98%
921
2 minutes
20
In the original publication [...].
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11048796 | PMC |
http://dx.doi.org/10.3390/cells13080714 | DOI Listing |
J Korean Med Sci
July 2025
Division of Endocrinology and Metabolism, Department of Internal Medicine, Jeonbuk National University Medical School, Jeonju, Korea.
Background: Cardiovascular autonomic neuropathy (CAN) is a frequently underdiagnosed complication of diabetes mellitus that contributes to increased mortality and morbidity rates. This multicenter study investigated the epidemiology and clinical characteristics of CAN in patients with long-term diabetes.
Methods: Retrospective data were collected from 884 individuals with diabetes who were assessed for CAN across eight hospitals in Korea.
J Clin Neurol
July 2025
Department of Neurology, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Busan, Korea.
This corrects the article on p. 190 in vol. 21, PMID: 40308014.
View Article and Find Full Text PDFCommun Med (Lond)
July 2025
Samsung Advanced Institute for Health Sciences and Technology (SAIHST), Sungkyunkwan University, Samsung Medical Center, Seoul, South Korea.
Background: Cancer is a polygenic disease that involves the dysregulation of multiple biological events, including aberrant cell proliferation and evasion of immune responses, which collectively contribute to cancer development and progression. Although the polygenic risk score (PRS) has enabled assessment of the effects of cancer risk loci, the potential impact of other genetic variants with functional relevance to cancer biology remains largely unexplored.
Methods: We conducted a large-scale analysis of UK Biobank data, including 61,249 cancer cases and 254,203 controls of European ancestry across 16 cancer types.
J Clin Invest
July 2025
Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Neurofibromatosis type 1 (NF1) is a genetic disorder caused by mutations of the NF1 tumor suppressor gene resulting in the loss of function of neurofibromin, a GTPase-activating protein (GAP) for Ras. While the malignant manifestations of NF1 are associated with loss of heterozygosity of the residual WT allele, the nonmalignant neurodevelopmental sequelae, including autism spectrum disorder (ASD) and/or attention deficit hyperactivity disorder (ADHD) are prevalent morbidities that occur in the setting of neurofibromin haploinsufficiency. We reasoned that augmenting endogenous levels of WT neurofibromin could serve as a potential therapeutic strategy to correct the neurodevelopmental manifestations of NF1.
View Article and Find Full Text PDF