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| 1 | Sevelamer Versus Calcium Carbonate in Incident Hemodialysis Patients : Results of an Open-Label 24-Month Randomized Clinical Trial 显示文摘 | Di Iorio B Molony D Bell C | 2013 | Am J Kidney Dis2013，62，4： | 1 |
| 2 | Sevelamer?versus calcium carbonate in incident hemodialysis patients: results of an open-label 24-month randomized clinical trial显示文摘 | Di Iofio B Molony D Bell C | 2013 | Am J Kidney Dis2013，62，4： | 1 |
| 3 | Sevelamer versus calcium carbonate in incident hemodialysis patients:results of an open-label 24-month randomized clinical trial显示文摘 | Di Iorio B Molony D Bell C | | 0，，04： | 1 |
| 4 | Molecular properties of Somatostatin revep-ors 显示文摘 | Resine Bell DI | 1995 | Neurosvience1995，67，： | 1 |
| 5 | Sevelamer Versus Calcium Carbonate in Incident Hemodialysis Patients: Results of an Open-Label, 24-Month Randomized Clinical Trial显示文摘 | Biagio Di Iorio Donald Molony Cynthia Bell Emanuele Cucciniello Vincenzo Bellizzi Domenico Russo Antonio Bellasi | 2013 | American Journal of Kidney Diseases2013，，： | 1 |
| 6 | Sevelamer Versus Calcium Carbonate in Incident Hemodialysis Patients:Results of an Open-Label 24-Month Randomized Clinical Trial显示文摘 | Di Iorio B Molony D Bell C | 2013 | Am J Kidney Dis2013，，： | 1 |
| 7 | Develop- ment of conductivity in low onversion temperature silver pastes via addition of nanoparticles显示文摘 | Bell Nelson B Di Antonio Dimos Duane B | 2002 | Journal of Materials Research2002，17，9： | 1 |
| 8 | Sevelamer versus calciumcarbonate in incident hemodialysis patients: results of an open-label 24-month randomized clinical trial显示文摘 | Di Iorio B Moiony D Bell C | 2013 | Am J Kidney Dis2013，62，4： | 1 |
| 9 | Sevelamer versus calcium carbonate in incident hemodialysis patients:results of an open-label24-month randomized clinical trial显示文摘 | Di Iorio B Molony D Bell C | 2013 | Am J Kidney Dis2013，62，4： | 1 |
| 10 | Restoration of Motor Function through Delayed Intraspinal Delivery of Human IL-10-Encoding Nucleoside-Modified mRNA after Spinal Cord Injury显示文摘Efficient in vivo delivery of anti-inflammatory proteins to modulate the microenvironment of an injured spinal cord and promote neuroprotection and functional recovery is a great challenge.Nucleoside-modified messenger RNA(mRNA)has become a promising new modality that can be utilized for the safe and efficient delivery of therapeutic proteins.Here,we used lipid nanoparticle(LNP)-encapsulated human interleukin-10(hIL-10)-encoding nucleoside-modified mRNA to induce neuroprotection and functional recovery following rat spinal cord contusion injury.Intralesional administration of hIL-10 mRNA-LNP to rats led to a remarkable reduction of the microglia/macrophage reaction in the injured spinal segment and induced significant functional recovery compared to controls.Furthermore,hIL-10 mRNA treatment induced increased expression in tissue inhibitor of matrix metalloproteinase 1 and ciliary neurotrophic factor levels in the affected spinal segment indicating a time-delayed secondary effect of IL-105 d after injection.Our results suggest that treatment with nucleoside-modified mRNAs encoding neuroprotective factors is an effective strategy for spinal cord injury repair. | LászlóGál Tamás Bellák Annamária Marton Zoltán Fekécs Drew Weissman Dénes Török Rachana Biju Csaba Vizler Rebeka Kristóf Mitchell B.Beattie Paulo J.C.Lin Norbert Pardi Antal Nógrádi Krisztián Pajer | 2023 | Research2023，，4： | 0 |
| 11 | The mutual interaction between the host spinal cord and grafted undifferentiated stem cells fosters the production of a lesion-induced secretome显示文摘Pathophysiology of spinal cord injury:Injury to the spinal cord results in loss of gray and white matter i.e.,it produces a segmental spinal cord lesion and,as a consequence leads to a fatal loss of motor,sensory and autonomic functions.Spinal cord injuries in humans and other mammals are not followed by the replacement of lost neurons and oligodendrocytes and regrowth of injured axons,instead they lead to permanent,fatal and incurable functional deficits.The primary physical injury is followed by a cascade of tissue-decaying events,called secondary injury,which leads to ischemia,vascular disruption,neuroinflammation,excitotoxicity,demyelination and death of neurons and glial cells(Silva et al.,2014;Figure 1A).The direct mechanical disruption of the vasculature results in the increased permeability of the blood-spinal cord barrier.Due to the leakiness of blood-spinal cord barrier and production of cytokines by activated microglia,a number of various immune cells(T lymphocytes,neutrophils and monocytes)invade the injury site.The macrophages generate a set of inflammatory cytokines such as tumor necrosis factor-α,interleukin(IL)-1α,IL-1β,and IL-6,which may further augment the secondary events(Ahuja et al.,2017).In addition,a number of other disruptive processes contribute to the heterogeneous and time-sensitive pathophysiology of spinal cord injury. | Krisztián Pajer Tamás Bellák Antal Nógrádi | 2020 | Neural Regeneration Research2020，15，10： | 0 |
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