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您的检索式：作者名="Milena Colombo"
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| 1 | Specifc inflammatory osteoclast precursors induced during chronic inflammation give rise to highly active osteoclasts associated with inflammatory bone loss显示文摘Elevated osteoclast(OC)activity is a major contributor to inflammatory bone loss(IBL)during chronic inflammatory diseases.However,the specific OC precursors(OCPs)responding to inflammatory cues and the underlying mechanisms leading to IBL are poorly understood.We identified two distinct OCP subsets:Ly6C^(hi)CD11b^(hi) inflammatory OCPs(iOCPs)induced during chronic inflammation,and homeostatic Ly6C^(hi)CD11b^(lo)OCPs(hOCPs)which remained unchanged.Functional and proteomic characterization revealed that while iOCPs were rare and displayed low osteoclastogenic potential under normal conditions,they expanded during chronic inflammation and generated OCs with enhanced activity.In contrast,hOCPs were abundant and manifested high osteoclastogenic potential under normal conditions but generated OCs with low activity and were unresponsive to the inflammatory environment.Osteoclasts derived from iOCPs expressed higher levels of resorptive and metabolic proteins than those generated from hOCPs,highlighting that different osteoclast populations are formed by distinct precursors.We further identified the TNF-αand S100A8/A9 proteins as key regulators that control the iOCP response during chronic inflammation.Furthermore,we demonstrated that the response of iOCPs but not that of hOCPs was abrogated in tnf-α^(-/-)mice,in correlation with attenuated IBL.Our findings suggest a central role for iOCPs in IBL induction.iOCPs can serve as potential biomarkers for IBL detection and possibly as new therapeutic targets to combat IBL in a wide range of inflammatory conditions. | Yaron Meirow Milena Jovanovic Yuval Zur Juliana Habib Daniele Filippo Colombo Nira Twaik Hadas Ashkenazi-Preiser Kerem Ben-Meir Ivan Mikula Jr. Or Reuven Guy Kariv Leonor Daniel Saja Baraghithy Yehuda Klein Jeroen Krijgsveld Noam Levaot Michal Baniyash | 2022 | Bone Research2022，10，3： | 2 |
| 2 | Distribution of catabolic pathways in some hydrocarbon degrading bacteria from a subsurface polluted soil显示文摘 | Lucia Cavaica Patrizia Di Gennaro Milena Colombo | 2000 | Res Microbiol2000，151，： | 1 |
| 3 | Endoscopic ultrasound-guided ablation of solid pancreatic lesions:A systematic review of early outcomes with pooled analysis显示文摘BACKGROUND Endoscopic ultrasound-guided radiofrequency ablation(EUS-RFA)is emerging as a complementary therapeutic approach for pancreatic solid masses.However,results of published data are difficult to interpret because of a retrospective design and small sample size.AIM To systematically review data on EUS-RFA for solid lesions and to pool the results of the different experiences in order to provide more consistent evidence in terms of safety and efficacy.METHODS A comprehensive systematic literature search on the main databases was performed to identify articles in which patients with pancreatic solid lesions underwent EUS-RFA.The primary outcomes were procedure-related adverse events(AEs)and mortality.Secondary outcomes were the technical success rate and the effects on primary tumor growth.Statistical analyses were performed using Stata version 14.0.RESULTS In total,14 studies were included,with 120 patients undergoing 153 ablations of 129 solid pancreatic lesions.The STARmed technology was used in seven studies,the Habib system in six studies,and the HybridTherm probe in one study.The pooled technical success rate was 99.0%(I2:25.82%).The pooled overall AE rate was 8.0%(I2:11.46%).Excluding mild AEs,the pooled rates of serious AEs was 1.0%(I2:0%).No mortality related to the procedure was reported.CONCLUSION The present pooled analysis confirms the safety and feasibility of EUS-RFA. | Marco Spadaccini Milena Di Leo Andrea Iannone Daan von den Hoff Alessandro Fugazza Piera Alessia Galtieri Gaia Pellegatta Roberta Maselli Andrea Anderloni Matteo Colombo Peter D Siersema Silvia Carrara Alessandro Repici | 2022 | World Journal of Gastrointestinal Oncology2022，14，2： | 0 |
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