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This study investigates the use of Long Short-Term Memory (LSTM) and Gated Recurrent Unit (GRU) models for predicting stadium attendance in National Football League (NFL) games. Using a comprehensive dataset spanning 26 years and incorporating various game-specific, economic, and temporal features, the performance of LSTM and GRU architectures in forecasting attendance rates is compared. The analysis reveals that both models effectively capture underlying patterns in attendance data, with the LSTM model demonstrating slightly superior predictive accuracy. Optimal configurations are identified through a comparative evaluation of different hidden sizes and layer counts. The best-performing models achieve a Root Mean Squared Error (RMSE) of 7.81% and a Mean Absolute Error (MAE) of 5.62%, representing a significant improvement over previous approaches. While the LSTM model exhibits better adaptability to sudden variations in attendance, the GRU model offers faster convergence and more consistent predictions. To enhance transparency, SHapley Additive exPlanations (SHAP) were used to interpret model outputs. The results revealed seasonality, team identity, and economic indicators as the most influential factors, aligning with domain knowledge and supporting practical applications. These findings contribute to the growing field of AI-driven demand forecasting in sports, offering valuable insights for financial decision-making and operational planning in the sports industry.

Probiotics have been reported to ameliorate symptoms of type 2 diabetes mellitus (T2DM) in animal models and human studies. We previously demonstrated that oral administration of Lactobacillus reuteri ADR-3 reduced insulin resistance in high-fructose-fed (HFD) rats. In the present study, we first identified another L . reuteri strain, ADR-1, which displayed anti-diabetes activity that reduced the levels of serum HbA1c and cholesterol and that increased antioxidant proteins in HFD rats. We further performed a randomized, double-blinded, placebo-controlled trial with a total of 68 T2DM patients to examine the beneficial effects of oral consumption of L . reuteri strains ADR-1 and ADR-3 and to investigate the associated changes in intestinal flora using a quantitative PCR method to analyze 16 S rRNA in fecal specimens. Significant reductions in HbA1c and serum cholesterol were observed in participants in the live ADR-1 consumption group (n = 22) after 3 months of intake when compared with those in the placebo group (n = 22). Although there was no significant difference in the HbA1c serum level among participants who consumed heat-killed ADR-3 (n = 24), the systolic blood pressure and mean blood pressure were significantly decreased after 6 months of intake. There was no obvious change in serum inflammatory cytokines or antioxidant proteins in participants after intaking ADR-1 or ADR-3, except for a reduction in IL-1β in the ADR-3 consumption group after 6 months of intake. With the analysis of fecal microflora, we found that L . reuteri or Bifidobacterium spp. were significantly increased in the ADR-1 and ADR-3 consumption groups, respectively, after 6 months of intake. Interestingly, a significant reduction in HbA1c was observed in the ADR-1 and ADR-3 consumption participants who displayed at least an 8-fold increase in fecal L . reuteri . We also observed that there was a significantly positive correlation between Bifidobacterium spp. and Lactobacillus spp. in participants with increased levels of fecal L . reuteri . In the ADR-1 intake group, the fecal Lactobacillus spp. level displayed a positive correlation with Bifidobacterium spp. but was negatively correlated with Bacteroidetes . The total level of fecal L . reuteri in participants in the ADR-3 consumption group was positively correlated with Firmicutes . In conclusion, L . reuteri strains ADR-1 and ADR-3 have beneficial effects on T2DM patients, and the consumption of different strains of L . reuteri may influence changes in intestinal flora, which may lead to different outcomes after probiotic intake.

The Global Navigation Satellite System (GNSS) cannot achieve accurate positioning and navigation in the indoor environment. Therefore, efficient indoor positioning technology has become a very active research topic. Bluetooth beacon positioning is one of the most widely used technologies. Because of the time-varying characteristics of the Bluetooth received signal strength indication (RSSI), traditional positioning algorithms have large ranging errors because they use fixed path loss models. In this paper, we propose an RSSI real-time correction method based on Bluetooth gateway which is used to detect the RSSI fluctuations of surrounding Bluetooth nodes and upload them to the cloud server. The terminal to be located collects the RSSIs of surrounding Bluetooth nodes, and then adjusts them by the RSSI fluctuation information stored on the server in real-time. The adjusted RSSIs can be used for calculation and achieve smaller positioning error. Moreover, it is difficult to accurately fit the RSSI distance model with the logarithmic distance loss model due to the complex electromagnetic environment in the room. Therefore, the back propagation neural network optimized by particle swarm optimization (PSO-BPNN) is used to train the RSSI distance model to reduce the positioning error. The experiment shows that the proposed method has better positioning accuracy than the traditional method.

The construction of water-soluble synthetic hosts with a stimuli-responsive endo -functionalized cavity is challenging. These hosts feature a switchable cavity and may bring new properties to the fields of self-assembly, molecular machines, and biomedical sciences. Herein, we report a pair of water-soluble naphthotubes with a pH-responsive endo -functionalized cavity. The inward-directing secondary amine group of the hosts can be protonated and deprotonated. Thus, the hosts have different cavity features at the two states and show drastically different binding preference and selectivity in water. We reveal that the binding difference of the two host states is originated from the differences in charge repulsion, hydrogen bonding and the hydrophobic effects. Moreover, the guest binding can be easily switched in a ternary mixture with two guest molecules by adjusting the pH value of the solution. These pH-responsive hosts may be used for the construction of smart self-assembly systems and water-soluble molecular machines. The development of synthetic host-guest systems for stimuli-responsive molecular recognition in water is challenging. Here, the authors report a pair of water-soluble naphthotubes with a pH-responsive cavity for which switchable bifunctional recognition in water is achieved.

Social exclusion has been found to impair working memory (WM). However, the emotional mechanism underlying this adverse effect remains unclear. Besides, little is known about how to alleviate this adverse effect. In the current study, 128 participants were randomly assigned to a social excluded group or an included group while they received anodal transcranial direct current stimulation (tDCS) or sham tDCS over the right ventrolateral pre-frontal cortex (rVLPFC), then they completed the 2-back task. ANOVA results showed that under the sham tDCS condition, mood rating score and 2-back task accuracy of excluded participants were both lower than included participants, and after anodal tDCS, mood rating score and 2-back task accuracy of excluded participants were both higher compared to sham tDCS. Besides, the mediation model showed that negative emotion mediated the relationship between social exclusion and WM under the sham tDCS condition, while the mediating effect disappeared under the anodal tDCS condition. Based on these results, we argued that anodal tDCS over the rVLPFC could alleviate the adverse effect of social exclusion on WM by reducing negative emotion. These findings contributed to further understanding of the emotional mechanism underlying the adverse effect of social exclusion on WM, and providing a clinical treatment in response to social exclusion.

Hydrogen embrittlement reduces the durability of the structural steels required for the hydrogen economy. Understanding how hydrogen interacts with the materials plays a crucial role in managing the embrittlement problems. Theoretical models have indicated that carbon vacancies in metal carbide precipitates are effective hydrogen traps in steels. Increasing the number of carbon vacancies in individual metal carbides is important since the overall hydrogen trapping capacity can be leveraged by introducing abundant metal carbides in steels. To verify this concept, we compare a reference steel containing titanium carbides (TiCs), which lack carbon vacancies, with an experimental steel added with molybdenum (Mo), which form Ti-Mo carbides comprising more carbon vacancies than TiCs. We employ theoretical and experimental techniques to examine the hydrogen trapping behavior of the carbides, demonstrating adding Mo alters the hydrogen trapping mechanism, enabling hydrogen to access carbon vacancy traps within the carbides, leading to an increase in trapping capacity. Understanding how hydrogen embrittles steels and developing the solutions are crucial for enabling the hydrogen economy. Here, the authors report a materials design strategy that can increase the hydrogen trapping capacity by creating carbon vacancies in metal carbide precipitates via microalloying.

Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) functions as a competing endogenous RNA to regulate target genes expression by sponging microRNAs (miRs) to play cancer-promoting roles in cancer stem cells. However, the regulatory mechanism of AFAP1-AS1 in cervical cancer (CC) stem cells is unknown. The present study aimed to provide a new therapeutic target for the clinical treatment of CC. Hyaluronic acid receptor cluster of differentiation 44 variant exon 6 (CD44v6)(+) CC cells were isolated by flow cytometry (FCM). Small interfering RNAs of AFAP1-AS1 (siAFAP1-AS1) were transfected into the (CD44v6)(+) cells. The levels of AFAP1-AS1 were measured by quantitative real-time PCR (qRT-PCR). Sphere formation assay, cell cycle analysis, and Western blotting were used to detect the effect of siAFAP1-AS1. RNA pull-down and luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor (VEGF)-C. CD44v6(+) CC cells had remarkable stemness and a high level of AFAP1-AS1. However, AFAP1-AS1 knockdown with siAFAP1-AS1 suppressed the cell cycle transition of G(1)/S phase and inhibited self-renewal of CD44v6(+) CC cells, the levels of the stemness markers octamer-binding transcription factor 4 (OCT4), osteopontin (OPN), and cluster of differentiation 133 (CD133), and the epithelial-mesenchymal transition (EMT)-related proteins Twist1, matrix metalloprotease (MMP)-9, and VEGF-C. In the mechanism study, miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+) CC cells. LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.

This paper presents a theoretical and numerical study on the stress intensity factors for double-edged cracked steel plates strengthened with fiber reinforced polymer (FRP) plates. Based on the stress intensity factor solution for infinite center-cracked steel plates strengthened with FRP plates, expressions of the stress intensity factors were proposed for double-edged cracked steel plates strengthened with FRP plates by introducing two correction factors: β and f. A finite element (FE) simulation was carried out to calculate the stress intensity factors of the steel plate specimens. Numerous combinations of the specimen width, crack length, FRP thickness and Young’s modulus, adhesive thickness, and shear modulus were considered to conduct the parametric investigation. The FE results were used to investigate the main influencing factors of the stress intensity factors and the correction factor, β. The expression of the correction factor, β, was formulated and calibrated based on the FE results. The proposed expressions of the stress intensity factors were a function of the applied stress, the crack length, the ratio between the crack length and the width of the steel plate, the stiffness ratio between the FRP plate and steel plate, the adhesive thickness, and the shear modulus. Finally, the theoretical results and numerical results were compared to validate the proposed expressions.

The relationship between orexin/hypocretin and rapid eye movement (REM) sleep remains elusive. Here, we find that a proportion of orexin neurons project to the sublaterodorsal tegmental nucleus (SLD) and exhibit REM sleep-related activation. In SLD, orexin directly excites orexin receptor-positive neurons (occupying ~3/4 of total-population) and increases gap junction conductance among neurons. Their interaction spreads the orexin-elicited partial-excitation to activate SLD network globally. Besides, the activated SLD network exhibits increased probability of synchronized firings. This synchronized excitation promotes the correspondence between SLD and its downstream target to enhance SLD output. Using optogenetics and fiber-photometry, we consequently find that orexin-enhanced SLD output prolongs REM sleep episodes through consolidating brain state activation/muscle tone inhibition. After chemogenetic silencing of SLD orexin signaling, a ~17% reduction of REM sleep amounts and disruptions of REM sleep muscle atonia are observed. These findings reveal a stabilization role of orexin in REM sleep. Orexin signaling is provided by diffusely distributed fibers and involved in different brain circuits that orchestrate sleep and wakefulness states. Here, the authors show that a proportion of orexin neurons project to the sublaterodorsal tegmental nucleus and exhibit rapid eye movement (REM) sleep-related actions.

To circumvent the devastating pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, a humanized decoy antibody (ACE2‐Fc fusion protein) was designed to target the interaction between viral spike protein and its cellular receptor, angiotensin‐converting enzyme 2 (ACE2). First, we demonstrated that ACE2‐Fc could specifically abrogate virus replication by blocking the entry of SARS‐CoV‐2 spike‐expressing pseudotyped virus into both ACE2‐expressing lung cells and lung organoids. The impairment of viral entry was not affected by virus variants, since efficient inhibition was also observed in six SARS‐CoV‐2 clinical strains, including the D614G variants which have been shown to exhibit increased infectivity. The preservation of peptidase activity also enables ACE2‐Fc to reduce the angiotensin II‐mediated cytokine cascade. Furthermore, this Fc domain of ACE2‐Fc was shown to activate NK cell degranulation after co‐incubation with Spike‐expressing H1975 cells. These promising characteristics potentiate the therapeutic prospects of ACE2‐Fc as an effective treatment for COVID‐19. Synopsis Currently, there is no effective strategy to fight against the COVID‐19 pandemic. We aim to design and develop a humanized decoy antibody to block SARS‐CoV‐2 infection. The ACE2‐Fc fusion protein can form a dimer that mimics a humanized antibody and specifically binds to the SARS‐CoV‐2 Spike protein. The ACE2‐Fc fusion protein abrogates virus replication by blocking SARS‐CoV‐2 entry in clinical isolates. The peptidase activity of ACE2‐Fc enables the decoy antibody to reduce angiotensin II‐mediated cytokine cascade. After binding to Spike‐expressing target cells, ACE2‐Fc activates degranulation of NK cells. Graphical Abstract Currently, there is no effective strategy to fight against the COVID‐19 pandemic. We aim to design and develop a humanized decoy antibody to block SARS‐CoV‐2 infection.