Search Results (1,222)

Prolonged inundations are altering coastal forest ecosystems of the southeastern US, causing extensive tree die-offs and the development of ghost forests. This hydrological stressor also alters carbon fluxes, threatening the stability of coastal carbon sinks. This study was conducted to investigate the interactions between hydrological drivers and ecosystem responses by analyzing daily eddy covariance flux data from a wetland forest in North Carolina, USA, spanning 2009–2019. We analyzed temporal patterns of net ecosystem exchange (NEE), gross primary productivity (GPP), and ecosystem respiration (RE) under both flooded and non-flooded conditions and evaluated their relationships with observed tree mortality. Generalized Additive Modeling (GAM) revealed that groundwater table depth (GWT), leaf area index (LAI), NEE, and net radiation (Rn) were key predictors of mortality transitions (R² = 0.98). Elevated GWT induces root anoxia; declining LAI reduces productivity; elevated NEE signals physiological breakdown; and higher Rn may amplify evapotranspiration stress. Receiver Operating Characteristic (ROC) analysis revealed critical early warning thresholds for tree mortality: GWT = 2.23 cm, LAI = 2.99, NEE = 1.27 g C m⁻² d⁻¹, and Rn = 167.54 W m⁻². These values offer a basis for forecasting forest mortality risk and guiding early warning systems. Our findings highlight the dominant role of hydrological variability in ecosystem degradation and offer a threshold-based framework for early detection of mortality risks. This approach provides insights into managing coastal forest resilience amid accelerating sea level rise. Full article

Hydrogen-rich water (HRW) has shown neuroprotective effects in acute brain injury, but its role in chronic radiation-induced brain injury (RIBI) remains unclear. This study investigated the long-term efficacy of HRW in mitigating cognitive impairment and neuronal damage caused by chronic RIBI. Fifty male Sprague Dawley rats were randomly divided into five groups: control, irradiation (IR), IR with memantine, IR with HRW, and IR with combined treatment. All but the control group received 20 Gy whole-brain X-ray irradiation, followed by daily interventions for 60 days. Behavioral assessments, histopathological analyses, oxidative stress measurements, ¹⁸F-FDG PET/CT imaging, transcriptomic sequencing, RT-qPCR, Western blot, and serum ELISA were performed. HRW significantly improved anxiety-like behavior, memory, and learning performance compared to the IR group. Histological results revealed that HRW reduced neuronal swelling, degeneration, and loss and enhanced dendritic spine density and neurogenesis. PET/CT imaging showed increased hippocampal glucose uptake in the IR group, which was alleviated by HRW treatment. Transcriptomic and molecular analyses indicated that HRW modulated key genes and proteins, including CD44, CD74, SPP1, and Wnt1, potentially through the MIF, Wnt, and SPP1 signaling pathways. Serum CD44 levels were also lower in treated rats, suggesting its potential as a biomarker for chronic RIBI. These findings demonstrate that HRW can alleviate chronic RIBI by preserving neuronal structure, reducing inflammation, and enhancing neuroplasticity, supporting its potential as a therapeutic strategy for radiation-induced cognitive impairment. Full article

Diabetes mellitus (DM) is a global health challenge marked by chronic hyperglycemia, which can result in complications such as diabetic cardiomyopathy. Sitagliptin, an oral anti-hyperglycemic drug, has demonstrated efficacy in alleviating cardiovascular complications associated with DM. This study explored the impact of Sitagliptin’s potential as a therapeutic agent, functioning not only to control blood sugar levels but also to enhance vascular health and strengthen cardiac resilience in diabetes. The investigation focused on alterations in the vascular endothelial growth factor (VEGF) and its receptor-1 (FLT-1) signaling pathways, as well as its potential to suppress inflammation and oxidative stress. A number of rats received a single dose of streptozotocin (STZ) 55 mg/kg (i.p.) to induce DM. Sitagliptin was administered orally (100 mg/kg/90 days) to normal and diabetic rats, after which samples were collected for investigation. Sitagliptin significantly mitigated weight loss in diabetic rats. Its administration significantly reduced blood glucose levels and improved serum troponin I and CK-MB levels. Heart sections from diabetic rats showed a marked increase in mTOR, VEGF, and FLT-1 immune reaction, while sitagliptin-treated diabetic rats’ heart sections showed moderate immune reactions. Sitagliptin’s protective effect was also associated with reduced inflammation, and apoptotic markers. In conclusion, Sitagliptin is suggested to offer beneficial effects on the vascular health of cardiac blood vessels, thereby potentially reducing myocardial stress in diabetic patients. Full article

In this paper, we present a system-level model of a digital multibeam antenna designed for Low Earth Orbit satellite communications operating in the Ka-band. We initially develop a suitable array topology, which is based on a thinned lattice, then adopt it as the foundation for evaluating its performance within a digital beamforming architecture. This architecture is implemented in a system-level simulator to evaluate the performance of the transmitter and receiver chains. This study advances the analysis of the digital antennas by incorporating both the RF front-end and digital sections non-idealities into a digital-twin framework. This approach enhances the designer’s ability to optimize the system with a holistic approach and provides insights into how various impairments affect the transmitter and receiver performance, identifying the subsystems’ parameter limits. To achieve this, we analyze several subsystems’ parameters and impairments, assessing their effects on both the antenna radiation and quality of the transmitted and received signals in a real applicative context. The results of this study reveal the sensitivity of the system to the impairments and suggest strategies to trade them off, emphasizing the importance of selecting appropriate subsystem features to optimize overall system performance. Full article

Reward processing is a vital function for health and survival and is impaired in various psychiatric and neurological disorders. Using a monetary gambling task, the current study aims to elucidate neural substrates in the reward network underlying the evaluation of win versus loss outcomes and their association with behavioral characteristics, such as impulsivity and task performance, and neuropsychological functioning. Functional MRI was recorded in thirty healthy, male community volunteers (mean age = 27.4 years) while they performed a monetary gambling task in which they bet with either 10 or 50 tokens and received feedback on whether they won or lost the bet amount. Results showed that a set of key brain structures in the reward network, including the putamen, caudate nucleus, superior and inferior parietal lobule, angular gyrus, and Rolandic operculum, had greater blood oxygenation level-dependent (BOLD) signals during win relative to loss trials, and the BOLD signals in most of these regions were highly correlated with one another. Furthermore, exploratory bivariate analyses between these reward-related regions and behavioral and neuropsychological domains showed significant correlations with moderate effect sizes, including (i) negative correlations between non-planning impulsivity and activations in the putamen and caudate regions, (ii) positive correlations between risky bets and right putamen activation, (iii) negative correlations between safer bets and right putamen activation, (iv) a negative correlation between short-term memory capacity and right putamen activity, and (v) a negative correlation between poor planning skills and left inferior occipital cortex activation. These findings contribute to our understanding of the neural underpinnings of monetary reward processing and their relationships to aspects of behavior and cognitive function. Future studies may confirm these findings with larger samples of healthy controls and extend these findings by investigating various clinical groups with impaired reward processing. Full article

Seasonal reproduction in sheep reduces reproductive efficiency. Melatonin (MT) plays a crucial role in reproductive processes. The purpose of this study was to assess the effects of a 5-day MT implant pretreatment on estrus synchronization and reproductive performance in sheep during seasonal anestrus. A total of 40 multiparous Mongolian sheep were selected and randomly divided into two groups. In the MT group (n = 20), the ewes received an MT implant for 5 days, and then, they were given a progesterone (P4)-containing vaginal sponge for 14 days with equine chorionic gonadotropin (eCG) administered (330 I.U. per ewe; I.M.) at sponge removal. Control (CON) ewes (n = 20) were similarly treated but did not receive MT implants. The results demonstrated that MT implantation significantly improved serum levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-Px), increased post-ovulatory luteal diameter and serum P4 levels, and reduced ovarian apoptosis. Compared with the CON group, the MT group showed significantly higher pregnancy (68.23% vs. 50.59%) and lambing rates (63.53% vs. 47.06%; number of lambed ewes/number of total ewes) following cervical-timed artificial insemination. Ovarian transcriptome analysis revealed 522 differentially expressed genes (DEGs) in the MT group compared with the CON group, including 355 upregulated and 167 downregulated DEGs. In addition, MT significantly enhanced proliferation and inhibited apoptosis in cultured granulosa cells (GCs) and luteal cells (LCs) in vitro. Moreover, it enhanced the antioxidant capacity of GCs and LCs probably by activating the NRF2 signaling pathway as well as stimulating steroid hormone synthesis. In conclusion, MT implantation 5 days before applying the conventional P4-eCG protocol enhances ovine reproductive outcomes during seasonal anestrus. MT implantation has a beneficial role on the growth and function of ovarian cells. These findings offer novel evidence supporting the functional role of MT in mammalian reproduction, and would be informative for optimizing estrus synchronization in sheep. Full article

Background: Coagulation disorders, including both bleeding and thrombotic complications, are common in patients undergoing hemodialysis (HD). Here, we aimed to characterize platelet function in patients undergoing hemodialysis three times per week, compared to healthy controls. Methods: Platelet function was assessed using the Multiplate analyzer (Roche), which is based on multiple electrode impedance aggregometry. Platelet aggregation was induced using adenosine diphosphate (ADP), and the area under the curve (AUC) served as the primary endpoint. In addition, platelet counts and C-reactive protein (CRP) levels were measured. To further evaluate nitric oxide (NO)-mediated inhibition of platelet aggregation, blood samples were incubated with the NO donor, sodium nitroprusside (SNP), and the phosphodiesterase 5A (PDE5A) inhibitor, sildenafil. Results: A total of 60 patients undergoing HD and 67 healthy controls were included in the analysis. Patients receiving HD treatment had significantly lower platelet counts compared to healthy controls (226.9 ± 53.47 vs. 246.7 ± 47.21 G/L, p = 0.029). Platelet aggregation was markedly reduced in patients undergoing HD compared to controls (462.0 ± 266.54 vs. 644.5 ± 254.44 AU × min, p < 0.001) with a significant correlation for platelet count (r = 0.42, p = 0.001) and systemic inflammation as indicated by CRP levels (r = 0.28, p = 0.035). Following SNP and sildenafil administration, inhibition of platelet aggregation remained more pronounced in patients undergoing HD. However, the change in platelet aggregation after SNP/sildenafil treatment did not differ significantly between the groups. Conclusions: Patients undergoing HD exhibit altered platelet function, indicated by reduced aggregation and platelet counts, as well as an association with systemic inflammation. Multiple electrode impedance aggregometry appears to be a feasible method for detecting platelet function alterations in patients receiving HD treatment. Responsiveness to NO donors was preserved in patients undergoing HD. Further studies are needed to identify the underlying mechanisms, particularly the role of NO signaling in platelet dysfunction in patients undergoing HD. Full article

Estrogen-related receptor γ (ERRγ) has been reported to regulate various inflammation-related diseases. Herein, we attempted to evaluate the effects of DN200434 as a modulator for ERRγ in mice with atopic dermatitis (AD). Levels of mRNA and protein expression for ERRγ were evaluated in normal and DNCB-induced AD-diagnosed skin. The effects of DN200434 on the chemokines, inflammatory cytokines, and AKT/MAPK/NFκB pathway signaling were investigated in TNF-α/IFN-γ-treated HaCaT cells. DNCB-induced AD mice received DN200434 intraperitoneally for 10 days. Epidermal thickness at the dorsal aspect of the inflamed skin, spleen index, serum IgE levels, and proinflammatory cytokine levels in the skin lesions were measured. Histopathological evaluations, including assessments of epidermal hyperplasia, dermal inflammation, hyperkeratosis, folliculitis, and mast cell counts, were performed to confirm diagnostic features. Significant elevations in ERRγ expression at the RNA and protein levels were observed in DNCB-induced AD lesions. DN200434 suppressed chemokine and inflammatory cytokine expression and inhibited the elevated phosphorylation levels of AKT, ERK, p38, and NFκB in TNF-α/IFN-γ-treated HaCaT cells. Treatment with DN200434 alleviated DNCB-induced AD symptoms. The histopathological score and levels of infiltrated mast cells were also markedly lower in DN200434-treated AD mice than in vehicle-treated AD mice. Consistently, DN200434 reduced the serum IgE level and mRNA expression of TNFα and IL-6 in AD-diagnosed lesions. Collectively, our findings indicated the feasibility of ERRγ as a therapeutic target for the regulation of AD and that DN200434 can be a useful therapeutic agent in treating AD. Full article

IgG antibodies, signaling via the inhibitory receptor, FcγRIIb, are potent inhibitors of IgE-mediated mast cell activation. We have previously reported that in addition to blocking mast cell degranulation, inhibitory IgG signals shut down a proinflammatory transcriptional program in which mast cells produce cytokines and chemokines known to drive type 2 tissue inflammation. To determine whether such effects of allergen-specific IgG can modulate allergic inflammation in vivo, we examined the airways of mice sensitized to ovalbumin (OVA) by intraperitoneal injection and then challenged with intranasal OVA. Pretreatment with allergen-specific IgG significantly reduced the recruitment of inflammatory cells, including macrophages and eosinophils, into the lungs of OVA-sensitized mice. The bronchoalveolar lavage fluid of OVA-challenged mice contained elevated levels of chemokine ligands (CCL2 and CCL24) and interleukin-5, a response that was markedly blunted in animals receiving allergen-specific IgG. IgG-treated animals exhibited attenuated allergen-induced production of IgE, IL-4, and IL-13, along with impaired OVA-induced goblet cell hyperplasia and Muc5ac expression and suppressed airway hyperresponsiveness, consistent with a shift away from a Th2 response. Using mice with a lineage-specific deletion of FcγRIIb, we demonstrated that each of these protective effects of IgG was dependent upon the expression of this receptor on mast cells. Overall, our findings establish that allergen-specific IgG can reduce allergen-driven airway inflammation and airway hyperresponsiveness and point to a mechanistic basis for the therapeutic benefit of aeroallergen-specific IgG therapy. Full article

Automatic modulation classification (AMC) is a fundamental technique in wireless communication systems, as it enables the identification of modulation schemes at the receiver without prior knowledge, thereby promoting efficient spectrum utilization. Recent advancements in deep learning (DL) have significantly enhanced classification performance by enabling neural networks (NNs) to learn complex decision boundaries directly from raw signal data. However, many existing NN-based AMC methods employ deep or specialized network architectures, which, while effective, tend to involve substantial structural complexity. To address this issue, we present a simple NN architecture that utilizes features derived from Hankelized matrices to extract informative signal representations. In the proposed approach, received signals are first transformed into Hankelized matrices, from which informative features are extracted using singular value decomposition (SVD). These features are then fed into a compact, fully connected (FC) NN for modulation classification across a wide range of signal-to-noise ratio (SNR) levels. Despite its architectural simplicity, the proposed method achieves competitive performance, offering a practical and scalable solution for AMC tasks at the receiver in diverse wireless environments. Full article

Acetaminophen (APAP) overdose is a major cause of drug-induced liver injury (DILI) globally, which necessitates effective therapies. Gallic acid (GA), a naturally abundant polyphenol, possesses potent antioxidant and anti-inflammatory properties that may overcome the limitations of N-acetylcysteine (NAC), such as its narrow therapeutic window. This study systematically investigated the hepatoprotective effects and underlying molecular mechanisms of GA against APAP-induced acute liver injury (ALI). Mice received an intraperitoneal injection of APAP (300 mg/kg), followed by an oral administration of GA (50 or 100 mg/kg) or NAC (150 mg/kg) 1 h post-intoxication. Both GA and NAC significantly ameliorated hypertrophy and histopathological damage, as evidenced by reduced serum ALT/AST levels and inflammatory cytokines. TUNEL staining revealed a marked suppression of apoptotic and necrotic cell death, further supported by the downregulation of pro-apoptotic Bax and the upregulation of anti-apoptotic Bcl-2 mRNA expression. GA and NAC treatment restored hepatic glutathione (GSH) content, enhanced antioxidant enzyme gene expression, and reduced malondialdehyde (MDA) accumulation. Mechanistically, GA and NAC inhibited MAPK phosphorylation while activating AMPK signaling. Taken together, these findings demonstrate that GA mitigates APAP-induced ALI by modulating oxidative stress and inflammation through the regulation of MAPK/AMPK signaling proteins. Full article

Wi-Fi fingerprinting is a widely adopted technique for indoor localization in location-based services (LBS) due to its cost-effectiveness and ease of deployment using existing infrastructure. However, the performance of these systems often suffers due to missing received signal strength indicator (RSSI) measurements, which can arise from complex indoor structures, device limitations, or user mobility, leading to incomplete and unreliable fingerprint data. To address this critical issue, we propose Feature-level Augmentation for Localization (FALoc), a novel framework that enhances Wi-Fi fingerprinting-based localization through targeted feature-level data augmentation. FALoc uniquely models the observation probabilities of RSSI signals by constructing a bipartite graph between reference points and access points, which is then processed by a variational graph auto-encoder (VGAE). Based on these learned probabilities, FALoc intelligently imputes likely missing RSSI values or removes unreliable ones, effectively enriching the training data. We evaluated FALoc using an MLP (Multi-Layer Perceptron)-based localization model on the UJIIndoorLoc and UTSIndoorLoc datasets. The experimental results demonstrate that FALoc significantly improves localization accuracy, achieving mean localization errors of 7.137 m on UJIIndoorLoc and 7.138 m on UTSIndoorLoc, which represent improvements of approximately 12.9% and 8.6% over the respective MLP baselines (8.191 m and 7.808 m), highlighting the efficacy of our approach in handling missing data. Full article

Per- and polyfluoroalkyl substances (PFASs) comprise a diverse array of synthetic chemicals that resist environmental degradation. They are increasingly recognised as endocrine-disrupting compounds (EDCs). These chemicals, found in non-stick cookware, food packaging, and industrial waste, accumulate in human tissues and fluids, raising substantial concerns regarding their impact on female reproductive health. Epidemiological studies have demonstrated associations between PFAS exposure and reduced fertility; nevertheless, the underlying molecular pathways remain inadequately understood. This narrative review investigates the multifaceted effects of PFASs on ovarian physiology, including its disruption of the hypothalamic–pituitary–ovarian (HPO) axis, alteration of anti-Müllerian hormone (AMH) levels, folliculogenesis, and gonadotropin receptor signalling. Significant attention is directed towards the emerging association between PFASs and polycystic ovarian syndrome (PCOS), wherein PFAS-induced hormonal disruption may exacerbate metabolic issues and elevated androgen levels. Furthermore, we analyse the current data regarding PFAS exposure in women undergoing treatment based on assisted reproductive technologies (ARTs), specifically in vitro fertilisation (IVF), highlighting possible associations with diminished oocyte quality, suboptimal embryo development, and implantation failure. We examine potential epigenetic and transgenerational alterations that may influence women’s reproductive capabilities over time. This study underscores the urgent need for further research and regulatory actions to tackle PFAS-related reproductive toxicity, particularly in vulnerable populations, such as women of reproductive age and those receiving fertility treatments. Full article

With the rapid expansion of Internet of Things (IoT) and edge computing applications, efficient video transmission under constrained bandwidth and limited computational resources has become increasingly critical. In such environments, perception-based video coding plays a vital role in maintaining acceptable visual quality while minimizing bit rate and processing overhead. Although newer video coding standards have emerged, H.264/AVC remains the dominant compression format in many deployed systems, particularly in commercial CCTV surveillance, due to its compatibility, stability, and widespread hardware support. Motivated by these practical demands, this paper proposes a perception-based video coding algorithm specifically tailored for low-bit-rate H.264/AVC applications. By targeting regions most relevant to the human visual system, the proposed method enhances perceptual quality while optimizing resource usage, making it particularly suitable for embedded systems and bandwidth-limited communication channels. In general, regions containing human faces and those exhibiting significant motion are of primary importance for human perception and should receive higher bit allocation to preserve visual quality. To this end, macroblocks (MBs) containing human faces are detected using the Viola–Jones algorithm, which leverages AdaBoost for feature selection and a cascade of classifiers for fast and accurate detection. This approach is favored over deep learning-based models due to its low computational complexity and real-time capability, making it ideal for latency- and resource-constrained IoT and edge environments. Motion-intensive macroblocks were identified by comparing their motion intensity against the average motion level of preceding reference frames. Based on these criteria, a dynamic quantization parameter (QP) adjustment strategy was applied to assign finer quantization to perceptually important regions of interest (ROIs) in low-bit-rate scenarios. The experimental results show that the proposed method achieves superior subjective visual quality and objective Peak Signal-to-Noise Ratio (PSNR) compared to the standard JM software and other state-of-the-art algorithms under the same bit rate constraints. Moreover, the approach introduces only a marginal increase in computational complexity, highlighting its efficiency. Overall, the proposed algorithm offers an effective balance between visual quality and computational performance, making it well suited for video transmission in bandwidth-constrained, resource-limited IoT and edge computing environments. Full article

Alzheimer’s disease (AD) is the most common cause of dementia in older adults and is becoming a major public health crisis as life expectancy increases worldwide. A major contributor to this disease is a deficiency in melatonin signaling. We have recently synthesised a series of melatonin analogs containing donepezil fragments. These compounds have been tested both in silico and in vitro. In this study, a particularly potent compound, 3a, was evaluated in a hybrid rat model of melatonin deficiency and AD. Rats underwent pinealectomy followed one week later by bilateral intracerebroventricular infusion of Aβ_1-42 (1 µg/µL). A 14-day subchronic treatment with compound 3a was started simultaneously with the neurotoxin infusion. Melatonin was used as a reference drug, while a matched sham group received vehicle treatment. One week after the Aβ_1-42 infusion, the rats’ cognitive functions were assessed using two Y-maze protocols, object recognition and object location tests. Markers of oxidative stress, including hippocampal glutathione, superoxide dismutase, and malondialdehyde, were assessed by ELISA. Compound 3a effectively prevented cognitive impairment induced by the AD model, and its effects were comparable to those of melatonin. In addition, this melatonin analogue with a donepezil fragment reduced AD-associated oxidative stress and suppressed model-associated increased Aβ_1-42 levels in the hippocampus. Our findings suggest that melatonin analogs containing donepezil fragments are promising therapeutic options for targeting oxidative stress associated with AD. Full article