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Pyrroline Ring Assembly via N-Prenylation and Oxidative Carbocyclization during Biosynthesis of Aeruginosin Derivatives
Covalent adduct Grob fragmentation underlies LSD1 demethylase-specific inhibitor mechanism of action and resistance
The impact of a high fat diet and platelet activation on pre-metastatic niche formation
Impact of prenatal phthalate exposure on newborn metabolome and infant neurodevelopment
Abstract We evaluated associations among exposure to prenatal phthalate metabolites, perturbations of the newborn metabolome, and infant neurobehavioral functioning in mother-newborn pairs enrolled in the Atlanta African American Maternal-Child Cohort during 2016–2018. We quantified eight phthalate metabolites in prenatal urine samples collected between 8- and 14-weeks’ (visit 1; n = 216) and 24- and 30-weeks’ gestation (visit 2; n = 145) and metabolite features in newborn dried-blood spot samples collected at delivery. Associations between phthalate metabolite concentrations and metabolic feature intensities at both visits were examined using adjusted generalized linear models (MWAS). Then, an exploratory meet-in-the-middle (MITM) analysis was conducted in a subset with NICU Neonatal Neurobehavioral Scale (NNNS) scores (visit 1 n = 81; visit 2 n = 71). In both the MWAS and MITM, many of the confirmed metabolites are involved in tyrosine and tryptophan metabolism, including tryptophan, tyrosine, thyroxine, and serine. This analysis elucidates how prenatal phthalate exposure disrupts the newborn metabolome and infant neurobehavioral outcomes.
Systems epigenetic approach towards non-invasive breast cancer detection
Layered Na2Ti3O7-supported Ru catalyst for ambient CO2 methanation
A LTR retrotransposon insertion leads to leafy phenotype in maize by elevating ZmOM66 expression
Retrievable hydrogel networks with confined microalgae for efficient antibiotic degradation and enhanced stress tolerance
Amyloid-reoriented enzyme catalysis
Drivers and impacts of sediment deposition in Amazonian floodplains
Abstract The Amazon River carries enormous amounts of sediment from the Andes mountains, much of which is deposited in its floodplains. However, accurate quantification of the sediment sink at fine spatiotemporal scales is still challenging. Here, we present a high-resolution hydrodynamic-sediment model to simulate sediment deposition in a representative Amazon/Solimões floodplain. The process is found to be jointly driven by inundation, suspended sediment concentration in the Amazon River, and floodplain hydrodynamics and only weakly correlated with inundation level. By upscaling the sediment deposition rate (1.33 ± 0.24 kg m−2 yr−1), we estimate the trapping of 77.3 ± 13.9 Mt (or 6.1 ± 1%) of the Amazon River sediment by the Amazon/Solimões floodplains every year. Widespread deforestation would reduce the trapping efficiency of the floodplains over time, exacerbating downstream river aggradation. Additionally, we show that the deposition of sediment-associated organic carbon plays a minor role in fueling carbon dioxide and methane emissions in the Amazon.
Flexible intelligent microwave metasurface with shape-guided adaptive programming
Molecular basis of SLC19A1-mediated folate and cyclic dinucleotide transport
Photocatalytic deoxygenative Z-selective olefination of aliphatic alcohols
Stabilization mechanism accommodating genome length variation in evolutionarily related viral capsids
Anionic high-entropy doping engineering for electromagnetic wave absorption
Cross-ancestry genome-wide association study identifies implications of SORL1 in cerebral beta-amyloid deposition
Distinct ventral tegmental area neuronal ensembles are indispensable for reward-driven approach and stress-driven avoidance behaviors
Abstract Assigning valence to stimuli for adaptive behavior is an essential function, involving the ventral tegmental area (VTA). VTA cell types are often defined through neurotransmitters (NT). However, valence function in VTA does not parse along NT-boundaries as, within each NT-class, certain neurons are excited by reward and others by stressors. Here we identify, in male mice, the co-activated VTA neuronal ensembles for reward and stress, and determine their role in adaptive behaviors. We show that stimuli of opposite valence (opioid vs acute social stress) recruit two distinct VTA neuronal ensembles. These two ensembles continue to be preferentially engaged by congruent valence stimuli. Stimulation of VTA stress- or reward ensembles is aversive/reinforcing, respectively. Strikingly, external valence stimuli fully require activity of these small discrete VTA ensembles for conferring approach/avoidance outcomes. Overall, our study identifies distinct VTA ensembles for positive and negative valence coding and shows their indispensability for adaptive behavior.