Arthroscopic Double-Row Suture Anchor Fixation of Minimally Displaced Greater Tuberosity Fractures

In cases of displaced greater tuberosity fractures, treatments by arthroscopic-assisted reduction and percutaneous screw fixation have been reported. However, in cases in which there is a comminuted fracture or a minimally displaced fracture combined with concomitant lesions such as rotator cuff tear or labral pathology, it is difficult to reduce the fracture and to treat other pathologies by use of a percutaneous screw. Recently, many surgeons have used the double-row repair method in rotator cuff repair, which provides a tendon-bone interface better suited for biologic healing and restoring normal anatomy. In accordance with this method, we used the arthroscopic technique of double-row suture anchor fixation for a minimally displaced greater tuberosity fracture without additional incision. Initially, debridement was performed on the fracture surface by use of a shaver, and the medial-row anchor was inserted through the anterior portal or the intact cuff. Two lateral-row anchors were inserted just anterior and posterior to the lower margin of the fractured fragment under C-arm guidance. The medial-row sutures and lateral-row sutures were then placed. Arthroscopic double-row suture anchor fixation of a displaced greater tuberosity fracture restores the original footprint of the rotator cuff and normal tendon-bone interface of the displaced greater tuberosity fracture.     

Differential gene expression in cultured osteoblasts and bone marrow stromal cells from patients with Paget's disease of bone.

Paget's disease is a focal condition of bone. To study changes in cells within pagetic lesions, we cultured osteoblasts and stromal cells from 22 patients and compared gene expression in these cells to cells from healthy bone. We identified several differentially regulated genes, and we suggest that these changes could lead to the formation of the lesions. INTRODUCTION: Paget's disease is a focal condition of bone of unknown cause. Although it is regarded as primarily an osteoclast disorder, the tight coupling of the activity of osteoclasts and osteoblasts suggests that the osteoblast could play a key role in its pathogenesis. The aim of the study was to identify possible changes in pagetic osteoblasts and stromal cells that might contribute to the development of pagetic lesions. MATERIALS AND METHODS: Candidate genes were identified based on known bone cell regulators, supplemented with microarray analysis. Gene expression was determined by real-time PCR in primary cultures of osteoblasts and bone marrow stromal cells from pagetic patients and control subjects. Concentrations of secreted proteins were determined by ELISA. RESULTS: Dickkopf1 mRNA and protein levels were increased in both pagetic osteoblast and stromal cell cultures, and interleukin (IL)-1 and IL-6 were overexpressed in pagetic osteoblasts. These changes parallel recent findings in myeloma bone disease, which shares some clinical similarities with Paget's disease. Alkaline phosphatase was overexpressed, and bone sialoprotein and osteocalcin were underexpressed in pagetic osteoblasts, consistent with their circulating levels in pagetic patients. It is hypothesized that overexpression of Dickkopf1, IL-1, and IL-6 would result in stimulation of osteoclast proliferation and inhibition of osteoblast growth, leading to the development of the characteristic lytic bone lesions. By stimulating osteoblast differentiation, Dickkopf1 and IL-6 may also promote mineralization, leading to the conversion of lytic lesions to sclerotic. CONCLUSIONS: These findings suggest that dysregulated gene expression in pagetic osteoblasts could cause the changes in bone cell number and function characteristic of Paget's disease.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.     

Enhanced chondrogenesis and Wnt signaling in PTH-treated fractures.

Studies have shown that systemic PTH treatment enhanced the rate of bone repair in rodent models. However, the mechanisms through which PTH affects bone repair have not been elucidated. In these studies we show that PTH primarily enhanced the earliest stages of endochondral bone repair by increasing chondrocyte recruitment and rate of differentiation. In coordination with these cellular events, we observed an increased level of canonical Wnt-signaling in PTH-treated bones at multiple time-points across the time-course of fracture repair, supporting the conclusion that PTH responses are at least in part mediated through Wnt signaling. INTRODUCTION: Since FDA approval of PTH [PTH(1-34); Forteo] as a treatment for osteoporosis, there has been interest in its use in other musculoskeletal conditions. Fracture repair is one area in which PTH may have a significant clinical impact. Multiple animal studies have shown that systemic PTH treatment of healing fractures increased both callus volume and return of mechanical competence in models of fracture healing. Whereas the potential for PTH has been established, the mechanism(s) by which PTH produces these effects remain elusive. MATERIALS AND METHODS: Closed femoral fractures were generated in 8-wk-old male C57Bl/6 mice followed by daily systemic injections of either saline (control) or 30 microg/kg PTH(1-34) for 14 days after fracture. Bones were harvested at days 2, 3, 5, 7, 10, 14, 21, and 28 after fracture and analyzed at the tissue level by radiography and histomorphometry and at the molecular and biochemical levels level by RNase protection assay (RPA), real-time PCR, and Western blot analysis. RESULTS: Quantitative muCT analysis showed that PTH treatment induced a larger callus cross-sectional area, length, and total volume compared with controls. Molecular analysis of the expression of extracellular matrix genes associated with chondrogenesis and osteogenesis showed that PTH treated fractures displayed a 3-fold greater increase in chondrogenesis relative to osteogenesis over the course of the repair process. In addition, chondrocyte hypertrophy occurred earlier in the PTH-treated callus tissues. Analysis of the expression of potential mediators of PTH actions showed that PTH treatment significantly induced the expression of Wnts 4, 5a, 5b, and 10b and increased levels of unphosphorylated, nuclear localized beta-catenin protein, a central feature of canonical Wnt signaling. CONCLUSIONS: These results showed that the PTH-mediated enhancement of fracture repair is primarily associated with an amplification of chondrocyte recruitment and maturation in the early fracture callus. Associated with these cellular effects, we observed an increase in canonical Wnt signaling supporting the conclusion that PTH effects on bone repair are mediated at least in part through the activation of Wnt-signaling pathways.     

供应室高护生实习大纲的设计与应用

目的 探讨供应室高护生实习大纲的设计与应用效果。方法 对64名高护生采用自行设计的供应室高护生实习大纲进行临床带教。结果 高护生对供应室实习的总满意率为96．8％，93．5～96．8％高护生对消毒灭菌知识、个人防护知识、无菌技术操作、手的卫生操作掌握良好。结论 供应室高护生实习大纲科学实用，其应用增强了高护生的无菌观念和个人防护意识。     

Radiation effects on the cosmetic outcomes of immediate and delayed autologous breast reconstruction: an argument about timing.

OBJECTIVE: To conduct a systematic review to gather the available evidence on the optimum timing of the radiotherapy in relation to autologous breast reconstruction. MATERIAL AND METHODS: The data was extracted from scientific databases, and a manual follow-up of references. The studies were selected which included at least 20 patients with any method of autologous breast reconstruction who were treated with adjuvant radiotherapy either before or after their reconstruction, and had addressed the effects of radiotherapy on the cosmetic outcome in their results. The principal outcome was cosmetic appearance. Secondary outcomes were immediate and delayed complications. RESULTS: We could not find any randomised controlled trial on this topic. Ten studies were included, most were retrospective, heterogeneous in terms of control groups, radiation doses, follow-up duration, and outcome measurements. Two studies included no control groups, and four studies compared the outcomes of patients with radiotherapy either before (n=3) or after (n=1) autologous breast reconstruction. The overall incidence of complications was increased in patients with radiotherapy in three out of these four studies. Only four studies directly compared the outcomes of patients who received radiotherapy before with patients who received radiotherapy after autologous breast reconstruction and two out of these reported worse outcomes associated with post-reconstruction radiotherapy. CONCLUSIONS: Despite the paucity of the published data, the current evidence suggests that the radiation has a deleterious effect on autologous flap reconstruction. Until better methods of radiation delivery can be devised to minimise the long term radiation sequelae in the irradiated tissue, delayed reconstruction seems to be a safe option in most of the cases. However, the findings from these studies should be interpreted with great caution before generalising from their results.     

雷公藤多甙联合中草药治疗IgA肾病的病例对照研究

IgA肾病(immunoglobulin A nephropathy,I-gAN)是肾小球系膜病变的一个特殊类型,其发病机制尚未完全明确,临床表现复杂多样。目前,临床上常用的药物主要有激素、雷公藤、环磷酰胺等,都具有一定的疗效,但在药物副作用、血尿的消退、肾功能的稳定及停药后复发等方面均有各自的缺陷。笔者所在科室在慢性肾炎型IgAN的治疗上进行探索,现将结果报告如下。1资料与方法1.1病例选择及分组73例均为铜陵市第一人民医院肾内科住院并经肾活检证实的IgAN患者,除外各种继发性IgAN,并符合以下条件:①按Lee氏分级均在Ⅲ~Ⅳ级间;②无严重的肝损害;③血…     

Effects of cerulenin on the endogenous fatty acid synthetic activity in squamous cell carcinoma of the oral cavity.

PURPOSES: Inhibition of cerulenin on the endogenous fatty acid synthetic activities of oral squamous cell carcinoma (OSCC) and normal oral mucosa was assayed. METHODS: Squamous cell carcinoma and normal oral mucosa were collected fresh from surgical specimens. The collected tissues were minced in RPMI 1640 and divided into 3 groups: cerulenin treated, dimethylsulfoxide treated, and control. The tissues were incubated in [1(2)-(14)C]acetic acid, sodium salt for the last 2.5 hours of the treatment at 37 degrees C in 5% CO(2). After labeling, total lipids were extracted and counted for (14)C by scintillation counting. RESULTS: Endogenous fatty acid synthetic activities of oral squamous cell caranoma in the cerulenin-treated group decreased by 19% at 1 hour, 64% at 2 hours, and 87% at 4 hours; remained nearly unchanged in the dimethylsulfoxide-treated group; and increased slightly in the control group. The oral mucosa tissues were only mildly affected by cerulenin in fatty acid synthesis. CONCLUSIONS: Cerulenin significantly inhibits fatty acid synthetic activity in squamous cell carcinoma and only mildly affected the oral mucosa, indicating that the fatty acid synthetic pathway may be exploited as a target for developing anticancer drugs.