Coastal recreational waters face increasing fecal contamination from poorly defined sources, yet most monitoring relies on fecal indicator bacteria (FIB) that cannot identify pollution origins. This study evaluated microbial water quality at 12 sites (six pore water, six surface water) along the Brazoria County, Texas coastline from July 2024 to June 2025, combining culturable enterococci with a general fecal marker (Entero1a) and two human-associated markers (HF183 and HumanmtND5), and integrating physicochemical parameters, precipitation, and Houston Freeport vessel-arrival data. Culturable enterococci were detected in 94% of pore and 100% of surface samples, with significantly higher concentrations in surface waters. Using the 104 MPN/100 mL marine recreational criterion as a reference benchmark, 58.1% of surface water samples exceeded this value compared with 10.4% of pore water samples. Marker concentrations differed significantly between water categories for all three assays. Among sites, pore waters showed no significant differences for any microbial parameter, whereas surface sites differed significantly in culturable enterococci and Entero1a, driven by elevated concentrations at S12 and S14.Spearman correlations among culturable enterococci, the three qPCR markers, physicochemical parameters and nitrogen species were stronger and more frequent in surface waters than pore waters. Principal component analysis placed 24-h and 7-day cumulative rainfall on the same component axes as the human-associated HF183 marker in both compartments, and vessel arrivals loaded together with HF183 and HumanmtND5 at surface sites nearest the Houston Freeport channel. Non-metric multidimensional scaling produced weak and largely non-significant ordination structure, indicating that the measured environmental conditions were relatively homogeneous across sites. Collectively, surface waters exhibited episodic microbial responses that co-varied with rainfall and vessel activity, whereas both compartments showed weak multivariate structure. Because the marker panel did not include non-human host-associated assays, these findings identify human-associated and hydrologically mediated pathways as detectable contributors rather than as the dominant sources of the observed contamination, and underscore the need for intensified, source-targeted coastal monitoring.

Fuel economy matters to both animals and machines, as the cost of transport can determine where, when, and how far locomotion is possible. However, established estimates of these values for animal flight come from laboratories and treat the atmosphere as constant, even though free-flying animals routinely extract energy from atmospheric flows. Using high-resolution movement data, we estimate the cost of transport for 50 bird and bat species flying in the wild. Our results revise the classic ranking of locomotion costs, suggesting that flying can be cheaper than swimming though almost as costly as running, depending on interactions between physical environment, morphology, and behavior. Linking transport costs to atmospheric conditions provides a mechanistic basis for predicting how changing windscapes will reshape the energetics, movements, and distributions of flying animals.

In the mediodorsal thalamus (MD), neurons of the medial (MD-M) and lateral (MD-L) subnuclei project to the medial prefrontal cortex (mPFC) to control complementary aspects of behavior, with MD-M supporting more of the social/emotional domain and MD-L promoting cognitive functions. Our recent work shows that MD-M and MD-L have differences in hyperpolarization-activated, cyclic nucleotide-gated (HCN) pacemaker channels that may enable their distinct roles in behavior. Low HCN channel activity in MD-M neurons makes them relatively sensitive and responsive to inputs, while higher HCN channel activity makes MD-L neurons more specific and selective for which inputs it transforms into outputs. Knockout (KO) of the fragile X syndrome-related gene Fmr1 decreased the activity of HCN channels in MD-L but not MD-M neurons, making MD-L neurons more like MD-M cells physiologically. We sought to understand if these Fmr1-related changes in MD function were accompanied by changes in subcellular structure. Here, we assessed the dendritic morphology of MD neurons in adult Fmr1 KO and wildtype (WT) littermate mice. In acute ex vivo brain slices, we filled MD neurons with biocytin via whole cell recording pipettes. We used Neurolucida to trace the dendrites, performed quantitative analysis of dendritic architecture, compared MD-M and MD-L neurons in wildtype mice, and compared WT to KO mice for each subnucleus. In WT mice, MD-M neurons showed more distal dendritic branching compared with MD-L neurons. In Fmr1 KO mice, MD-M neurons lost their distal dendritic branching and exhibited significant reductions in multiple measures of dendritic complexity compared to WT controls (total dendritic length, number of nodes, and number of terminals), while MD-L neurons showed no morphological differences between WT and KO animals. Notably, these morphological changes show a double dissociation with our previous physiological findings: MD-M neurons exhibit structural but not functional changes, while MD-L neurons show functional but not structural changes in Fmr1 KO mice. Together, these findings suggest that FMRP regulates structure and function through independent, circuit-specific mechanisms in thalamocortical neurons, with implications for understanding the diverse cellular and network consequences of Fmr1 loss in fragile X syndrome.

In rectifying power electronics, wider-bandgap (Eg) semiconductors allow higher efficiency and power density with the Baliga figure of merit proportional to Eg[5.5] (refs. [1,2]). Unfortunately, the unique ability of semiconductors to have their conductivities controllably modulated over orders of magnitude by equilibrium doping methods becomes increasingly elusive as the bandgap increases. Increasing demand for wider-bandgap semiconductors has led to many materials previously considered insulators-including GaN, SiC, AlN, Ga2O3 and GeO2-to emerge as useful semiconductors after decreasing defect densities and finding appropriate dopants. Here we report silicon-doped α-(AlxGa1-x)2O3 films with bandgaps exceeding 7.0 eV grown by suboxide molecular-beam epitaxy, surpassing that of cubic boron nitride, the next-widest-bandgap semiconductor known[3-5]. In the colossal-bandgap regime, >6 eV, our silicon-doped α-(AlxGa1-x)2O3 films have room-temperature conductivities over 100 million times higher than all previous reports[6]. We fabricate a Schottky diode and a field-effect transistor (the AlphaFET) with colossal-bandgap channels. These α-(AlxGa1-x)2O3 films and devices use sapphire, an abundant, inexpensive substrate with excellent quality that is produced at massive scale, facilitating the development and adoption of colossal-bandgap electronics. Our achievement breaks the trend of increasing synthesis difficulty, cost and small size of ever-wider-bandgap semiconductors, for example, diamond and cubic boron nitride.

Borehole detection in textured quarry reconstructions is challenging because shadows, rocks, and fractured ground can resemble visible surface openings. We introduce GeoBoreNet, which augments RGB with four pixel-aligned inputs derived from reconstructed surface height: local residual relief, spatial gradient magnitude, spatial Laplacian response, and mesh support. Plane removal and resolution-adapted local-background subtraction encode surface morphology, and an expanded first convolution incorporates these channels into standard detectors. Experiments evaluate DINO-R50 and YOLO11x across 11 source scenes using scene-disjoint leave-one-scene-out testing, with five paired training seeds for DINO-R50. In pooled cross-fold evaluation, adding geometry increases AP from 0.483 to 0.548 for DINO-R50 and from 0.385 to 0.450 for YOLO11x, an absolute gain of 0.065 for each detector. Component and local-background scale studies further assess the geometry representation. DINO-R50 source-object-unique AP increases from 0.448 to 0.493 at cross-patch NMS IoU 0.4. In evaluated search regions containing zero-object tiles, AP increases from 0.380 to 0.430 for DINO-R50 and from 0.300 to 0.360 for YOLO11x. These results show that local surface morphology complements RGB for two-dimensional borehole detection in the evaluated scenes.

Pollination is a key ecological process sustaining biodiversity and food security, yet global patterns of plant-pollinator specialization remain unresolved. Using a global dataset of quantitative plant-pollinator networks (>3,400 networks, >110,000 interactions), we show that specialization is latitudinally structured, but not as a single directional pattern. We find no consistent monotonic increase or decrease in specialization towards the Equator. Instead, network-level and pollinator specialization peak at low northern latitudes near the tropical-subtropical boundary, whereas plant specialization is hemispherically asymmetric. Climate is most often the best-supported predictor of specialization compared with latitude, biodiversity and environmental productivity. Network-level specialization declines with increasing mean annual temperature, with strong group-specific differences. Precipitation exerts nonlinear effects: plant specialization peaks at intermediate precipitation but is lower at the wettest sites, whereas pollinator specialization is lower at intermediate precipitation, although often in interaction with temperature. Pollinator groups diverge strongly, especially in contrasting precipitation-related patterns between birds and insects. These findings show that global plant-pollinator specialization is structured by latitude and climate in complex and taxon-specific ways, with implications for uneven responses of pollination networks to future climatic change.

IntroductionAdolescent and young adult (AYA) cancer survivors (ages 15-39 at diagnosis) who identify as sexual and gender minorities [SGM] and/or Black, Indigenous, and Persons of Color [BIPOC]) experience survivorship challenges compounded by discrimination, mistrust, and culturally incongruent care. These factors contribute to inequities in health outcomes and research participation. This qualitative study explored the experiences of underrepresented AYA cancer survivors and key stakeholders in research engagement.MethodsParticipants were recruited through five US-based academic cancer centers and five community-based organizations. Interviews were conducted via two-way video conferencing, and transcripts were analyzed using inductive thematic analysis. A Community Advisory Panel (CAP) consisting of 10 underrepresented AYAs co-developed semi-structured interview guides and contributed to study interpretation.ResultsTwenty-eight participants completed interviews (n=22 survivors, n=5 healthcare professionals, n=1 caregiver). Participants identified as BIPOC (64.3%), SGM (46.4%), and both (23.1%). Four themes shaped research engagement: (1) Awareness (visibility and pathways to research opportunities); (2) Accessibility (emotional, logistical, and institutional feasibility); (3) Authenticity (trust and perceived legitimacy); and (4) Appropriateness (alignment with identity and lived context).ConclusionResearch engagement among underrepresented AYA cancer survivors is shaped by interconnected multilevel factors. Advancing equity requires moving beyond recruitment to redesign research approaches that enhance visibility, reduce structural barriers, build trust, and align participation with AYAs' identities and lived experiences.

Recognizing familiar faces is a fundamental social function that depends on interactions between perceptual and memory systems, yet the underlying neural mechanisms remain poorly understood. Here, we combine single-neuron recordings, intracranial electroencephalography (iEEG), and multi-scale connectivity analyses in the human ventral temporal cortex (VTC) and medial temporal lobe (MTL) to investigate the neural dynamics underlying face familiarity. Theta-frequency phase locking of MTL neurons is associated with face familiarity and familiarization, complementing firing-rate signals. The VTC represents visual features through an axis-based code that disproportionately contributes to familiarity representations. Familiarity is further associated with enhanced theta synchronization between the VTC and MTL, particularly between VTC visual-feature-coding and MTL familiarity-coding channels. Enhanced theta-frequency spike-iEEG coherence for familiar faces suggests that MTL phase locking is coordinated with large-scale VTC activity. Together, these findings identify theta synchronization as a key mechanism coordinating the neural dynamics underlying face familiarity processing in humans.

Pancreatic β-cell mass and glucose-stimulated insulin secretion strongly increase during postnatal development. Voltage-gated calcium channels (CaV) are the key determinants of pancreatic β-cell electrical activity, insulin granule exocytosis, β-cell proliferation and survival. Here we show that β-cells of 1-day-old mice have significantly smaller CaV currents compared to 14-day (juvenile) or 3-month-old (adult) mice, as well as a different CaV isoform composition. In neonates, P/Q-type channels contribute ~53% of the whole-cell current while L-type channels contribute only ~25%. The reduced L-type current is associated with a complete absence of β-cell-specific glucose-induced excitability even though the β-cells depolarize at a lower glucose threshold. By postnatal day 14, the L-type contribution increases to ~44%, reaching ~50% in adults, and P/Q-type currents decrease to ~20%. Nevertheless, the total β-cell calcium influx density is largest in juvenile mice consistent with a lower-threshold glucose dependence of the electrical activity compared to adults. Despite the larger calcium influx, the islets of 14-day-old mice show significantly reduced vesicle exocytosis, insulin release and insulin content. Our data show extensive postnatal remodeling in β-cell mass and glucose sensitivity, and an age-dependent refinement of CaV isoform composition, electrical activity, and insulin release. The cumulative increase in β-cell mass and insulin release causes a ~ 7-fold increase in plasma insulin levels between 14-day- and 3-month-old mice.

Mitochondria are essential for cardiac myocyte function, providing the continuous ATP supply required for contraction and cellular homeostasis. Regulation of the proton motive force, which is critical for ATP synthesis, depends on multiple ion transport mechanisms, including those mediating H[+] flux. The voltage-gated proton channel (Hv1), encoded by the Hvcn1 gene, is known to regulate cytosolic pH and membrane potential in several cell types. Here, using isolated mouse cardiac mitochondria, we demonstrate for the first time that Hv1 is functionally expressed in cardiac mitochondria. Pharmacological inhibition of Hv1 enhanced matrix alkalinization and induced mitochondrial hyperpolarization during succinate-driven mitochondrial energization. Importantly, a similar hyperpolarization was also observed under basal conditions in intact cardiac myocytes.

The pancreas consists of exocrine and endocrine compartments. In the exocrine pancreas, cystic fibrosis transmembrane conductance regulator (CFTR) functions mainly in ductal epithelial cells as a chloride and bicarbonate channel. Its activity depends on proper protein folding, trafficking, and localization to the apical membrane. This systematic narrative review aims to synthesize the available evidence on the role of protein sorting machinery in CFTR channelopathies and its contribution to exocrine pancreatic dysfunction. A thorough search was conducted using PRISMA criteria on PubMed, Wiley Online Library, and Scopus for studies published in English between January 2000 and November 2025. Twenty studies that met the inclusion criteria were included in this review. Pathogenic CFTR variants impair protein folding, endoplasmic reticulum (ER) exit, and endosomal recycling, resulting in reduced apical membrane expression and stability. These defects disrupt the localization of associated transporters and secretory proteins, impair ductal bicarbonate secretion, alter zymogen handling, and promote acinar injury, although these claims are supported mainly by indirect experimental models and therefore require clinical confirmation. CFTR channelopathies in the exocrine pancreas encompass both ion transport defects and broader disruptions of protein sorting machinery. CFTR may contribute to the assembly, stabilization, or localization of selected apical transport complexes, and its loss can secondarily alter epithelial organization. Therapeutic approaches targeting both channel correction and intracellular trafficking may improve pancreatic function and mitigate disease progression.