Mccallhartmann7498

To increase fitness, animals use both internal and external states to coordinate reproductive behaviors. The molecular mechanisms underlying this coordination remain unknown. Here, we focused on pheromone-sensing Drosophila Or47b neurons, which exhibit age- and social experience-dependent increase in pheromone responses and courtship advantage in males. FruitlessM (FruM), a master regulator of male courtship behaviors, drives the effects of social experience and age on Or47b neuron responses and function. We show that simultaneous exposure to social experience and age-specific juvenile hormone (JH) induces chromatin-based reprogramming of fruM expression in Or47b neurons. Group housing and JH signaling increase fruM expression in Or47b neurons and active chromatin marks at fruM promoter. Conversely, social isolation or loss of JH signaling decreases fruM expression and increases repressive marks around fruM promoter. Our results suggest that fruM promoter integrates coincident hormone and pheromone signals driving chromatin-based changes in expression and ultimately neuronal and behavioral plasticity.Increasing occurrence of moderate to severe intrauterine adhesion (IUA) is seriously affecting the quality of human life. The aim of the study was to establish IUA models in nonhuman primates and to explore the dual repair effects of human umbilical cord-derived mesenchymal stem cells (huMSCs) loaded on autocrosslinked hyaluronic acid gel (HA-GEL) on endometrial damage and adhesion. Here, we recorded the menstrual cycle data in detail with uterine cavities observed and endometrial tissues detected after intervention, and the thicker endometria, decreased amount of fibrotic formation, increased number of endometrium glands, etc., suggested that both HA-GEL and huMSC/HA-GEL complexes could partially repair IUA caused by mechanical injury, but huMSC/HA-GEL complex transplantation had notable dual repair effects a reliable antiadhesion property and the promotion of endometrial regeneration.Safety concerns about organic media-based batteries are the key public arguments against their widespread usage. Aqueous batteries (ABs), based on water which is environmentally benign, provide a promising alternative for safe, cost-effective, and scalable energy storage, with high power density and tolerance against mishandling. Research interests and achievements in ABs have surged globally in the past 5 years. However, their large-scale application is plagued by the limited output voltage and inadequate energy density. We present the challenges in AB fundamental research, focusing on the design of advanced materials and practical applications of whole devices. Potential interactions of the challenges in different AB systems are established. A critical appraisal of recent advances in ABs is presented for addressing the key issues, with special emphasis on the connection between advanced materials and emerging electrochemistry. Last, we provide a roadmap starting with material design and ending with the commercialization of next-generation reliable ABs.Phenotypic plasticity refers to environment-induced phenotypic changes without mutation and is present in all organisms. The role of phenotypic plasticity in organismal adaptations to novel environments has attracted much attention, but its role in readaptations to ancestral environments is understudied. To address this question, we use the reciprocal transplant approach to investigate the multitissue transcriptomes of chickens adapted to the Tibetan Plateau and adjacent lowland. While many genetic transcriptomic changes had occurred in the forward adaptation to the highland, plastic changes largely transform the transcriptomes to the preferred state when Tibetan chickens are brought back to the lowland. The same trend holds for egg hatchability, a key component of the chicken fitness. These findings, along with highly similar patterns in comparable experiments of guppies and Escherichia coli, demonstrate that organisms generally "remember" their ancestral environments via phenotypic plasticity and reveal a mechanism by which past experience affects future evolution.Trans-4-hydroxy-l-proline is produced by trans-proline-4-hydroxylase with l-proline through glucose fermentation. Here, we designed a thorough "from A to Z" strategy to significantly improve trans-4-hydroxy-l-proline production. Through rare codon selected evolution, Escherichia coli M1 produced 18.2 g L-1 l-proline. Metabolically engineered M6 with the deletion of putA, proP, putP, and aceA, and proB mutation focused carbon flux to l-proline and released its feedback inhibition. It produced 15.7 g L-1 trans-4-hydroxy-l-proline with 10 g L-1 l-proline retained. Furthermore, a tunable circuit based on quorum sensing attenuated l-proline hydroxylation flux, resulting in 43.2 g L-1 trans-4-hydroxy-l-proline with 4.3 g L-1 l-proline retained. Finally, rationally designed l-proline hydroxylase gave 54.8 g L-1 trans-4-hydroxy-l-proline in 60 hours almost without l-proline remaining-the highest production to date. The de novo engineering carbon flux through rare codon selected evolution, dynamic precursor modulation, and metabolic engineering provides a good technological platform for efficient hydroxyl amino acid synthesis.Neurovascular coupling, the close spatial and temporal relationship between neural activity and hemodynamics, is disrupted in pathological brain states. To understand the altered neurovascular relationship in brain disorders, longitudinal, simultaneous mapping of neural activity and hemodynamics is critical yet challenging to achieve. Here, we use a multimodal neural platform in a mouse model of stroke and realize long-term, spatially resolved tracking of intracortical neural activity and cerebral blood flow in the same brain regions. We observe a pronounced neurovascular dissociation that occurs immediately after small-scale strokes, becomes the most severe a few days after, lasts into chronic periods, and varies with the level of ischemia. this website Neuronal deficits extend spatiotemporally, whereas restoration of cerebral blood flow occurs sooner and reaches a higher relative value. Our findings reveal the neurovascular impact of ministrokes and inform the limitation of neuroimaging techniques that infer neural activity from hemodynamic responses.Interpreting how multicellular interactions in the tumor affect resistance pathways to BRAF and MEK1/2 MAPK inhibitors (MAPKi) remains a challenge. To investigate this, we profiled global ligand-receptor interactions among tumor and stromal/immune cells from biopsies of MAPK-driven disease. MAPKi increased tumor-associated macrophages (TAMs) in some patients, which correlated with poor clinical response, and MAPKi coamplified bidirectional tumor-TAM signaling via receptor tyrosine kinases (RTKs) including AXL, MERTK, and their ligand GAS6. In xenograft tumors, intravital microscopy simultaneously monitored in situ single-cell activities of multiple kinases downstream of RTKs, revealing MAPKi increased TAMs and enhanced bypass signaling in TAM-proximal tumor cells. As a proof-of-principle strategy to block this signaling, we developed a multi-RTK kinase inhibitor nanoformulation that accumulated in TAMs and delayed disease progression. Thus, bypass signaling can reciprocally amplify across nearby cell types, offering new opportunities for therapeutic design.While there has been impressive progress connecting bacterial behavior with electrodes, an attractive observation to facilitate advances in synthetic biology is that the growth of a bacterial colony can be determined from impedance changes over time. Here, we interface synthetic biology with microelectronics through engineered population dynamics that regulate the accumulation of charged metabolites. We demonstrate electrical detection of the bacterial response to heavy metals via a population control circuit. We then implement this approach to a synchronized genetic oscillator where we obtain an oscillatory impedance profile from engineered bacteria. We lastly miniaturize an array of electrodes to form "bacterial integrated circuits" and demonstrate its applicability as an interface with genetic circuits. This approach paves the way for new advances in synthetic biology, analytical chemistry, and microelectronic technologies.Thermal turbulence is well known as a potent means to convey heat across space by a moving fluid. The existence of the boundary layers near the plates, however, bottlenecks its heat-exchange capability. Here, we conceptualize a mechanism of thermal vibrational turbulence that breaks through the boundary-layer limitation and achieves massive heat-transport enhancement. When horizontal vibration is applied to the convection cell, a strong shear is induced to the body of fluid near the conducting plates, which destabilizes thermal boundary layers, vigorously triggers the eruptions of thermal plumes, and leads to a heat-transport enhancement by up to 600%. We further reveal that such a vibration-induced shear can very efficiently disrupt the boundary layers. The present findings open a new avenue for research into heat transport and will also bring profound changes in many industrial applications where thermal flux through a fluid is involved and the mechanical vibration is usually inevitable.Despite great progress in biomaterial design strategies for replacing damaged articular cartilage, prevention of stem cell-derived chondrocyte hypertrophy and resulting inferior tissue formation is still a critical challenge. Here, by using engineered biomaterials and a high-throughput system for screening of combinatorial cues in cartilage microenvironments, we demonstrate that biomaterial cross-linking density that regulates matrix degradation and stiffness-together with defined presentation of growth factors, mechanical stimulation, and arginine-glycine-aspartic acid (RGD) peptides-can guide human mesenchymal stem cell (hMSC) differentiation into articular or hypertrophic cartilage phenotypes. Faster-degrading, soft matrices promoted articular cartilage tissue formation of hMSCs by inducing their proliferation and maturation, while slower-degrading, stiff matrices promoted cells to differentiate into hypertrophic chondrocytes through Yes-associated protein (YAP)-dependent mechanotransduction. in vitro and in vivo chondrogenesis studies also suggest that down-regulation of the Wingless and INT-1 (WNT) signaling pathway is required for better quality articular cartilage-like tissue production.Coastal marshes are threatened by relative sea-level (RSL) rise, yet recent studies predict marsh survival even under the high rates of RSL rise expected later in this century. However, because these studies are mostly based on short-term records, uncertainty persists about the longer-term vulnerability of coastal marshes. We present an 8500-year-long marsh record from the Mississippi Delta, showing that at rates of RSL rise exceeding 6 to 9 mm year-1, marsh conversion into open water occurs in about 50 years. At rates of RSL rise exceeding ~3 mm year-1, marsh drowning occurs within a few centuries. Because present-day rates of global sea-level rise already surpass this rate, submergence of the remaining ~15,000 km2 of marshland in coastal Louisiana is probably inevitable. RSL-driven tipping points for marsh drowning vary geographically, and those for the Mississippi Delta may be lower than elsewhere. Nevertheless, our findings highlight the need for consideration of longer time windows in determining the vulnerability of coastal marshes worldwide.