Recently, the LHCb collaboration reported the first observation of CP violation in baryon decays, with a significance of more than 5σ. This strongly motivates us to investigate the CP violation in more baryon decay processes. In this work, we employ the final-state rescattering mechanism with introducing two model parameters, Λ_charm and Λ_charmless, and calculate two-body non-leptonic baryon decays Λ^0_b → Λ(1520) π^0/κ(700)/f_0(500, 980)/ρ^0/K^*0/ϕ and Ξ^-_b → Λ(1520) K^-. Consequently, we evaluate the corresponding branching ratios, CP asymmetries, and interference effects between different decay amplitudes. Our theoretical predictions for certain decay channels are in good agreement with current experimental measurements, while the remaining processes–particularly the remarkably large CP violation observable revealed by the kinematic analysis are expected to be tested in future experiments.

SASH1 is a signal adaptor protein involved in cell growth, apoptosis, and immune regulation, and has been increasingly studied in tumor and immune cells. Emerging evidence suggests that SASH1 plays an important role in inflammatory responses and cellular homeostasis, processes that are closely associated with the development of PE. This study aimed to determine whether SASH1 contributes to trophoblast apoptosis and inflammatory responses in PE and whether P-EXOS exerts protective effects through SASH1 regulation. In this study, three PE-related transcriptomic datasets (GSE75010, GSE10588, and GSE60438) were analyzed to identify shared differentially expressed genes (DEGs), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Machine learning algorithms were further applied to screen key candidate genes, and single-cell RNA sequencing data were used to characterize cellular heterogeneity in placental tissue and to determine cell type-specific expression patterns. SASH1 was identified as a consensus candidate gene and was significantly upregulated in trophoblast cells from PE samples. In vitro, a hypoxia-treated HTR-8/SVneo trophoblast cell model was established, combined with SASH1 knockdown, SASH1 overexpression, and co-culture with P-EXOS. Functional experiments showed that knockdown of SASH1 significantly suppressed hypoxia-induced trophoblast apoptosis and reduced the secretion of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α, whereas SASH1 overexpression promoted apoptosis and inflammatory responses. In addition, P-EXOS treatment markedly reduced SASH1 expression at both mRNA and protein levels and attenuated hypoxia-induced trophoblast injury, while SASH1 overexpression largely abolished these protective effects. Taken together, these findings indicate that SASH1 plays a critical role in trophoblast apoptosis and inflammatory responses in PE. P-EXOS may alleviate hypoxia-induced trophoblastic injury by suppressing SASH1 expression, providing new insights into the molecular mechanisms and potential therapeutic targets for PE.

In this work, we investigate the charmless non-leptonic two-body Λ_b decays within the framework of final-state rescattering mechanism. In contrast to the Cutkosky cutting method, we compute both the absorptive and dispersive parts of the hadronic rescattering triangle diagrams. Based on the established formalism, we analyze the Λ_b → N^*(1535,1520)M decay processes with M =K_S, K^*_0(700), f_0(500,980), ρ(770), K̅^*0, ϕ, and predict various physical observables, such as their branching ratios, direct and partial-wave CP asymmetries, as well as decay asymmetry parameters. These two-body decay processes are expected to contribute primarily to the subsequent four-body decay channels, such as Λ_b^0 → p π^- π^+ π^-, whose CP asymmetry measurements will be accessible at the LHCb experiment.

Lithium-rich disordered rock salt Li 1.25 V 0.5 Nb 0.25 O 2 is synthesized as a high-performance LIC anode, enabling 178 mAh g −1 capacity (0.1 A g −1 ) and stable cycling for over 1000 cycles, advancing sustainable energy storage.

Honey bees are frequently exposed to multiple stressors in natural habitats, such as pesticides and parasites, which may potentially interact and lead to synergistic effects. Tropilaelaps mercedesae is an ectoparasitic mite that severely affects Apis mellifera, feeding on hemolymph and fat bodies of honey bee larvae and pupae, and carrying honey bee viruses. Chlorantraniliprole, a diamide insecticide widely used in agricultural production, poses potential long-term risks to bee health. In this study, we investigated the combined impacts of T. mercedesae and chlorantraniliprole on Apis mellifera. Co-exposure to T. mercedesae and chlorantraniliprole resulted in a synergistic effect, significantly reducing the survival of honey bees, while increasing the activities of oxidative stress-related enzymes, including catalase, peroxidase, and superoxide dismutase. In addition, the expression levels of abaecin and defensin 1 were suppressed, whereas vitellogenin was significantly upregulated. These findings deepen our understanding of how biotic and abiotic stressors interact to affect honey bees and provide valuable insights for developing more effective strategies for their conservation.

This study investigates the toxicological effects of Triflumezopyrim (TRF), a novel mesoionic insecticide, on two closely related honey bee species, Apis mellifera and Apis cerana. In acute oral toxicity assays, A. cerana exhibited a lower LC50 value (3.413 mg/L) compared to A. mellifera (17.495 mg/L), indicating approximately 5-fold higher sensitivity to TRF. Transcriptomic analysis revealed differential gene expression patterns related to detoxification, neurotransmission, and immune responses between A. mellifera and A. cerana following TRF exposure, suggesting potential differences in molecular responses that require further validation. A. mellifera displayed enhanced cytochrome P450 and UGT expression, which likely contribute to its higher tolerance, while A. cerana showed obvious downregulation of genes involved in neurotransmission and immune function. Additionally, sublethal TRF exposure caused an initial oxidative imbalance, as indicated by significantly upregulated P450 activity in A. mellifera but a strong reduction in A. cerana, while GST activity was significantly upregulated in both species, alongside decreased GSH levels and reduced LPO, suggesting that different antioxidant and detoxification responses may occur in the two species after TRF exposure. Moreover, the downregulation of neurotransmission related genes (i.e., ACHE, GAD, and GLS) indicated the disruption of synaptic transmission in A. cerana. Consistent with the molecular differences, both the two honey bees exhibited reduced climbing ability and sucrose responsiveness after chronic TRF exposure, with the effects being more pronounced in A. cerana. These laboratory-based hazard identification findings reveal the differential susceptibility of A. mellifera and A. cerana to TRF under controlled conditions, providing foundational data for future refinements of pollinator hazard assessment protocols in regions where both species coexist.

Neonicotinoid imidacloprid is an environmentally contaminant that poses a high toxicity to non-target organisms, honey bees (Apis mellifera). Newly emerged bees are critical for colony resilience but vulnerable. This study evaluated the potential of phytochemical resveratrol in mitigating the toxicity induced by imidacloprid in newly emerged bees. To simulate a combined-stress scenario, bees were exposed to imidacloprid at a concentration (0.25 mg/L) that represents elevated field residues. Newly emerged bees were administered a diet supplemented with resveratrol. A series of assays were conducted to evaluate survival rate, physiological indices, histomorphological alterations, enzyme activities, and transcriptomic profiles. The results demonstrated that dietary supplementation with resveratrol (0.6 mg/L resveratrol and 0.25 mg/L imidacloprid) exhibited significantly higher survival rates and improved food utilization efficiency compared to bees exposed to imidacloprid alone. Resveratrol mitigated imidacloprid-induced midgut injury, aberrant sucrose enzyme activity, and restored homeostasis of genes involved in energy and nutrient metabolism (e.g. ATP synthesis, lipid, carbohydrate, and tyrosine metabolism), which were dysregulated by imidacloprid. Resveratrol alleviated oxidative stress via modulated CAT/GST activity and normalized MDA level, and upregulated genes in phase I and II detoxification pathways (e.g. GST, UGTs, P450). Notably, resveratrol attenuated imidacloprid-induced brain injury and alleviated neurotoxicity by preserving cholinergic integrity and modulating gene expression associated with neural signaling pathway (e.g. AChE activity and the expression of nAChR and GABA receptor genes). The present work suggested the protective effects of resveratrol on the newly emerged bees in agroecosystems contaminated with neonicotinoid and provided a promising practical strategy.

Recent work on B → π, K and B → D form factors from lattice QCD and light-cone sum rules has made it possible to constrain the inverse moment λB of the B-meson light-cone distribution amplitudes by performing a global fit of B → π, K, D form factors. We have compiled the B → π, K, D form factors calculated by the HPQCD, MILC, and RBC/UKQCD collaborations in the large q2 region. By employing an three-parameter ansatz of the B-meson light-cone distribution amplitudes, we express the B → π, K, D form factors at q2 = 0 that are calculated from light-cone sum rules, in terms of the inverse moment λB of the leading-twist B-meson light-cone distribution amplitude. In the B → πℓν channel, we also include the available q2-binned experimental data from the BaBar, Belle, and Belle II collaborations. Using the Bourrely-Caprini-Lellouch parametrization, we perform a global fit and obtain λB = 217(19)_-17^+82 MeV and |Vub| = 3.68(13)_-1^+0 × 10−3. The second uncertainty is obtained by constraining λB > 200 MeV and varying the inverse logarithmic moments σ̂_1 ∈ [−0.7, 0.7] and σ̂_2 ∈ [−6, 6], which represents the model-dependent uncertainty from the B-meson light-cone distribution amplitudes. When taking into account λB and σ̂_1 as fitting parameters simultaneously, the intervals of our preditions are λB = [208, 324] MeV and σ̂_1 = [−0.7, 0.27].

DRX-Li1.25V0.5Nb0.25O2 is innovatively deployed as a lithium-ion capacitor (LIC) anode, exhibiting a specific capacity of 178 mAh g-1 at 0.1 A g-1 with unattenuated cycling over 1000 cycles. Full LIC devices achieve 45.1 mAh g-1 and 76.3% capacity retention after 2000 cycles, expanding the application scope of DRX materials as anodes.

Pesticides represent a major threat to pollinators' health. Bumblebees, as essential pollinators, are one of the bees severely impacted by pesticide exposure. The lack of sensitivity data across diverse species hinders the breeding and application of pesticide-tolerance pollinators trains. This study assessed the acute oral toxicity of dimethoate, an organophosphorus insecticide and a positive control in environmental risk assessments, in five bumblebee species: the commercial European bumblebee species Bombus terrestris and four wild Chinese native bumblebee species (B. ignitus, B. ganjsuensis, B. pyrosoma, and B. lantschouensis). The 48-h median lethal doses (LD50) were determined as follows: 1.64 μg/bee for B. terrestris, 0.98 μg/bee for B. ignitus, 0.91 μg/bee for B. ganjsuensis, 0.71 μg/bee for B. pyrosoma and 0.70 μg/bee for B. lantschouensis. Morphological traits including body wight and forewing length were measured, revealing a positive correlation between them and a negative relationship between body weight and sensitivity to dimethoate. These results indicate that easily measurable morphological traits like body weight could serve as potential indicators to predicting dimethoate tolerance in bumblebees. Our findings are of importance for bumblebee toxicology, addressing the knowledge gap in non-commercial bumblebees of pesticide sensitivity. By expanding acute toxicity data to include underrepresented wild species, this study provided valuable insights for selecting and breeding pollinator strains with enhanced insecticide tolerance, highlighting the need for a broader species range in toxicity tests.

Honey bees in agroecosystems face increasingly exposure to multiple stressors, such as pesticides and pathogens, making it crucial to assess their combined impacts rather than focusing on individual factors alone. This study examined the adverse effects of single exposure acetamiprid, Varroa destructor, and Nosema ceranae, both individually and in combination, on honey bee survival, midgut integrity and transcriptomic changes to understand the molecular mechanisms involved. The findings revealed that combination of acetamiprid and N. ceranae induced significant energetic stress, as evidenced by disruptions in energy metabolism. The synergistic effects of V. destructor and N. ceranae led to severe alterations in midgut histomorphology, particularly damaging the midgut epithelium. Concurrent exposure to acetamiprid and V. destructor inhibited the immune response and energy metabolism of honey bees, thereby exacerbating the vulnerability to pathogens and destabilizing their physiological equilibrium. The combination of all three stressors caused the most dramatic damage, disrupting midgut structure as well as aromatic amino acids and lipid metabolism. Our study underscored the complexity and unpredictability of stressor interactions, emphasizing the need to consider environmental context when assessing the risks of honey bee health.

Solid-state lithium-ion batteries (SSLIBs) employing silicon anodes and sulfide solid electrolytes (SEs) have garnered significant attention due to their exceptional energy density and intrinsic safety, rendering them highly promising for large-scale applications. However, substantial challenges persist, particularly the pronounced volumetric expansion of silicon during cycling, which leads to severe interfacial delamination. In this study, we developed a novel ion-conducting polymeric binder engineered with a LiTFSI-Pyr14TFSI system to address these interfacial challenges. This innovative binder design features high ionic conductivity at room temperature, enabling effective infiltration and stabilization of the solid-solid interfaces. The incorporated ionic liquid serves as an interfacial filler phase, accommodating mechanical strain from silicon expansion while maintaining continuous ion transport pathways. Notably, the binder fulfills dual functionalities: simultaneous ionic conduction and robust mechanical adhesion. Furthermore, advanced characterization revealed the in situ formation of a Li3N-LiF hybrid interphase at the anode during lithiation. This nanocomposite passivation layer significantly enhances lithium-ion transport kinetics, as evidenced by the substantially improved ionic conductivity. The synergistic interplay between the viscoelastic ionic liquid phase and the in situ-derived lithium salts collectively optimizes interfacial stability and charge transfer efficiency. The resultant electrochemical performance demonstrates remarkable improvements: the nano-silicon (nSi) anode achieves an exceptional discharge capacity of 4174.2 mAh g(-1), a substantial increase from 3267.9 mAh g(-1). Moreover, the system retains 70.4% of its initial capacity after 80 cycles, highlighting superior cycling stability. This work presents a groundbreaking interfacial engineering strategy for SSLIBs, combining dynamic ionic liquid mediation with in situ-generated conductive interphases to overcome long-standing challenges in silicon-based solid-state batteries. The findings provide critical insights into multifunctional binder design and pave the way for high-performance, durable energy storage systems.

The widespread use of pesticides poses a significant threat to honeybee health by impacting their survival, behavior, immune function, and detoxification capacity. While phytochemicals such as resveratrol (RSV) have shown potential in mitigating oxidative stress and enhancing antioxidant defenses, their role in improving honeybee tolerance to pesticide exposure remains underexplored. In this study, we investigated the effects of RSV supplementation on honeybees exposed to three pesticides: dinotefuran (DIN), tebuconazole (TEB), and deltamethrin (DEL). The results showed that RSV supplementation significantly improved survival, feed intake, mobility, and gustatory sensitivity, indicating its protective effects against pesticide toxicity. Furthermore, RSV helped normalize impaired detoxification enzyme activities, including SOD, POD, catalase, and glutathione reductase, and reduced ROS levels and lipid peroxidation. Gene expression analysis revealed that RSV modulates Toll pathway-related genes like defensin and apidaecin, alleviating immune suppression caused by pesticides. Additionally, RSV influenced the insulin/insulin-like growth factor signaling (IIS) pathway by reducing ilp1 and inr1 expression, potentially mitigating metabolic stress. These findings demonstrate that protective effects of RSV may be linked to its ability to counter oxidative stress, restore mitochondrial function, and enhance energy metabolism. Furthermore, RSV is widely available, cost-effective, and easily incorporated into bee feed, making it feasible for large-scale application. This study highlights the protective role of RSV in pesticide detoxification in honeybees, offering new perspectives for honeybee health management and environmental toxicology research. By reducing the adverse effects of pesticides on honeybees, the application of RSV not only contributes to maintaining ecological balance but also supports sustainable agricultural practices. Future research should focus on optimizing its dosage, evaluating long-term effects, and investigating its impact on colony dynamics to facilitate its practical implementation in apiculture.

Background Cerebral palsy (CP) is a prevalent cause of physical disability in children, often resulting from hypoxic-ischemic encephalopathy, with current therapies often failing to address the underlying pathophysiology. This study aimed to investigate the potential synergistic effects of human amnion-derived mesenchymal stem cells (hAMSCs) combined with scalp acupuncture in a rat model of CP. Methods Twenty male Sprague-Dawley rats were randomly divided into four groups: Sham, CP, hAMSCs, and hAMSCs+scalp acupuncture (hAMSCs+AP). The CP model was induced via left common carotid artery ligation. hAMSCs were administered through tail vein injection, followed by scalp acupuncture at Baihui (GV20) and Qubin (GB7) points. Neurobehavioral function was assessed using the Bederson score, and brain tissues were analyzed using hematoxylin and eosin (H&E) staining, TUNEL staining, and RT-qPCR for apoptosis-related genes. Results The CP group exhibited significant neurobehavioral deficits and increased apoptosis. Both hAMSCs and hAMSCs+AP treatments improved neurobehavioral function and reduced apoptosis. The combination therapy further decreased apoptosis levels, normalized mRNA expression of Bax, Caspase 9, and Caspase 3, and alleviated histological damage. Conclusions The combination of hAMSCs and scalp acupuncture provides a promising treatment for CP, potentially alleviating brain damage through apoptosis regulation. Further studies are required to elucidate the detailed mechanisms and assess clinical feasibility and safety.

Previous studies have confirmed the excellent biocompatibility, osteogenic properties, and angiogenic ability of hydroxyapatite (HAP), as well as the good osteoblast differentiation ability of dental pulp stem cells. We hypothesized that combining dental pulp stem cells with ultralong hydroxyapatite nanowires and cellulose fibers could more effectively promote osteoblast differentiation, making it a potential biomaterial for enhancing bone wound healing. Therefore, based on the optimal ratio of ultralong hydroxyapatite nanowires and cellulose fibers (HAPNW/CF) determined in previous studies, we added human dental pulp stem cells (hDPSCs) to investigate whether this combination can accelerate cell osteogenic differentiation. hDPSCs were introduced into HAPNW/CF scaffolds, and in vitro experiments revealed that: (1) HAPNW/CF scaffolds exhibited no cytotoxicity toward hDPSCs; (2) HAPNW/CF scaffolds enhanced alkaline phosphatase staining activity, an early marker of osteogenic differentiation, and significantly upregulated the expression level of osteogenic-related proteins; (3) co-culturing with hDPSCs in HAPNW/CF scaffolds significantly increased the expression of angiogenesis-related factors compared to hDPSCs alone when tested using human umbilical vein endothelial cells (hUVECs). Our study demonstrates that combining hDPSCs with HAPNW/CF can enhance osteogenic differentiation more effectively, potentially through increased secretion of angiogenesis-related factors promoting osteoblast differentiation.

Growing evidences have shown that the decline in honey bee populations is mainly caused by the combination of multiple stressors. However, the impacts of parasitic Nosema ceranae to host fitness during long-term pesticide exposure-induced stress is largely unknown. In this study, the effects of chronic exposure to a sublethal dose of dinotefuran, in the presence or absence of N. ceranae, was examined in terms of survival, food consumption, detoxification enzyme activities and gut microbial community. The interaction between dinotefuran and Nosema ceranae on the survival of honey bee was synergistic. Co-exposure to dinotefuran and N. ceranae led to less food consumption and greater changes of enzyme activities involved in defenses against oxidative stress. Particularly, N. ceranae and dinotefuran-N. ceranae co-exposure significantly impacted the gut microbiota structure and richness in adult honey bees, while dinotefuran alone did not show significant alternation of core gut microbiota compared to the control group. We herein demonstrated that chronical exposure to dinotefuran decreases honey bee's survival but is not steadily associated with the gut microbiota dysbiosis; by contrast, N. ceranae parasitism plays a dominant role in the combination in influencing the gut microbial community of the host honey bee. Our findings provide a comprehensive understanding of combinatorial effects between biotic and abiotic stressors on one of the most important pollinators, honey bees.

The combined effects of mite infestation and viral transmission can lead to a rapid decline in colony health. There is growing concern about the decline of Western honey bees (Apis mellifera) caused by an emerging pathogen, Tropilaelaps mercedesae. So far, it is unclear whether T. mercedesae transmits viruses and which viruses might facilitate increased transmission. Here, we found that T. mercedesae harbored six common honey bee viruses. Furthermore, viral proliferation analysis by RT-qPCR showed that viral loads in T. mercedesae was higher than in A. mellifera, especially for deformed wing virus (DWV). Subsequently, we verified that DWV can be transferred between A. mellifera and T. mercedesae during the mite parasitism process by employing an infectious clone of DWV with Green fluorescent protein (GFP). Our findings not only contribute to the understanding of the bee-mite-virus interplay but also highlight the potential role of T. mercedesae as a vector for DWV, similar to Varroa destructor. Due to their ability to transmit viral infections, coupled with their direct parasitic effects, more research is needed for effective management strategies to protect honey bees and ensure the sustainability of apiculture and agriculture.

Objectives This study aimed to investigate changes in the blood metabolic profiles of newborns with varying intrauterine growth conditions. Specifically, we analyzed the levels of amino acids, carnitine, and succinylacetone among full-term newborns, including small for gestational age (SGA), appropriate for gestational age (AGA), and large for gestational age (LGA). We aim to identify differential metabolites and metabolic pathways that may offer insights into clinical interventions. Methods A total of 5106 full-term newborns were included in the study. Blood samples were obtained from all newborns between 3 and 5 days after birth and analyzed using tandem mass spectrometry to detect blood metabolites. Subsequently, we screened for different metabolites and metabolic pathways among the groups using the MetaboAnalystR package (Version 1.0.1) in R software (R-3.6.0). Results The levels of blood amino acids and carnitine metabolism differed significantly among newborns with varying intrauterine growth conditions. Full-term SGA newborns exhibited a decrease in multiple amino acids and an increase in multiple carnitines, while full-term LGA newborns showed an increase in multiple amino acids and acylcarnitines. Conclusion Continuous monitoring of the short-term and long-term growth and metabolic status of full-term SGA and LGA newborns is warranted with individualized dietary and nutritional adjustments to promote healthy growth in a timely manner. The findings of this research contribute to the broader understanding of SGA/LGA and shall inform future research on metabolomics, interventions, and long-term outcomes.

BACKGROUND:Cerebral palsy (CP) is a condition resulting from perinatal brain injury and can lead to physical disabilities. Exosomes derived from human amniotic mesenchymal stromal cells (hAMSC-Exos) hold promise as potential therapeutic options. OBJECTIVE:This study aimed to investigate the impact of hAMSC-Exos on neuronal cells and their role in regulating apoptosis both in vitro and in vivo. METHODS:hAMSC-Exos were isolated via ultracentrifugation and characterized via transmission electron microscopy, particle size analysis, and flow cytometry. In vitro, neuronal damage was induced by lipopolysaccharide (LPS). CP rat models were established via left common carotid artery ligation. Apoptosis levels in cells and CP rats were assessed using flow cytometry, quantitative reverse transcription polymerase chain reaction (RT-qPCR), Western blotting, and TUNEL analysis. RESULTS:The results demonstrated successful isolation of hAMSC-Exos via ultracentrifugation, as the isolated cells were positive for CD9 (79.7%) and CD63 (80.2%). Treatment with hAMSC-Exos significantly mitigated the reduction in cell viability induced by LPS. Flow cytometry revealed that LPS-induced damage promoted apoptosis, but this effect was attenuated by treatment with hAMSC-Exos. Additionally, the expression of caspase-3 and caspase-9 and the Bcl-2/Bax ratio indicated that excessive apoptosis could be attenuated by treatment with hAMSC-Exos. Furthermore, tail vein injection of hAMSC-Exos improved the neurobehavioral function of CP rats. Histological analysis via HE and TUNEL staining showed that apoptosis-related damage was attenuated following hAMSC-Exo treatment. CONCLUSIONS:In conclusion, hAMSC-Exos effectively promote neuronal cell survival by regulating apoptosis, indicating their potential as a promising therapeutic option for CP that merits further investigation.

We employ vacuum-to-B meson correlation functions with interpolating currents q̅'nq and q̅'nγ_⊥q to construct light-cone sum rules (LCSR) for calculating the B→ K^* form factors in the large recoil region. We investigate several subleading-power corrections to these form factors at tree level, including the next-to-leading power contributions from the hard-collinear propagator, the subleading power corrections from the effective current q̅Γ[iD_⊥/(2m_b)]h_v, and four-body higher-twist effects. By utilizing the available leading-power results at 𝒪(α_s) and the power corrections from higher-twist B-meson light-cone distribution amplitudes from our previous work, we further derive the improved numerical predictions for B→ K^* form factors by applying the three-parameter model for B-meson light-cone distribution amplitudes (LCDAs). The subleading-power contribution is about 30% relative to the corresponding leading-power result. Taking the well-adopted Bourrely-Caprini-Lellouch (BCL) parametrization, we then provide the numerical results of B→ K^* form factors in the entire kinematic range, by adopting the combined fit to both LCSR predictions and lattice QCD results. Taking advantage of the newly obtained B→ K^* form factors, we analyse the rare exclusive decay B → K^* ν_ℓν̅_ℓ and estimate the Standard Model predictions of ℬℛ(B̅^0 →K̅^*0ν_ℓν̅_ℓ)=7.54(86)× 10^-6, ℬℛ(B̅^+ →K̅^*+ν_ℓν̅_ℓ)=9.35(94)× 10^-6 and longitudinal K^* polarization fraction F_L=0.44(4).