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1. A 5:2 intermittent fasting regimen ameliorates NASH and fibrosis and blunts HCC development via hepatic PPARα and PCK1

2. Intestinal B cells license metabolic T-cell activation in NASH microbiota/antigen-independently and contribute to fibrosis by IgA-FcR signalling

4. Lack of Cyclin E1 in hepatocytes aggravates ethanol-induced liver injury and hepatic steatosis in experimental murine model of acute and chronic alcohol-associated liver disease

6. XCR1.sup.+ type 1 conventional dendritic cells drive liver pathology in non-alcoholic steatohepatitis

7. Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH

8. Beneficial effects of intermittent fasting in NASH and subsequent HCC development are executed by concerted PPAR alpha and PCK1 action in hepatocytes

10. Publisher Correction: XCR1+ type 1 conventional dendritic cells drive liver pathology in non-alcoholic steatohepatitis

11. Author Correction: Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH

13. Nrf2 induces malignant transformation of hepatic progenitor cells by inducing β-catenin expression

15. Hepatocytes

17. Guidelines and Considerations for Metabolic Tolerance Tests in Mice

19. Corrigendum to ‘Molecular characterisation of hepatocellular carcinoma in patients with non-alcoholic steatohepatitis’ [J Hepatol 75 (2021) 865–878]

21. Molecular characterisation of hepatocellular carcinoma in patients with non-alcoholic steatohepatitis

27. Corrigendum to 'Molecular characterisation of hepatocellular carcinoma in patients with non-alcoholic steatohepatitis' [J Hepatol 75 (2021) 865-878]

32. Guidelines and Considerations for Metabolic Tolerance Tests in Mice

39. An Immune Gene Expression Signature Associated With Development of Human Hepatocellular Carcinoma Identifies Mice That Respond to Chemopreventive Agents

41. FRI-089-Genetic deletion of Keap in hepatocytes improves liver damage, but triggers hepatitis in an Nrf2-dependent manner, in experimental toxic liver injury

42. THU-254-Cumulative effects of western diet and alcohol abuse: A novel model of ASH/NASH-derived liver injury

43. Alcohol and Hepatocellular Carcinoma: Adding Fuel to the Flame

44. Genetic Nrf2 Overactivation Inhibits the Deleterious Effects Induced by Hepatocyte-Specific c-met Deletion during the Progression of NASH

45. Auto-aggressive CXCR6+CD8 T cells cause liver immune pathology in NASH

46. Reflectance confocal microscopy for noninvasive examination of nonmelanocytic tumors and virus‐associated skin lesions in organ transplant recipients.

47. XCR1+type 1 conventional dendritic cells drive liver pathology in non-alcoholic steatohepatitis

48. Immunoregulation by lipids during the development of non-alcoholic steatohepatitis

49. Stress-activatedmiR-21/miR-21*in hepatocytes promotes lipid and glucose metabolic disorders associated with high-fat diet consumption

50. Hepatocyte-specific Keap1 deletion reduces liver steatosis but not inflammation during non-alcoholic steatohepatitis development

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