Intervertebral disc degeneration (IVDD) is a primary contributor to low back pain, posing significant social and economic burdens. Increasing evidence shows that obesity contributes to IVDD, yet the underlying mechanisms remain elusive. Here, we firstly revealed a causal correlation between obesity and IVDD via a two-sample mendelian randomization analysis and identified fatty acid-binding protein 4 (FABP4) as the potential regulator to associate IVDD and obesity.
View Article and Find Full Text PDFBackground And Aims: Metastatic cancers arise from a decades-long succession of increasingly virulent precursor lesions, each of which represents prospective targets for therapeutic intervention. This evolutionary process has been particularly vivid in esophageal adenocarcinoma (EAC), as this cancer and associated precursor lesions, including Barrett's esophagus (BE), low-grade dysplasia (LGD), and high-grade dysplasia (HGD), co-exist in an accessible, two-dimensional pattern in esophageal mucosa. Given the durability of these precursor lesions, it is likely that they, like EAC, rely on stem cells for their regenerative growth.
View Article and Find Full Text PDFMol Phylogenet Evol
March 2025
Species delimitation in plants is sometimes challenging due to morphological convergence, interspecific gene flow, and historically limited sampling. Bredia Blume as currently defined comprises 27 species and has been resolved as monophyletic in previous phylogenomic studies. However, relationships among several major lineages in the genus remain elusive, and the species boundaries of some problematic taxa have not been tested.
View Article and Find Full Text PDFAims: Circulating biochemistry markers are commonly used to monitor and detect disease-induced dysfunctions including osteoarthritis (OA). However, the causal nature of this relationship is nevertheless largely unknown, due to unmeasured confounding factors from observational studies. We aimed to reveal the causal relationship between 28 circulating biochemistry markers and OA pathogenesis.
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