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We conducted a meta-analysis of carbon and oxygen isotopes from tree ring chronologies representing 34 species across 10 biomes to better understand the environmental drivers and physiological mechanisms leading to historical changes in tree intrinsic water use efficiency (iWUE), or the ratio of net photosynthesis () to stomatal conductance (), over the last century. We show a ∼40% increase in tree iWUE globally since 1901, coinciding with a ∼34% increase in atmospheric CO (C), although mean iWUE, and the rates of increase, varied across biomes and leaf and wood functional types. While C was a dominant environmental driver of iWUE, the effects of increasing C were modulated either positively or negatively by climate, including vapor pressure deficit (VPD), temperature, and precipitation, and by leaf and wood functional types. A dual carbon-oxygen isotope approach revealed that increases in dominated the observed increased iWUE in ∼83% of examined cases, supporting recent reports of global increases in , whereas reductions in occurred in the remaining ∼17%. This meta-analysis provides a strong process-based framework for predicting changes in tree carbon gain and water loss across biomes and across wood and leaf functional types, and the interactions between C and other environmental factors have important implications for the coupled carbon-hydrologic cycles under future climate. Our results furthermore challenge the idea of widespread reductions in as the major driver of increasing tree iWUE and will better inform Earth system models regarding the role of trees in the global carbon and water cycles.
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http://dx.doi.org/10.1073/pnas.2014286118 | DOI Listing |
Clin Orthop Relat Res
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Leni & Peter W. May Department of Orthopaedic Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
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Section of Brain Function Information, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan.
This study aimed to identify brain activity modulations associated with different types of visual tracking using advanced functional magnetic resonance imaging techniques developed by the Human Connectome Project (HCP) consortium. Magnetic resonance imaging data were collected from 27 healthy volunteers using a 3-T scanner. During a single run, participants either fixated on a stationary visual target (fixation block) or tracked a smoothly moving or jumping target (smooth or saccadic tracking blocks), alternating across blocks.
View Article and Find Full Text PDFMol Biol Rep
September 2025
School of Pharmacy, Heilongjiang University of Chinese Medicine, NO 24 Heping Road, 150040, Harbin, P. R. China.
Lysosome-dependent cell death (LDCD) is a regulated form of cell death initiated by increased lysosomal membrane permeability, leading to the cytoplasmic release of lysosomal enzymes and subsequent cellular damage. Molecular mechanisms controlling LDCD include lysosomal membrane instability and lysosomal enzyme release, which together lead to cell damage. A more profound comprehension of these underlying mechanisms may reveal new therapeutic targets for diseases associated with lysosomal dysfunction.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA, 91766-1854, USA.
Regenerative cardiology has emerged as a novel strategy to improve cardiac healing following ischemic injury. While stem-cell-mediated cardiac regeneration has garnered much attention as a promising strategy, its value remains debated owing to the lack of ideal stem cell source candidates. Resident/endogenous cardiac-derived stromal cells (CSCs) exhibit superior therapeutic potential due to their innate abilities to differentiate into cardiac cells, especially cardiomyocytes (CM).
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Department of Plastic Surgery, the First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, China.
Keloid scarring and Metabolic Syndrome (MS) are distinct conditions marked by chronic inflammation and tissue dysregulation, suggesting shared pathogenic mechanisms. Identifying common regulatory genes could unveil novel therapeutic targets. Methods.
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