22 results on '"Nepali, Prerna"'
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2. Chemotherapeutic Agents-Induced Ceramide-Rich Platforms (CRPs) in Endothelial Cells and Their Modulation
3. Reduced activin receptor-like kinase 1 activity promotes cardiac fibrosis in heart failure
4. Endothelial mechanisms for inactivation of inflammation-induced hyperpermeability
5. Abstract 15364: Radiation Exposure of the Base of the Heart Accelerates Coronary Atherosclerosis
6. Review of: "[Review] Investigating the Role of Urokinase in Cancer Metastasis: A Review"
7. Anoikis in phenotypic reprogramming of the prostate tumor microenvironment
8. Conditional knockout of activin like kinase-1 (ALK-1) leads to heart failure without maladaptive remodeling
9. Abstract 6056: Activation of Sting in response to partial-tumor radiation exposure
10. eNOS Location is a Fundamental Mechanism for Inactivation of Inflammation‐induced Hyperpermeability
11. Abstract 38: Radiation Exposure And Coronary Atherosclerosis: Differential Effect Of The Radiation Site
12. Abstract 1663: Activation of STING in response to partial-tumor radiation exposure
13. Abstract 3069: Radiation exposure of the base of the heart accelerates coronary atherosclerosis
14. Radiation exposure of the base of the heart accelerates coronary atherosclerosis
15. Endothelial Barrier Restoration after Inflammation‐Induced Hyperpermeability
16. Endothelial cAMP deactivates ischemia-reperfusion-induced microvascular hyperpermeability via Rap1-mediated mechanisms
17. Abstract 64: Conditional Knockout of Activin Like Kinase-1 (ALK-1) Leads to Heart Failure Without Maladaptive Remodeling
18. ASMase is Essential for the Immune Response to Partial-Tumor Radiation Exposure.
19. Kinesin Facilitates Phenotypic Targeting of Therapeutic Resistance in Advanced Prostate Cancer.
20. Endothelial mechanisms for inactivation of inflammation-induced hyperpermeability.
21. Chemotherapeutic Agents-Induced Ceramide-Rich Platforms (CRPs) in Endothelial Cells and Their Modulation.
22. Endothelial cAMP deactivates ischemia-reperfusion-induced microvascular hyperpermeability via Rap1-mediated mechanisms.
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