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Environmental drivers of spatial variation in tropical forest canopy height: Insights from NASA’s GEDI spaceborne LiDAR

Forest canopy height is a fundamental ecosystem property—influencing patterns of forest carbon storage and forest ecosystem responses to climate variability and change. Previous studies have analyzed environmental drivers influencing spatial variation in canopy height at landscape-to-regional scales; however, far less is known about the environmental determinants underlying regional and global scale variation in forest canopy height. Using the canopy height metrics products from Global Ecosystem Dynamics Investigation (GEDI), a space-borne Light Detection and Ranging (LiDAR) instrument specifically designed to characterize forest structure, we analyze the environmental correlates of spatial variation of global tropical forest canopy height. Our study demonstrates that climate, topography, and soil properties account for 75% of the variation in tropical forest canopy height. Elevation, dry season length, and solar radiation are the most important drivers in determining canopy height both locally and regionally. These results emphasize the vulnerability of tropical forest structure to ongoing changes in the earth’s climate and provide a valuable empirical baseline for tropical forest management.

Navigating artificial general intelligence development: societal, technological, ethical, and brain-inspired pathways

Cluster dynamical mean-field study of intra-unit-cell charge nematicity in hole-doped cuprates

Recent scanning-tunneling microscopy on hole-doped Bi 2 Sr 2 CaCu 2 O 8 , one of the materials of the cuprate family, finds a long-range ordered spontaneous splitting of the energy levels of oxygen orbitals inside the CuO 2 unit cells [S. Wang et al ., Nat. Mat. 23, 492–498 (2024)]. This spontaneous intra-unit-cell orbital ordering, also known as electronic nematicity, breaks C 4 symmetry and is thought to arise from the Coulomb interaction (denoted by V pp ) between oxygen p x and p y electrons. In this work, we study the spontaneous emergence of electronic nematicity within the three-band Hubbard [aka the Emery-VSA (Varma-Schmitt-Rink-Abrahams) model], using cluster dynamical mean-field theory. This method incorporates short-range electronic correlations and gives us access to the density of states, a quantity that is directly probed in experiments. We argue that there is a delicate competition between V pp and V pd (the latter being the Coulomb interaction between copper d x 2 − y 2 and oxygen p x , y electrons) that must be taken into account in order to find a Zhang-Rice singlet band well-resolved from the upper Hubbard band, and a splitting of the charge-transfer band (one of the signatures of charge nematicity) by roughly 50 meV, as observed recently.

Efficient remote sensing image classification using the novel STConvNeXt convolutional network

Stereospecific control of microbial growth by a combinatoric suite of chiral siderophores

Bacteria compete for iron by producing small-molecule chelators known as siderophores. The triscatechol siderophores trivanchrobactin and ruckerbactin, produced by Vibrio campbellii DS40M4 and Yersinia ruckeri YRB, respectively, are naturally occurring diastereomers that form chiral ferric complexes in opposing enantiomeric configurations. Chiral recognition is a hallmark of specificity in biological systems, yet the biological consequences of chiral coordination compounds are relatively unexplored. We demonstrate stereoselective discrimination of microbial growth and iron uptake by chiral Fe(III)–siderophores. The siderophore utilization pathway in V. campbellii DS40M4 is stereoselective for Λ-Fe(III)–trivanchrobactin, but not the mismatched Δ-Fe(III)–ruckerbactin diastereomer. Chiral recognition is likely conferred by the stereospecificity of both the outer membrane receptor (OMR) protein FvtA and the periplasmic binding protein (PBP) FvtB, both of which must interact preferentially with the Λ-configured Fe(III)-coordination complexes.

Darcy number effects on natural convection around a porous cylinder in L-shaped enclosure using Lattice Boltzmann method

Independent and combined effects of long-term air pollution exposure and genetic predisposition on COVID-19 severity: A population-based cohort study

The relationships between air pollution, genetic susceptibility, and COVID-19-related outcomes, as well as the potential interplays between air pollution and genetic susceptibility, remain largely unexplored. The Cox proportional hazards model was used to assess associations between long-term exposure to air pollutants and the risk of COVID-19 outcomes (infection, hospitalization, and death) in a COVID-19-naive cohort (n = 458,396). Additionally, associations between air pollutants and the risk of COVID-19 severity (hospitalization and death) were evaluated in a COVID-19 infection cohort (n = 110,216). Furthermore, this study investigated the role of host genetic susceptibility in the relationships between exposure to air pollutants and the development of COVID-19-related outcomes. Long-term exposure to air pollutants was significantly associated with an increased risk of COVID-19-related outcomes in the COVID-19 naive cohort. Similarly, in COVID-19 infection cohort, hazard ratios (HRs) for COVID-19 hospital admission were 1.23 (1.19, 1.27) for PM 2.5 and 1.22 (1.17, 1.26) for PM 10 , whereas HRs for COVID-19 death were 1.28 (1.18, 1.39) for PM 2.5 and 1.25 (1.16, 1.36) for PM 10 . Notably, significant interactions were found between PM 2.5 /PM 10 and genetic susceptibility in COVID-19 death. In COVID-19 infection cohort, participants with both high genetic risk and high air pollutants exposure had 1.86- to 1.97-fold and 1.91- to 2.14-fold higher risk of COVID-19 hospitalization and death compared to those with both low genetic risk and low air pollutants exposure. Exposure to air pollution is significantly associated with an increased burden of severe COVID-19, and air pollution–gene interactions may play a crucial role in the development of COVID-19-related outcomes.

Publisher Correction: A hybrid explainable model based on advanced machine learning and deep learning models for classifying brain tumors using MRI images

Inhibition of amyloid beta oligomer accumulation by NU-9: A unifying mechanism for the treatment of neurodegenerative diseases

Protein aggregation is a hallmark of neurodegenerative diseases, which connects these neuropathologies by a common phenotype. Various proteins and peptides form aggregates that are poorly degraded, and their ensuing pathological accumulation underlies these neurodegenerative diseases. Similarities may exist in the mechanisms responsible for the buildup of these aggregates. Therefore, therapeutics designed to treat one neurodegenerative disease may be beneficial to others. In ALS models, the compound NU-9 was previously shown to block neurodegeneration produced by aggregation-inducing mutations of SOD-1 and TDP-43 [B. Genç et al., Clin. Transl. Med. 11 , e336 (2021)]. Here, we report that NU-9 also prevents the accumulation of amyloid beta oligomers (AβOs), small peptide aggregates that are instigators of Alzheimer’s disease neurodegeneration [M. Tolar et al., Int. J. Mol. Sci. 22 , 6355 (2021)]. AβO buildup was measured by immunofluorescence imaging of cultured hippocampal neurons exposed to exogenous monomeric Aβ. In this model, AβO buildup occurs via cathepsin L- and dynamin-dependent trafficking. This is prevented by NU-9 through a cellular mechanism that is cathepsin B- and lysosome-dependent, suggesting that NU-9 enhances the ability of endolysosomal trafficking to protect against AβO buildup. This possibility is strongly supported by a quantitative assay for autophagosomes that shows robust stimulation by NU-9. These results contribute additional understanding to the mechanisms of protein aggregation and suggest that multiple neurodegenerative diseases might be treatable by targeting common pathogenic mechanisms responsible for protein aggregation.

TMPRSS4 as a prognostic biomarker after gastric cancer surgery in a multicenter retrospective study

Reply to Johnson: Holistic evaluation of ecological models in paleobiology

The correlation between calcaneocuboid joint involvement and sustentacular fragment displacement among male patients with displaced intra-articular calcaneal fractures

Vimentin undergoes liquid–liquid phase separation to form droplets which wet and stabilize actin fibers

The cytoskeleton is composed of F-actin, microtubules, and intermediate filaments (IFs). Vimentin is one of the most ubiquitous and well-studied IFs. It is involved in many activities including wound healing, tissue fibrosis, and cancer metastasis, all of which require rapid vimentin IF assembly. In this paper, we report that vimentin forms liquid condensates which appear to enable rapid filament growth. Given the transient nature of these droplets, we focus on properties of vimentin-Y117L, which has a point mutation that leads to formation of condensates but not IFs, enabling us to study these droplets in detail. The droplets dissolve under 1,6-Hexanediol treatment and under decreasing concentration, confirming that they are liquid, and phase separated. These condensates extensively wet actin stress fibers, rendering them resistant to actin-binding drugs and protecting them from depolymerization. We show similar behavior occurs in wild-type vimentin during its assembly into filaments.

Widely accessible prognostication using medical history for fetal growth restriction and small for gestational age in nationwide insured women

Novel 5-HT6R modulators as mTOR-dependent neuronal autophagy inductors

Early evidence of avocado domestication from El Gigante Rockshelter, Honduras

Molecular research suggests that avocados ( Persea americana Mill.) were domesticated multiple times in the Americas. Seed exchange, hybridization, and cloning have played an essential role across their wild distribution from Mexico to South America to create the modern varieties of today. Archaeological sites with well-preserved and directly radiocarbon-dated botanical assemblages are rare, however, so we know very little about the complexities of the domestication process. Here, we define an early locus of avocado domestication using well-dated desiccated and carbonized avocado remains from El Gigante rockshelter in western Honduras spanning the last 11,000 y. Measurements of avocado seeds and rinds show evidence for long-term management resulting in selection for larger, more robust fruits through time that culminated by 2,250 to 2,080 calendar B.P. (cal. B.P.). However, human-directed selection for larger fruits with thicker rinds is evident as early as 7,565 to 7,265 cal. B.P. Seed morphology is similar to P. americana var. guatemalensis and is congruent with genetic data for the development of this variety in both the highlands of Guatemala and Honduras. Increases in seed size and rind thickness through time are consistent with genetic evidence for the enrichment of putative candidate genes for fruit development and ripening in this variety.

Tick-borne encephalitis virus seroprevalence and infection incidence in Switzerland, 2020–2021

EGFR-induced lncRNA <i>TRIDENT</i> promotes drug resistance in non–small cell lung cancer via phospho-TRIM28-mediated DNA damage repair

Long noncoding RNAs (lncRNAs) play numerous roles in cellular biology and alterations in lncRNA expression profiles have been implicated in a variety of cancers. Here, we identify and characterize a lncRNA, TRIM28 Interacting DNA damage repair Enhancing Noncoding Transcript ( TRIDENT ), whose expression is induced upon epithelial growth factor receptor (EGFR) activation, and which exerts pro-oncogenic functions in EGFR-driven non–small cell lung cancer. Knocking down TRIDENT leads to decreased tumor-cell proliferation in both in vitro and in vivo model systems and induces sensitization to chemotherapeutic drugs. Using ChIRP-MS analysis we identified TRIM28 as a protein interactor of TRIDENT . TRIDENT promotes phosphorylation of TRIM28 and knocking down TRIDENT leads to accumulation of DNA damage in cancer cells via decreased TRIM28 phosphorylation. Altogether, our results reveal a molecular pathway in which TRIDENT regulates TRIM28 phosphorylation to promote tumor cell growth and drug resistance. Our findings suggest that TRIDENT can be developed as a biomarker or therapeutic target for EGFR mutant non–small cell lung cancer.

The virome investigation of the globally endangered Eld’s deer (Rucervus eldii) on Hainan Island, China

The NAE1-mediated neddylation operates as an essential post-translational modification checkpoint for effector CD8 ⁺ T cells

Optimal activation of CD8+ T cells is crucial for immunity-mediated destruction of cancer, requiring a substantial amount of proteins involved in metabolism, proliferation, and effector function. Despite extensive studies emphasizing the role of transcriptional regulation in this process, paired transcriptomic and proteomic analyses reveal that the RNA profile is poorly correlated with protein levels. This discrepancy underscores the importance of post-translational modifications (PTMs) in controlling protein abundance during activation. However, the impact of PTMs on the CD8+ T cell protein dynamic remains underexplored. We identify that neddylation, a recently discovered PTM, is activated in response to T cell receptor (TCR) stimulation and enriched in effector CD8+ T cells from colon cancer patients. Mechanistically, we found the rate-limiting enzyme of neddylation, neural precursor cell expressed developmentally down-regulated protein 8 activating enzyme E1 (NAE1), is induced by the NFATc1, a critical transcription factor downstream of TCR signaling. Our observation revealed that genetic ablation of NAE1 significantly disturbed the proteomic landscape related to activation and mitochondrial function. As a result, CD8+ T cells lacking NAE1 exhibited severely compromised activation, proliferation, and survival, which was accompanied by impaired mitochondrial function. Consistently, deletion of NAE1 in CD8+ T cells abolished their antitumor function and promoted tumor progression. By contrast, the overexpression of NAE1 significantly improved the function of tumor-infiltrating CD8+ T cells. Overall, we uncovered neddylation, a previously underappreciated PTM, as a proteomic checkpoint for CD8+ T cell activation. Enforced expression of NAE1 offers promising therapeutic potential for boosting the antitumor CD8+ T cell responses.