Best bone of acetabulum for cup component placement in Crowe types I to III dysplastic hips: a computer simulation study.

BACKGROUND: During cup implantation, vertical height of the cup center (V-HCC) should be precisely controlled to achieve sufficient bone-cup coverage (BCC). Our study aimed to investigate the acetabular bone stock and the quantitative relationship between V-HCC and BCC in Crowe types I to III hips. METHODS: From November 2013 to March 2016, pelvic models of 51 patients (61 hips) with hip dysplasia were retrospectively reconstructed using a computer software. Acetabular height and doom thickness were measured on the mid-acetabular coronal cross section. V-HCC was defined as the vertical distance of cup rotational center to the interteardrop line (ITL). In the cup implantation simulation, the cup was placed at the initial preset position, with a V-HCC of 15 mm, and moved proximally by 3-mm increments. At each level, the BCC was automatically calculated by computer. Analysis of variance and Kruskal-Wallis test were used to compare the differences between groups. RESULTS: There were no significant between-group differences in maximum thickness of the acetabular doom; however, peak bone stock values were obtained at heights of 41.63 ±â€Š5.14 mm (Crowe type I), 47.58 ±â€Š4.10 mm (Crowe type II), and 55.78 ±â€Š3.64 mm (Crowe type III) above the ITL. At 15 mm of V-HCC, median BCC was 78% (75-83%) (Crowe type I), 74% (66-71%) (Crowe type II), and 61% (57-68%) (Crowe type III). To achieve 80% of the BCC, the median V-HCC was 16.27 (15.00-16.93) mm, 18.19 (15.01-21.53) mm, and 24.13 (21.02-28.70) mm for Crowe types I, II, and III hips, respectively. CONCLUSION: During acetabular reconstruction, slightly superior placement with V-HCC <25 mm retained sufficient bone coverage in Crowe I to III hips.

Identification of Leptospira interrogans phospholipase C as a novel virulence factor responsible for intracellular free calcium ion elevation during macrophage death.

BACKGROUND: Leptospira-induced macrophage death has been confirmed to play a crucial role in pathogenesis of leptospirosis, a worldwide zoonotic infectious disease. Intracellular free Ca(2+) concentration ([Ca(2+)]i) elevation induced by infection can cause cell death, but [Ca(2+)]i changes and high [Ca(2+)]i-induced death of macrophages due to infection of Leptospira have not been previously reported. METHODOLOGY/PRINCIPAL FINDINGS: We first used a Ca(2+)-specific fluorescence probe to confirm that the infection of L. interrogans strain Lai triggered a significant increase of [Ca(2+)]i in mouse J774A.1 or human THP-1 macrophages. Laser confocal microscopic examination showed that the [Ca(2+)]i elevation was caused by both extracellular Ca(2+) influx through the purinergic receptor, P2X7, and Ca(2+) release from the endoplasmic reticulum, as seen by suppression of [Ca(2+)]i elevation when receptor-gated calcium channels were blocked or P2X7 was depleted. The LB361 gene product of the spirochete exhibited phosphatidylinositol phospholipase C (L-PI-PLC) activity to hydrolyze phosphatidylinositol-4,5-bisphosphate (PIP2) into inositol-1,4,5-trisphosphate (IP3), which in turn induces intracellular Ca(2+) release from endoplasmic reticulum, with the Km of 199 µM and Kcat of 8.566E-5 S(-1). Secretion of L-PI-PLC from the spirochete into supernatants of leptospire-macrophage co-cultures and cytosol of infected macrophages was also observed by Western Blot assay. Lower [Ca(2+)]i elevation was induced by infection with a LB361-deficient leptospiral mutant, whereas transfection of the LB361 gene caused a mild increase in [Ca(2+)]i. Moreover, PI-PLCs (PI-PLC-ß3 and PI-PLC-γ1) of the two macrophages were activated by phosphorylation during infection. Flow cytometric detection demonstrated that high [Ca(2+)]i increases induced apoptosis and necrosis of macrophages, while mild [Ca(2+)]i elevation only caused apoptosis. CONCLUSIONS/SIGNIFICANCE: This study demonstrated that L. interrogans infection induced [Ca(2+)]i elevation through extracellular Ca(2+) influx and intracellular Ca(2+) release cause macrophage apoptosis and necrosis, and the LB361 gene product was shown to be a novel PI-PLC of L. interrogans responsible for the [Ca(2+)]i elevation.

Classification of pilon fractures by computed tomography and its guide to clinical treatment / 中国骨伤

<p><b>OBJECTIVE</b>To introduce a method of three-column classifications for Pilon fractures and observe clinical utility on column fixation.</p><p><b>METHODS</b>From June 2007 to March 2010,a total of 27 patients (29 ankles, 26 males and 1 female,ranging in age from 23 to 59 years, with an average of 33.1 years) with Pilon fractures were treated through column fixation by using semitubular plates or screws with anteromedial, anterior, posterolateral,posteromedial approach. And postoperative follow up were carried out.</p><p><b>RESULTS</b>The mean follow up was 17.5 months(ranged,5 to 33 months). According to the Mazur ankle grading system, the outcome was excellent in 20, good in 4 and fair in 5 ankles. Patients in this group did not have complications of wound dehiscence, deep infection, osteomyelitis, nonunion, ankylosis, and joint instability.</p><p><b>CONCLUSION</b>Based on the three-column classification, the clinical results for the treatment of Pilon fractures demonstrate the rationality and efficiency of this method.</p>