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101.
Background
Prevention, early identification, and effective management of periprosthetic joint infection (PJI) in patients with inflammatory joint disease (IJD) present unique challenges for physicians. Discontinuing disease-modifying anti-rheumatoid drugs (DMARDs) perioperatively may reduce immunosuppression and infection risk at the expense of increasing disease flares. Interpreting traditional diagnostic markers of PJI can be difficult due to disease-related inflammation.Purposes
This review is designed to answer how to (1) manage immunosuppressive/DMARD therapy perioperatively, (2) diagnose PJI in patients with IJD, and (3) treat PJI in this population.Methods
The PubMed database was searched for relevant articles with subsequent review by independent authors.Results
While there is evidence to support the use of methotrexate perioperatively in RA patients, it remains unclear whether using anti-tumor necrosis factor medications perioperatively increases the risk of surgical site infections. Serum erythrocyte sedimentation rate and C-reactive protein can be useful for diagnosis of PJI in this population, but only as part of comprehensive workup that ultimately relies upon sampling of joint fluid. Management of PJI depends on several clinical factors including duration of infection and the likelihood of biofilm presence, the infecting organism, sensitivity to antibiotic therapy, and host immune status. The evidence suggests that two-stage revision or resection arthroplasty is more likely to eradicate infection, particularly when MRSA is the pathogen.Conclusion
Immunosuppression and baseline inflammatory changes in the IJD population can complicate the prevention, diagnosis, and treatment of PJI. Understanding the increase in risk associated with IJD and its treatment is essential for proper management when patients undergo lower extremity arthroplasty.Electronic supplementary material
The online version of this article (doi:10.1007/s11420-013-9338-8) contains supplementary material, which is available to authorized users. 相似文献102.
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Kamrul Hasan Shivakumar Shankar Aadhar Sharma Alison Carter Razi Zaidi Suzie Cro John Skinner Andy Goldberg 《Journal of orthopaedics and traumatology》2016,17(4):291-295
Background
The burden of traumatic and elective hip surgery is set to grow. With an increasing number of techniques and implants against the background of an aging population, the emphasis on evidence-based treatment has never been greater. The purpose of this study was to assess changes in the levels of evidence in the hip literature over a decade.Materials and methods
Articles pertaining to hip surgery from the years 2000 and 2010 in Hip International, Journal of Arthroplasty, Journal of Bone and Joint Surgery and The Bone and Joint Journal were analysed. Articles were ranked by a five-point level of evidence scale and by type of study, according to guidelines from the Centre for Evidence-based Medicine.Results
531 articles were analysed from 48 countries. The kappa value for the inter-observer reliability showed excellent agreement between the reviewers for study type (κ = 0.956, P < 0.01) and for levels of evidence (κ = 0.772, P < 0.01). Between 2000 and 2010, the overall percentage of high-level evidence (levels I and II) studies more than doubled (12 to 31 %, P < 0.001). The most frequent study type was therapeutic; the USA and UK were the largest producers of published work in these journals, with contributions from other countries increasing markedly over the decade.Conclusions
There has been a significant increase in high levels of evidence in hip surgery over a decade (P < 0.001). We recommend that all orthopaedic journals consider implementing compulsory declaration by authors of the level of evidence to help enhance quality of evidence.Level of evidence
Level 2: economic and decision analysis.106.
107.
Long‐term functional results after open partial horizontal laryngectomy type IIa and type IIIa: A comparison study 下载免费PDF全文
108.
Schaber JA Triffo WJ Suh SJ Oliver JW Hastert MC Griswold JA Auer M Hamood AN Rumbaugh KP 《Infection and immunity》2007,75(8):3715-3721
Biofilms are bacterial communities residing within a polysaccharide matrix that are associated with persistence and antibiotic resistance in chronic infections. We show that the opportunistic pathogen Pseudomonas aeruginosa forms biofilms within 8 h of infection in thermally injured mice, demonstrating that biofilms contribute to bacterial colonization in acute infections as well. Using light, electron, and confocal scanning laser microscopy, P. aeruginosa biofilms were visualized within burned tissue surrounding blood vessels and adipose cells. Although quorum sensing (QS), a bacterial signaling mechanism, coordinates differentiation of biofilms in vitro, wild-type and QS-deficient P. aeruginosa strains formed similar biofilms in vivo. Our findings demonstrate that P. aeruginosa forms biofilms on specific host tissues independently of QS. 相似文献
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Liu Y Purvis J Shih A Weinstein J Agrawal N Radhakrishnan R 《Annals of biomedical engineering》2007,35(6):1012-1025
We describe a hierarchical multiscale computational approach based on molecular dynamics simulations, free energy-based molecular
docking simulations, deterministic network-based kinetic modeling, and hybrid discrete/continuum stochastic dynamics protocols
to study the dimer-mediated receptor activation characteristics of the Erb family receptors, specifically the epidermal growth
factor receptor (EGFR). Through these modeling approaches, we are able to extend the prior modeling of EGF-mediated signal
transduction by considering specific EGFR tyrosine kinase (EGFRTK) docking interactions mediated by differential binding and
phosphorylation of different C-terminal peptide tyrosines on the RTK tail. By modeling signal flows through branching pathways
of the EGFRTK resolved on a molecular basis, we are able to transcribe the effects of molecular alterations in the receptor
(e.g., mutant forms of the receptor) to differing kinetic behavior and downstream signaling response. Our molecular dynamics
simulations show that the drug sensitizing mutation (L834R) of EGFR stabilizes the active conformation to make the system
constitutively active. Docking simulations show preferential characteristics (for wildtype vs. mutant receptors) in inhibitor
binding as well as preferential enhancement of phosphorylation of particular substrate tyrosines over others. We find that
in comparison to the wildtype system, the L834R mutant RTK preferentially binds the inhibitor erlotinib, as well as preferentially
phosphorylates the substrate tyrosine Y1068 but not Y1173. We predict that these molecular level changes result in preferential
activation of the Akt signaling pathway in comparison to the Erk signaling pathway for cells with normal EGFR expression.
For cells with EGFR over expression, the mutant over activates both Erk and Akt pathways, in comparison to wildtype. These
results are consistent with qualitative experimental measurements reported in the literature. We discuss these consequences
in light of how the network topology and signaling characteristics of altered (mutant) cell lines are shaped differently in
relationship to native cell lines.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
These authors contributed equally 相似文献