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1. Skeletal muscle hypertrophy rewires glucose metabolism: An experimental investigation and systematic review

3. Age But Not Menopausal Status Is Linked to Lower Resting Energy Expenditure

5. NAD+ repletion with niacin counteracts cancer cachexia

10. Age but not menopausal status is linked to lower resting energy expenditure

11. Skeletal muscle hypertrophy rewires glucose metabolism: an experimental investigation and systematic review

12. NAD+ repletion with niacin counteracts cancer cachexia

19. List of Contributors

20. Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

23. Blocking Activin Receptor Ligands Is Not Sufficient to Rescue Cancer-Associated Gut Microbiota—A Role for Gut Microbial Flagellin in Colorectal Cancer and Cachexia?

24. Molecular Pathways Mediating Immunosuppression in Response to Prolonged Intensive Physical Training, Low-Energy Availability, and Intensive Weight Loss

27. Systemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury

32. Morphological, molecular and hormonal adaptations to early morning versus afternoon resistance training

37. Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

38. Effects of resistance training on expression of IGF-I splice variants in younger and older men

39. Heterogeneity in resistance training-induced muscle strength and mass responses in men and women of different ages

40. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

42. PGC-1 isoforms and their target genes are expressed differently in human skeletal muscle following resistance and endurance exercise

43. Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling

47. Myostatin/activin blocking combined with exercise reconditions skeletal muscle expression profile of mdx mice

50. VEGF ‐B‐induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart

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