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151.
Yongseok Jang Daniel Owuor Jenora T. Waterman Leon White Boyce Collins Jagannathan Sankar Thomas W. Gilbert Yeoheung Yun 《Materials》2014,7(8):5866-5882
The biodegradable ability of magnesium alloys is an attractive feature for tracheal stents since they can be absorbed by the body through gradual degradation after healing of the airway structure, which can reduce the risk of inflammation caused by long-term implantation and prevent the repetitive surgery for removal of existing stent. In this study, the effects of bicarbonate ion (HCO3−) and mucin in Gamble’s solution on the corrosion behavior of AZ31 magnesium alloy were investigated, using immersion and electrochemical tests to systematically identify the biodegradation kinetics of magnesium alloy under in vitro environment, mimicking the epithelial mucus surfaces in a trachea for development of biodegradable airway stents. Analysis of corrosion products after immersion test was performed using scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDX) and X-ray diffraction (XRD). Electrochemical impedance spectroscopy (EIS) was used to identify the effects of bicarbonate ions and mucin on the corrosion behavior of AZ31 magnesium alloys with the temporal change of corrosion resistance. The results show that the increase of the bicarbonate ions in Gamble’s solution accelerates the dissolution of AZ31 magnesium alloy, while the addition of mucin retards the corrosion. The experimental data in this work is intended to be used as foundational knowledge to predict the corrosion behavior of AZ31 magnesium alloy in the airway environment while providing degradation information for future in vivo studies. 相似文献
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153.
Peter G. Alexander Jamie D. Bulken‐Hoover Jared A. Vogler Youngmi Ji Patricia McKay Leon J. Nesti Rocky S. Tuan 《Journal of tissue engineering and regenerative medicine》2013,7(6):443-451
The success of peripheral nerve regeneration is governed by the rate and quality of axon bridging and myelination that occurs across the damaged region. Neurite growth and the migration of Schwann cells is regulated by neurotrophic factors produced as the nerve regenerates, and these processes can be enhanced by mesenchymal stem cells (MSCs), which also produce neurotrophic factors and other factors that improve functional tissue regeneration. Our laboratory has recently identified a population of mesenchymal progenitor cells (MPCs) that can be harvested from traumatized muscle tissue debrided and collected during orthopaedic reconstructive surgery. The objective of this study was to determine whether the traumatized muscle‐derived MPCs exhibit neurotrophic function equivalent to that of bone marrow‐derived MSCs. Similar gene‐ and protein‐level expression of specific neurotrophic factors was observed for both cell types, and we localized neurogenic intracellular cell markers (brain‐derived neurotrophic factor and nestin) to a subpopulation of both MPCs and MSCs. Furthermore, we demonstrated that the MPC‐secreted factors were sufficient to enhance in vitro axon growth and cell migration in a chick embryonic dorsal root ganglia (DRG) model. Finally, DRGs in co‐culture with the MPCs appeared to increase their neurotrophic function via soluble factor communication. Our findings suggest that the neurotrophic function of traumatized muscle‐derived MPCs is substantially equivalent to that of the well‐characterized population of bone marrow‐derived MPCs, and suggest that the MPCs may be further developed as a cellular therapy to promote peripheral nerve regeneration. Copyright © 2012 John Wiley & Sons, Ltd. 相似文献
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158.
Contreras G Pardo V Cely C Borja E Hurtado A De La Cuesta C Iqbal K Lenz O Asif A Nahar N Leclerq B Leon C Schulman I Ramirez-Seijas F Paredes A Cepero A Khan T Pachon F Tozman E Barreto G Hoffman D Almeida Suarez M Busse JC Esquenazi M Esquenazi A Garcia Mayol L Garcia Estrada H 《Lupus》2005,14(11):890-895
The objective of this study was to identify the factors associated with important clinical outcomes in a case-control study of 213 patients with lupus nephritis. Included were 47% Hispanics, 44% African Americans and 9% Caucasians with a mean age of 28 years. Fifty-four (25%) patients reached the primary composite outcome of doubling serum creatinine, end-stage renal disease or death during a mean follow-up of 37 months. Thirty-four percent African Americans, 20% Hispanics and 10% Caucasians reached the primary composite outcome (P < 0.05). Patients reaching the composite outcome had predominantly proliferative lupus nephritis (WHO classes: 30% III, 32% IV, 18% V and 5% II, P < 0.025) with higher activity index score (7 +/- 6 versus 5 +/- 5, P < 0.05), chronicity index (CI) score (4 +/- 3 versus 2 +/- 2 unit, P < 0.025), higher baseline mean arterial pressure (MAP) (111 +/- 21 versus 102 +/- 14 mmHg, P < 0.025) and serum creatinine (1.9 +/- 1.3 versus 1.3 +/- 1.0 mg/dL, P < 0.025), but lower baseline hematocrit (29 +/- 6 versus 31 + 5%, P < 0.025) and complement C3 (54 +/- 26 versus 65 + 33 mg/dL, P < 0.025) compared to controls. More patients reaching the composite outcome had nephrotic range proteinuria compared to controls (74% versus 56%, P < 0.025). By multivariate analysis, CI (hazard ratio [95% CI] 1.18 [1.07-1.30] per point), MAP (HR 1.02 [1.00-1.03] per mmHg), and baseline serum creatinine (HR 1.26 [1.04-1.54] per mg/dL) were independently associated with the composite outcome. We concluded that hypertension and elevated serum creatinine at the time of the kidney biopsy as well as a high CI are associated with an increased the risk for chronic renal failure or death in patients with lupus nephritis. 相似文献
159.
The association between glutathione S-transferase P1, M1 polymorphisms and asthma in Taiwanese schoolchildren 总被引:2,自引:0,他引:2
STUDY OBJECTIVES: Genetic polymorphisms in the glutathione S-transferase P1 gene (GSTP1) and the glutathione S-transferase M1 gene (GSTM1) have been implicated as risk factors for asthma. However, their roles in asthma pathogenesis and the interaction between these two genes have not been extensively investigated. This study, therefore, examined the relationship among GSTP1 and GSTM1 genotypes and childhood asthma, and evaluated their gene-gene interactions. SETTING: The population from three southern Taiwan communities of a 2001 national survey. SUBJECTS AND METHODS: Two hundred sixty-six fourth-grade to ninth-grade schoolchildren were recruited for oral mucosa samplings based on questionnaire information. Polymerase chain reaction-based assays were performed to determine GSTP1 and GSTM1 genotypes among asthmatic subjects and nonasthmatic control subjects. Multiple logistic regression was used to adjust for potential confounding factors. RESULTS: All of the participants were homozygous at the GSTP1 Ala-114 locus. After controlling for age, sex, and atopic eczema, compared with participants carrying any Val-105 allele, children who were homozygotic for GSTP1 Ile-105 had a significantly increased risk of physician-diagnosed asthma (adjusted odds ratio [adjOR], 1.94; 95% confidence interval [CI], 1.08 to 3.59). A positive risk for childhood asthma was also noted on the GSTM1 null genotype but did not reach statistical significance (adjOR, 1.37; 95% CI, 0.80 to 2.38). Among children with GSTM1 present genotypes, GSTP1-105 polymorphisms were associated with the increased risk of asthma. However, the reduced and statistically insignificant asthma risk was observed among those with GSTM1 null genotype. CONCLUSIONS: We concluded that GSTP1-105 was a predictor for childhood asthma, whereas GSTM1 polymorphism might modify the risk. Our study also suggested a competitive effect for homozygous GSTP1 Ile-105 and GSTM1 null genotypes on childhood asthma. 相似文献
160.
Leticia Leon Marta Redondo Alberto Garcia-Vadillo Miguel A. Perez-Nieto Luis Rodriguez-Rodriguez Juan A. Jover Isidoro Gonzalez-Alvaro Lydia Abasolo 《Rheumatology international》2016,36(11):1549-1555
Individualized treatment of rheumatoid arthritis (RA) based on genetic/serologic factors is increasingly accepted. Moreover, patients are more actively involved in the management of their disease. However, personality has received little attention with respect to perception of the need and adherence to treatment. Our objective was to evaluate whether patient personality was associated with the acceptance or rejection of more aggressive early treatment. We performed a cross-sectional study in two hospitals with early arthritis clinics where sociodemographic, clinical, and therapeutic variables are systematically recorded. Patients completed Eysenck Personality Questionnaire, Multidimensional Health Locus of Control, Pain-Related Self-Statement Scale and Pain-Related Control Scale. Aggressive treatment was considered if patients received more than two DMARDs or biological agents during the first year of follow-up. Multivariate logistic regression analysis was performed to determine predictors of aggressive treatment. One hundred seventy-six RA patients were included (80 % women, disease begin median age 55 years). Treatment was considered aggressive in 57.9 % of the sample. Scores were high in extraversion in 50.8 % of patients, neuroticism in 29.5 % and psychoticism in 14.7 %. Neuroticism was the only factor associated with aggressive treatment, which was less probable (p = 0.04, OR = 0.40). Neuroticism also decreased the possibility of receiving a combination of biologics and DMARDs (p = 0.04, OR = 0.28). Patients with high scores on neuroticism are more worried, obsessive and hypochondriac, leading them to reject more aggressive therapy. It is important to educate about their disease so that they will accept more aggressive approaches in clear cases of poor outcome. 相似文献