 cells.</p> <p>Methods</p> <p>HT-29 cells were cultured with various concentrations of DIM (0 ā 30 Ī¼mol/L) and the DNA was stained with propidium iodide, followed by flow cytometric analysis. [<sup>3</sup>H]Thymidine incorporation assays, Western blot analyses, immunoprecipitation and <it>in vitro </it>kinase assays for cyclin-dependent kinase (CDK) and cell division cycle (CDC)2 were conducted.</p> <p>Results</p> <p>The percentages of cells in the G1 and G2/M phases were dose-dependently increased and the percentages of cells in S phase were reduced within 12 h in DIM-treated cells. DIM also reduced DNA synthesis in a dose-dependent fashion. DIM markedly reduced CDK2 activity and the levels of phosphorylated retinoblastoma proteins (Rb) and E2F-1, and also increased the levels of hypophosphorylated Rb. DIM reduced the protein levels of cyclin A, D1, and CDK4. DIM also increased the protein levels of CDK inhibitors, p21<sup>CIP1/WAF1 </sup>and p27<sup>KIPI</sup>. In addition, DIM reduced the activity of CDC2 and the levels of CDC25C phosphatase and cyclin B1.</p> <p>Conclusion</p> <p>Here, we have demonstrated that DIM induces G1 and G2/M phase cell cycle arrest in HT-29 cells, and this effect may be mediated by reduced CDK activity.</p
Shared decision-making in urology and female pelvic floor medicine and reconstructive surgery.
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Amplification of TGF beta Induced ITGB6 Gene Transcription May Promote Pulmonary Fibrosis
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Reduced Ets Domain-containing Protein Elk1 Promotes Pulmonary Fibrosis via Increased Integrin alpha v beta 6 Expression
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Reduced Ets Domain-containing Protein Elk1 Promotes Pulmonary Fibrosis via Increased Integrin alpha v beta 6 Expression
Reduced ets domain-containing protein Elk1 promotes pulmonary fibrosis via increased integrin alpha v beta 6 expression
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease with high mortality. Active TGFĪ²1 is considered central to the pathogenesis of IPF. A major mechanism of TGFĪ²1 activation in the lung involves the epithelially restricted Ī±vĪ²6 integrin. Expression of the Ī±vĪ²6 integrin is dramatically increased in IPF. How Ī±vĪ²6 integrin expression is regulated in the pulmonary epithelium is unknown. Here we identify a region in the Ī²6 subunit gene (ITGB6) promoter acting to markedly repress basal gene transcription, which responds to both the Ets domain-containing protein Elk1 (Elk1) and the glucocorticoid receptor (GR). Both Elk1 and GR can regulate Ī±vĪ²6 integrin expression in vitro. We demonstrate Elk1 binding to the ITGB6 promoter basally and that manipulation of Elk1 or Elk1 binding alters ITGB6 promoter activity, gene transcription, and Ī±vĪ²6 integrin expression. Crucially, we find that loss of Elk1 causes enhanced Itgb6 expression and exaggerated lung fibrosis in an in vivo model of fibrosis, whereas the GR agonist dexamethasone inhibits Itgb6 expression. Moreover, Elk1 dysregulation is present in epithelium from patients with IPF. These data reveal a novel role for Elk1 regulating ITGB6 expression and highlight how dysregulation of Elk1 can contribute to human disease