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http://dx.doi.org/10.1089/cmb.2018.0170 | DOI Listing |
Diabetes Res Clin Pract
January 2025
Department of Medicine, Division of Endocrinology, Diabetes and Clinical Nutrition, Oregon Health & Science University, Portland USA.
Background: Diabetic neuropathy (DN) affects up to half of individuals with type 1 and type 2 diabetes. Despite evidence that improving metabolic and cardiovascular health can slow its progression, DN remains a significant clinical challenge due to the lack of disease-modifying therapies and effective pain management strategies. This consensus aimed to identify gaps and recommend strategies to address these challenges.
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
Zoophysiology, Department of Biology, Aarhus University, Aarhus C, Denmark.
Aim: Snakes exhibit remarkable physiological shifts when their large meals induce robust postprandial growth after prolonged fasting. To understand the regulatory mechanisms underlying this rapid metabolic transition, we examined the regulation of protein synthesis in pythons, focusing on processes driving early postprandial tissue remodeling and growth.
Methods: Using the SUnSET method with puromycin labeling, we measured in vivo protein synthesis in fasting and digesting snakes at multiple post-feeding intervals.
J Anat
January 2025
Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital - Bispebjerg-Frederiksberg, Copenhagen, Denmark.
Tendon injuries and disorders associated with mechanical tendon overuse are common musculoskeletal problems. Even though tendons play a central role in human movement, the intrinsic healing process of tendon is very slow. So far, it is known that tendon cell activity is supported by several interstitial cells within the tendon.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Center for Cooperative Research in Biosciences (CIC BioGUNE), Basque Research and Technology Alliance (BRTA), Derio, Spain.
Prion diseases, particularly sporadic cases, pose a challenge due to their complex nature and heterogeneity. The underlying mechanism of the spontaneous conversion from PrPC to PrPSc, the hallmark of prion diseases, remains elusive. To shed light on this process and the involvement of cofactors, we have developed an in vitro system that faithfully mimics spontaneous prion misfolding using minimal components.
View Article and Find Full Text PDFDiscov Immunol
December 2024
Laboratory of Functional Genomics and Medicine, Division of Biological Science, Nara Institute of Science and Technology (NAIST), Ikoma-shi, Nara, Japan.
Introduction: Programmed death-1 (PD-1) is a negative regulator of immune responses. Upon deletion of PD-1 in mice, symptoms of autoimmunity developed only after they got old. In a model experiment in cancer immunotherapy, PD-1 was shown to prevent cytotoxic T lymphocytes from attacking cancer cells that expressed neoantigens derived from genome mutations.
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