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Margaret L Novak Eileen M Weinheimer‐Haus Timothy J Koh 《The Journal of pathology》2014,232(3):344-355
Following injury to different tissues, macrophages can contribute to both regenerative and fibrotic healing. These seemingly contradictory roles of macrophages may be related to the markedly different phenotypes that macrophages can assume upon exposure to different stimuli. We hypothesized that fibrotic healing after traumatic muscle injury would be dominated by a pro‐fibrotic M2a macrophage phenotype, with M1 activation limited to the very early stages of repair. We found that macrophages accumulated in lacerated mouse muscle for at least 21 days, accompanied by limited myofibre regeneration and persistent collagen deposition. However, muscle macrophages did not exhibit either of the canonical M1 or M2a phenotypes, but instead up‐regulated both M1‐ and M2a‐associated genes early after injury, followed by down‐regulation of most markers examined. Particularly, IL‐10 mRNA and protein were markedly elevated in macrophages from 3‐day injured muscle. Additionally, though flow cytometry identified distinct subpopulations of macrophages based on high or low expression of TNFα, these subpopulations did not clearly correspond to M1 or M2a phenotypes. Importantly, cell therapy with exogenous M1 macrophages but not non‐activated macrophages reduced fibrosis and enhanced muscle fibre regeneration in lacerated muscles. These data indicate that manipulation of macrophage function has potential to improve healing following traumatic injury. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. 相似文献
84.
Use of a Learning Network to Improve Variation in Interstage Weight Gain after the Norwood Operation
Jeffrey B. Anderson MD Robert H. Beekman III MD John D. Kugler MD Geoffrey L. Rosenthal MD PhD Kathy J. Jenkins MD Thomas S. Klitzner MD PhD Gerard R. Martin MD Steven R. Neish MD Lynn Darbie MS Eileen King PhD Carole Lannon MD National Pediatric Cardiology Quality Improvement Collaborative 《Congenital heart disease》2014,9(6):512-520
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Watson L Leone V Pilkington C Tullus K Rangaraj S McDonagh JE Gardner-Medwin J Wilkinson N Riley P Tizard J Armon K Sinha MD Ioannou Y Archer N Bailey K Davidson J Baildam EM Cleary G McCann LJ Beresford MW;UK Juvenile-Onset Systemic Lupus Erythematosus Study Group 《Arthritis and rheumatism》2012,64(7):2356-2365
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Baba M Keller JR Sun HW Resch W Kuchen S Suh HC Hasumi H Hasumi Y Kieffer-Kwon KR Gonzalez CG Hughes RM Klein ME Oh HF Bible P Southon E Tessarollo L Schmidt LS Linehan WM Casellas R 《Blood》2012,120(6):1254-1261
Birt-Hogg-Dubé (BHD) syndrome is an autosomal dominant disorder characterized by cutaneous fibrofolliculomas, pulmonary cysts, and kidney malignancies. Affected individuals carry germ line mutations in folliculin (FLCN), a tumor suppressor gene that becomes biallelically inactivated in kidney tumors by second-hit mutations. Similar to other factors implicated in kidney cancer, FLCN has been shown to modulate activation of mammalian target of rapamycin (mTOR). However, its precise in vivo function is largely unknown because germ line deletion of Flcn results in early embryonic lethality in animal models. Here, we describe mice deficient in the newly characterized folliculin-interacting protein 1 (Fnip1). In contrast to Flcn, Fnip1(-/-) mice develop normally, are not susceptible to kidney neoplasia, but display a striking pro-B cell block that is entirely independent of mTOR activity. We show that this developmental arrest results from rapid caspase-induced pre-B cell death, and that a Bcl2 transgene reconstitutes mature B-cell populations, respectively. We also demonstrate that conditional deletion of Flcn recapitulates the pro-B cell arrest of Fnip1(-/-) mice. Our studies thus demonstrate that the FLCN-FNIP complex deregulated in BHD syndrome is absolutely required for B-cell differentiation, and that it functions through both mTOR-dependent and independent pathways. 相似文献
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Quynh T. Vo Christopher Cox Xiuhong Li Lisa P. Jacobson Rosemary McKaig Ned Sacktor Ola A. Selnes Eileen Martin James T. Becker Eric N. Miller 《Journal of neurovirology》2013,19(1):24-31
The objective of this study is to compare neuropsychological test performance before and after HIV-1 seroconversion in order to identify possible acute changes in psychomotor speed, memory, attention, and concentration secondary to seroconversion. The study utilized mixed effects models to examine longitudinal neuropsychological test data. We conducted a nested cohort study of 362 male HIV-1 seroconverters enrolled in the Multicenter AIDS Cohort Study. We used linear mixed models with random subject effects to compare repeated neuropsychological test outcomes from 5 years before seroconversion to 2 years after seroconversion on the Trail Making Test (parts A and B), Symbol-Digit Test, Grooved Pegboard (dominant and non-dominant hands), Stroop Color-Interference Test, Rey Auditory Verbal Learning Test, and the CalCAP Reaction Time Test. We found no significant changes in the time-dependent score after seroconversion for the majority of neuropsychological tests used in the Multicenter AIDS Cohort Study. There was a significant change in time trend after seroconversion on part B of the Trail Making Test (p?=?0.042), but the difference only represented a 2 % decrease in performance. We found the following characteristics to be associated with worse neuropsychological test performance: lower education levels, history of depression, older age, and no previous neurocognitive testing (p?<?.05). Our results suggest that despite a 50 % decrease in CD4 cell count immediately following infection, HIV-1 does not appear to have a measurable effect on psychomotor or complex cognitive processing for up to 2 years following infection, using this set of neurocognitive measures. 相似文献
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Diane Mullins Eileen Daly Andrew Simmons Felix Beacher Catherine ML Foy Simon Lovestone Brian Hallahan Kieran C Murphy Declan G Murphy 《Journal of Neurodevelopmental Disorders》2013,5(1):19