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排序方式: 共有426条查询结果,搜索用时 31 毫秒
1.
Ann E Barr Fayez F Safadi Irene Gorzelany Mamta Amin Steven N Popoff Mary F Barbe 《Journal of bone and mineral research》2003,18(11):2023-2032
Work-related repetitive motion disorders are costly. Immunohistochemical changes in bones resulting from repetitive reaching and grasping in 17 rats were examined. After 3-6 weeks, numbers of ED1+ macrophages and osteoclasts increased at periosteal surfaces of sites of muscle and interosseous membrane attachment and metaphyses of reach and nonreach forelimbs. These findings indicate pathological overloading leading to inflammation and subsequent bone resorption. INTRODUCTION: Sixty-five percent of all occupational illnesses in U.S. private industry are attributed to musculoskeletal disorders arising from the performance of repeated motion, yet the precise mechanisms of tissue pathophysiology have yet to be determined for work-related musculoskeletal disorders. This study investigates changes in upper extremity bone tissues resulting from performance of a voluntary highly repetitive, negligible force reaching and grasping task in rats. MATERIALS AND METHODS: Seventeen rats reached an average of 8.3 times/minute for 45-mg food pellets for 2 h/day, 3 days/week for up to 12 weeks. Seven rats served as normal or trained controls. Radius, ulna, humerus, and scapula were collected bilaterally as follows: radius and ulna at 0, 3, 4, 5, 6, and 12 weeks and humerus and scapula at 0, 4, and 6 weeks. Bones were examined for ED1-immunoreactive mononuclear cells and osteoclasts. Double-labeling immunohistochemistry was performed for ED1 (monocyte/macrophage lineage cell marker) and TRACP (osteoclast marker) to confirm that ED1+ multinucleated cells were osteoclasts. Differences in the number of ED1+ cells over time were analyzed by ANOVA. RESULTS: Between 3 and 6 weeks of task performance, the number of ED1+ mononuclear cells and osteoclasts increased significantly at the periosteal surfaces of the distal radius and ulna of the reach and nonreach limbs compared with control rats. These cells also increased at periosteal surfaces of humerus and scapula of both forelimbs by 4-6 weeks. These cellular increases were greatest at muscle attachments and metaphyseal regions, but they were also present at some interosseous membrane attachments. The number of ED1+ cells decreased to control levels in radius and ulna by 12 weeks. CONCLUSIONS: Increases in ED1+ mononuclear cells and osteoclasts indicate that highly repetitive, negligible force reaching causes pathological overloading of bone leading to inflammation and osteolysis of periosteal bone tissues. 相似文献
2.
Serum CA-125 antigen levels increase during menses 总被引:4,自引:0,他引:4
Serum CA-125 antigen levels were measured by radioimmunoassay before and during menses in women with and without endometriosis. Mean CA-125 levels were significantly increased in both groups during menses. Samples obtained during menses represent a potential source of elevated levels and false positive results. 相似文献
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Costa MA Angiolillo DJ Tannenbaum M Driesman M Chu A Patterson J Kuehl W Battaglia J Dabbons S Shamoon F Flieshman B Niederman A Bass TA;STLLR Investigators 《The American journal of cardiology》2008,101(12):1704-1711
Drug-eluting stent failures were associated with various clinical factors. However, the clinical impact of stent deployment technique was unknown. This study was designed to evaluate the frequency and impact of suboptimal percutaneous coronary intervention on long-term outcomes of 1,557 patients treated with sirolimus-eluting stents (SESs) in 41 US hospitals. All steps of the interventional procedure were scrutinized by an independent core laboratory to determine the occurrence of geographic miss (GM). GM included longitudinal (LGM; injured or diseased segment not covered by SES) or axial GM (balloon-artery size ratio <0.9 or >1.3) mismatches. Patients with and without GM were stratified (GM vs no-GM group). Patients, investigators, and the independent clinical event adjudication committee were blind to study group assignments. The primary end point was 1-year target-vessel revascularization (TVR) rate. Incidences and predictors of GM and safety outcomes were secondary end points. GM occurred in 943 patients (66.5%): 47.6% had LGM, 35.2% had axial GM, and 16.5% had both. One-year TVR rates were 5.1% in the GM group versus 2.5% in the no-GM group (p=0.025). TVR was 6.1% in the LGM versus 2.6% in the no-LGM subgroups (p=0.001). The association of GM with 1-year TVR was independent of clinical or anatomic factors (hazard ratio 2.0, 95% confidence interval 1.0 to 4.02, p=0.05). There was a 3-fold increase in myocardial infarction rates associated with GM (2.4% vs 0.8%; p=0.04). In conclusion, GM occurred frequently during SES implantation and was associated with increased risk of TVR and myocardial infarction at 1 year. These results emphasized the need for improvement in contemporary percutaneous coronary intervention practices and technologies. 相似文献
6.
The Use of Sodium Tetradecyl Sulphate for the Treatment of Venous Malformations of the Head and Neck
Xena Alakailly Raja Kummoona Faisal A. Quereshy Dale A. Baur Ariadne E. González 《Journal of maxillofacial and oral surgery》2015,14(2):332-338
Introduction
Vascular malformations have devastating cosmetic effects in addition to being associated with pain and bleeding. Sclerotherapy has been used as an effective therapeutic modality for the management of vascular malformations. The purpose of this case series is to describe our clinical experience of using sodium tetradecyl sulphate (STS) 3 % in the treatment of venous malformation lesions of head and neck.Materials and Methods
Thirteen patients were included in this study (three male and ten female; age range between 8 months and 54 years; mean age 18.2 years, ±SD 15.71). The patients were treated by 3 % STS intralesional injections. Of the thirteen patients treated, complete resolution occurred in four patients (28.57 %), a good response occurred in five patients (35.7 %), a moderate response in two patients (14.28 %), a mild response in two patients (14.28 %) and no response in one patient (7.14 %). The side effects encountered in all patients were pain and edema after injection which was controlled by oral analgesics and an intramuscular injection of dexamethasone. In addition, two patients developed a superficial ulceration (11.76 %) which healed uneventfully, and one patient developed ecchymosis after injection (5.88 %).Conclusion
Sclerotherapy with 3 % STS is a simple, safe, and effective modality for the treatment of venous malformations. 相似文献7.
Samir M. Abdelmagid Joyce Y. Belcher Fouad M. Moussa Suzanne L. Lababidi Gregory R. Sondag Kimberly M. Novak Afif S. Sanyurah Nagat A. Frara Roshanak Razmpour Fabiola E. Del Carpio-Cano Fayez F. Safadi 《The American journal of pathology》2014,184(3):697-713
We have previously identified osteoactivin (OA), encoded by Gpnmb, as an osteogenic factor that stimulates osteoblast differentiation in vitro. To elucidate the importance of OA in osteogenesis, we characterized the skeletal phenotype of a mouse model, DBA/2J (D2J) with a loss-of-function mutation in Gpnmb. Microtomography of D2J mice showed decreased trabecular mass, compared to that in wild-type mice [DBA/2J-Gpnmb+/SjJ (D2J/Gpnmb+)]. Serum analysis showed decreases in OA and the bone-formation markers alkaline phosphatase and osteocalcin in D2J mice. Although D2J mice showed decreased osteoid and mineralization surfaces, their osteoblasts were increased in number, compared to D2J/Gpnmb+ mice. We then examined the ability of D2J osteoblasts to differentiate in culture, where their differentiation and function were decreased, as evidenced by low alkaline phosphatase activity and matrix mineralization. Quantitative RT-PCR analyses confirmed the decreased expression of differentiation markers in D2J osteoblasts. In vitro, D2J osteoblasts proliferated and survived significantly less, compared to D2J/Gpnmb+ osteoblasts. Next, we investigated whether mutant OA protein induces endoplasmic reticulum stress in D2J osteoblasts. Neither endoplasmic reticulum stress markers nor endoplasmic reticulum ultrastructure were altered in D2J osteoblasts. Finally, we assessed underlying mechanisms that might alter proliferation of D2J osteoblasts. Interestingly, TGF-β receptors and Smad-2/3 phosphorylation were up-regulated in D2J osteoblasts, suggesting that OA contributes to TGF-β signaling. These data confirm the anabolic role of OA in postnatal bone formation.Osteoporosis is a growing public health problem, in part because of the increasing numbers of people living beyond the age of 65 years.1 It is characterized by low bone mass due to increased bone resorption by osteoclasts and decreased bone formation by osteoblasts, with significant deterioration in the bone microarchitecture leading to high bone fragility and increased fracture risk.1,2 The net effect of osteoporosis is low bone mass.1 There is an increasing demand for identifying novel bone anabolic factors with potential therapeutic benefits in treating generalized bone loss, such as osteoporosis and/or major skeletal fracture.Osteoactivin is a novel glycoprotein first identified in natural mutant osteopetrotic rats.3 The same protein has been identified and named separately in several other species: as dendritic cell heparan sulfate proteoglycan integrin dependent ligand (DCHIL) in mouse dendritic cells,4 as transmembrane glycoprotein NMB (GPNMB) in human melanoma cell lines and melanocytes,5 and as hematopoietic growth factor inducible neurokinin (HGFIN) in human tumor cells.6 The current recommended name for the protein encoded by Gpnmb in mouse is transmembrane glycoprotein NMB (http://www.ncbi.nlm.nih.gov/protein/Q99P91.2); here, we continue to use osteoactivin (OA) for the protein and Gpnmb for the gene. OA is a type I transmembrane protein that consists of multiple domains, including an extracellular domain, transmembrane domain, and protein sorting signal sequence.7 Within the C-terminal domain, OA has an RGD motif, predicting an integrin attachment site.3,7–9Our research group initially reported on the novel role of OA in osteoblast differentiation and function.7–10 We demonstrated that OA expression has a temporal pattern during osteoblast differentiation, being highest during matrix maturation and culture mineralization in vitro.7–11 Using loss-of–function and gain-of–function approaches in osteoblasts, we reported that OA overexpression increases osteoblast differentiation and function and that OA down-regulation decreases nodule formation, alkaline phosphatase (ALP) activity, osteocalcin (OC) production, and matrix mineralization in vitro.7 We also reported on the positive role of OA in mesenchymal stem cell (MSCs) differentiation into osteoblasts in vitro.12 In another study, we showed that recombinant OA protein induces higher osteogenic potential of fetal-derived MSCs, compared with bone marrow–derived MSCs13 and its osteogenic effects in the mouse C3H10T1/2 MSC cell line were similar to those of recombinant BMP-2.12 We also localized OA protein as associated predominately with osteoblasts lining trabecular bones in vivo,11 and showed that local injection of recombinant OA increased bone mass in a rat model.14 Moreover, in a fracture repair model OA expression increased over time, reaching a maximum 2 weeks after fracture.11 In a parallel study, recombinant OA supported bone regeneration and formation in a rat critical-size calvarial defect model.15 Others have shown that OA is highly expressed by osteoclasts in vitro, suggesting that it may regulate osteoclast formation and activity.16There is urgent need for an animal model to fully examine the role of OA in osteogenesis. Interestingly, a natural mutation of the Gpnmb gene has been identified in the DBA/2J (D2J) mouse strain.17 These mice exhibit high-frequency hearing loss, which begins at the time of weaning and becomes severe by 2 to 3 months of age.18,19 Aged D2J mice also develop progressive eye abnormalities that closely mimic human hereditary glaucoma. The onset of disease symptoms falls roughly between 3 and 4 months of age, and disease becomes severe by 6 months of age.5,20 D2J mice are homozygous for a nonsense mutation in the Gpnmb gene sequence that induces an early stop codon, generating a truncated protein sequence of 150 amino acids (aa) instead of the full-length 562-aa OA protein.5 The control for the D2J mouse is the wild-type DBA/2J-Gpnmb+/SjJ mouse (D2J/Gpnmb+), homozygous for the wild-type Gpnmb gene.21 These Gpnmb wild-type mice do not develop glaucoma, as D2J mice do, although they exhibit mild iris stromal atrophy.21In the present study, we used Gpnmb mutant (D2J) and Gpnmb wild-type (D2J/Gpnmb+) mice to gain insight into the role of OA in osteogenesis and in osteoblast differentiation and function. Here, we report that loss-of–function mutation of Gpnmb suppresses bone formation by directly affecting osteoblast proliferation and survival, leading to a decreased number of differentiated osteoblasts with suppressed activity in bone mineralization. Thus, our data point to OA as a novel and positive regulator of postnatal bone formation. 相似文献
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9.
Soroush Assari Alan Kaufmann Kurosh Darvish Jung Park Jonathan Haw Fayez Safadi Saqib Rehman 《Injury》2013
Objective
Biomechanical comparison between locked plating and retrograde nailing of supracondylar femur fractures with simulated postoperative weight-bearing.Methods
The Locking Condylar Plate (LCP) and Retrograde/Antegrade EX Femoral Nail (RAFN) were tested using 10 paired elderly cadaveric femurs, divided into Normal and Low Bone Mineral Density (BMD) groups, with a simulated AO/OTA type 33-A3 supracondylar femur fracture. Each specimen was subjected to 200,000 loading cycles in an attempt to simulate six weeks of postoperative recovery with full weight-bearing for an average individual. The construct's subsidence due to cyclic loading, and axial stiffness before and after the cyclic loading were measured and their correlation with BMD was studied. The two implants were compared in a paired study within each BMD group.Results
LCP constructs showed higher axial stiffness compared to RAFN for both Normal and Low BMD groups (80% and 57%, respectively). After cyclic loading, axial stiffness of both constructs decreased by 20% and RAFN constructs resulted in twice as much subsidence (1.9 ± 0.6 mm). Two RAFN constructs with Low BMD failed after a few cycles whereas the matched pairs fixed with LCP failed after 70,000 cycles.Conclusions
The RAFN constructs experienced greater subsidence and reduced axial stiffness compared to the LCP constructs. In Low BMD specimens, the RAFN constructs had a higher risk of failure. 相似文献10.