Feed-forward Mechanism Research Articles

Sparse Cascade: Multi-stage cascade fusion and shape dictionary guided network for segmentation of microscopic cytology images

Microscopic cytology image instance segmentation is critical for clinical diagnosis, treatment planning, and biomedical research. However, challenges such as cell overlapping, external interferences, and irregular shapes hinder accurate segmentation. In this paper, a microscopic cytology image instance segmentation algorithm based on a multi-stage cascaded fusion and shape-guided strategy is proposed to improve instance segmentation accuracy. To mitigate the issue of external interference and cell overlap, a feedforward fusion mechanism is introduced in the multi-stage cascade architecture to effectively integrate the mask features from multiple stages. To make the shape of the segmentation result more consistent with the shape of the cell, and to alleviate the issues of unclear boundaries and incomplete shape segmentation caused by cellular overlap and irregular shapes, the sparse code guidance branch based on the explicit shape guidance strategy is introduced. Experiments on the private embryonic cell dataset and the ISBI2014 dataset indicate that the network has achieved improvements over the Cascade Mask R-CNN, with enhancements of 2.51% and 3.92% in bounding boxes mean Average Precision (mAP), and 2.82% and 4.70% in segmentation mAP, respectively. The experimental results indicate that the network proposed in this paper can output more accurate bounding boxes and instance masks.

Ubiquitin-Specific Protease 15 Plays an Important Role in Controlling the Tolerance to Salt, Drought and Abscisic Acid in Arabidopsis thaliana.

Ubiquitin-specific proteases (UBPs), the largest subfamily of deubiquitinating enzymes (DUBs), are critical for plant growth and development as well as abiotic-stress responses. In this study, we discovered that the expression of the ubiquitin-specific protease 15 (UBP15) gene of the gene ubiquitin-specific protease 15 (UBP15) was induced by salt, mannitol and abscisic acid (ABA) treatments. Further research revealed that UBP15 is involved in modulation of salt, drought tolerance and ABA signaling during seed germination, early seedling development, post-germination root growth or adult-plant stage. Enrichment analysis showed that many genes related to abiotic stresses and metabolic pathways were altered in the ubp15-1 mutant. Through the joint analysis of the quantitative real-time polymerase chain reaction (qRT-PCR) and differentially-expressed gene relationship network, we found that UBP15 may mainly regulate salt-stress tolerance by modulating the dwarf and delayed flowering 1 (DDF1) pathway through a cascade reaction. In the regulation of drought-stress responses, ring domain ligase1 (RGLG1) may be a direct substrate of UBP15. Moreover, we cannot exclude the possibility that UBP15 acts in a feed-forward loop mechanism in the regulation of drought-stress responses via ethylene response factor 53 (ERF53) and its ubiquitin (Ub) ligase RGLG1. In ABA signal transduction, UBP15 may play a role in at least three aspects of the ABA signaling pathway: ABA synthesis, stomatal closure regulated by ABA signaling, and transcription factors in the ABA pathway. Taken together, our results suggest that UBP15 is involved in salt, osmotic, and drought-stress tolerance and the ABA signaling pathway by directly regulating the stability of key substrates or indirectly affecting the expression of genes related to abiotic stresses in Arabidopsis thaliana. Our research provides new germplasm resources for stress-resistant crops cultivation. These results demonstrate that UBP15 is a key regulator of salt, drought and ABA tolerance in Arabidopsis.

NMDA receptor antagonist high-frequency oscillations are transmitted via bottom-up feedforward processing

In mammals, NMDA receptor antagonists have been linked to the emergence of high-frequency oscillations (HFO, 130–180 Hz) in cortical and subcortical brain regions. The extent to which transmission of this rhythm is dependent on feedforward (bottom-up) or feedback (top-down) mechanisms is unclear. Previously, we have shown that the olfactory bulb (OB), known to orchestrate oscillations in many brain regions, is an important node in the NMDA receptor-dependent HFO network. Since the piriform cortex (PC) receives major input from the OB, and can modulate OB activity via feedback projections, it represents an ideal site to investigate transmission modalities. Here we show, using silicon probes, that NMDA receptor antagonist HFO are present in the PC associated with current dipoles, although of lower power than the OB. Granger causality and peak-lag analyses implicated the OB as the driver of HFO in the PC. Consistent with this, reversible inhibition of the OB resulted in a reduction of HFO power both locally and in the PC. In contrast, inhibition of the PC had minimal impact on OB activity. Collectively, these findings point to bottom-up mechanisms in mediating the transmission of NMDA receptor antagonist-HFO, at least in olfactory circuits.

Seamless switching, feedforward, and feedback mechanisms: Enhancing task performance and user perception in device switch

In an era where digital multitasking is universal, the necessity to switch between devices is vital. The effect of switching modes between devices on the user experience remains unclear. This study investigates the impact of switching modes on task performance and user perception within interconnected device environments. A within-subject experiment utilizing memory recall tasks was implemented to test three switching modes: seamless switching, passive switching, and switching with feedforward and feedback. Task accuracy rate, perceived interruption, perceived control, and behavioral intention were measured. Results indicated that seamless switching outperformed passive switching in task accuracy rate. Passive switching elicited the highest level of perceived interruption, while switching with feedforward and feedback substantially improved the perceived control of users over seamless switching. The behavioral intention to use seamless switching and switching with feedforward and feedback was considerably higher than that for passive switching. This research provides insights into the comparative benefits of seamless switching and switching with feedforward and feedback, particularly regarding their influence on user perception. Practical implications for the design of interconnected device switching and the management of device ecosystems are also presented.

Additional feedforward mechanism of Parkin activation via binding of phospho-UBL and RING0 in trans.

Loss-of-function Parkin mutations lead to early-onset of Parkinson's disease. Parkin is an auto-inhibited ubiquitin E3 ligase activated by dual phosphorylation of its ubiquitin-like (Ubl) domain and ubiquitin by the PINK1 kinase. Herein, we demonstrate a competitive binding of the phospho-Ubl and RING2 domains towards the RING0 domain, which regulates Parkin activity. We show that phosphorylated Parkin can complex with native Parkin, leading to the activation of autoinhibited native Parkin in trans. Furthermore, we show that the activator element (ACT) of Parkin is required to maintain the enzyme kinetics, and the removal of ACT slows the enzyme catalysis. We also demonstrate that ACT can activate Parkin in trans but less efficiently than when present in the cis molecule. Furthermore, the crystal structure reveals a donor ubiquitin binding pocket in the linker connecting REP and RING2, which plays a crucial role in Parkin activity.

Additional feedforward mechanism of Parkin activation via binding of phospho-UBL and RING0 in trans

Loss-of-function Parkin mutations lead to early-onset of Parkinson’s disease. Parkin is an auto-inhibited ubiquitin E3 ligase activated by dual phosphorylation of its ubiquitin-like (Ubl) domain and ubiquitin by the PINK1 kinase. Herein, we demonstrate a competitive binding of the phospho-Ubl and RING2 domains towards the RING0 domain, which regulates Parkin activity. We show that phosphorylated Parkin can complex with native Parkin, leading to the activation of autoinhibited native Parkin in trans. Furthermore, we show that the activator element (ACT) of Parkin is required to maintain the enzyme kinetics, and the removal of ACT slows the enzyme catalysis. We also demonstrate that ACT can activate Parkin in trans but less efficiently than when present in the cis molecule. Furthermore, the crystal structure reveals a donor ubiquitin binding pocket in the linker connecting REP and RING2, which plays a crucial role in Parkin activity.

Feedforward inhibition of stress by brainstem neuropeptide Y neurons

Resistance to stress is a key determinant for mammalian functioning. While many studies have revealed neural circuits and substrates responsible for initiating and mediating stress responses, little is known about how the brain resists to stress and prevents overreactions. Here, we identified a previously uncharacterized neuropeptide Y (NPY) neuronal population in the dorsal raphe nucleus and ventrolateral periaqueductal gray region (DRN/vlPAG) with anxiolytic effects in male mice. NPYDRN/vlPAG neurons are rapidly activated by various stressful stimuli. Inhibiting these neurons exacerbated hypophagic and anxiety responses during stress, while activation significantly ameliorates acute stress-induced hypophagia and anxiety levels and transmits positive valence. Furthermore, NPYDRN/vlPAG neurons exert differential but synergic anxiolytic effects via inhibitory projections to the paraventricular thalamic nucleus (PVT) and the lateral hypothalamic area (LH). Together, our findings reveal a feedforward inhibition neural mechanism underlying stress resistance and suggest NPYDRN/vlPAG neurons as a potential therapeutic target for stress-related disorders.

Spatial transcriptomic validation of a biomimetic model of fibrosis enables re-evaluation of a therapeutic antibody targeting LOXL2

Matrix stiffening by lysyl oxidase-like 2 (LOXL2)-mediated collagen cross-linking is proposed as a core feedforward mechanism that promotes fibrogenesis. Failure in clinical trials of simtuzumab (the humanized version of AB0023, a monoclonal antibody against human LOXL2) suggested that targeting LOXL2 may not have disease relevance; however, target engagement was not directly evaluated. We compare the spatial transcriptome of active human lung fibrogenesis sites with different human cell culture models to identify a disease-relevant model. Within the selected model, we then evaluate AB0023, identifying that it does not inhibit collagen cross-linking or reduce tissue stiffness, nor does it inhibit LOXL2 catalytic activity. In contrast, it does potently inhibit angiogenesis consistent with an alternative, non-enzymatic mechanism of action. Thus, AB0023 is anti-angiogenic but does not inhibit LOXL2 catalytic activity, collagen cross-linking, or tissue stiffening. These findings have implications for the interpretation of the lack of efficacy of simtuzumab in clinical trials of fibrotic diseases.

An incoherent feed-forward loop involving bHLH transcription factors, Auxin and CYCLIN-Ds regulates style radial symmetry establishment in Arabidopsis.

The bilateral-to-radial symmetry transition occurring during the development of the Arabidopsis thaliana female reproductive organ (gynoecium) is a crucial biological process linked to plant fertilization and seed production. Despite its significance, the cellular mechanisms governing the establishment and breaking of radial symmetry at the gynoecium apex (style) remain unknown. To fill this gap, we employed quantitative confocal imaging coupled with MorphoGraphX analysis, in vivo and in vitro transcriptional experiments, and genetic analysis encompassing mutants in two bHLH transcription factors necessary and sufficient to promote transition to radial symmetry, SPATULA (SPT) and INDEHISCENT (IND). Here, we show that defects in style morphogenesis correlate with defects in cell-division orientation and rate. We showed that the SPT-mediated accumulation of auxin in the medial-apical cells undergoing symmetry transition is required to maintain cell-division-oriented perpendicular to the direction of organ growth (anticlinal, transversal cell division). In addition, SPT and IND promote the expression of specific core cell-cycle regulators, CYCLIN-D1;1 (CYC-D1;1) and CYC-D3;3, to support progression through the G1 phase of the cell cycle. This transcriptional regulation is repressed by auxin, thus forming an incoherent feed-forward loop mechanism. We propose that this mechanism fine-tunes cell division rate and orientation with the morphogenic signal provided by auxin, during patterning of radial symmetry at the style.

Study on phase selection control characteristics of fast vacuum circuit breakers suitable for new power systems

Abstract With a high proportion of new energy access to the power system, the user side of the randomness and volatility of distributed photovoltaic large-capacity access to the 10 kV medium-voltage distribution grid operation results in more frequent fluctuations in the system voltage and more frequent switching of reactive compensation of the shunt capacitor bank on the 10 kV side of the conventional substation. Conventional reactive compensation switching circuit breakers adopt a spring mechanism whose mechanical stability is insufficient and the selection of the relevant fit capacitor bank accuracy is not enough. The 12 kV fast vacuum circuit breaker of small mechanical dispersion for selection related to the combination was proposed. First of all, based on the neutral grounded and ungrounded system of the capacitor bank, the strategy of capacitor bank phase selection closing was developed. For the action characteristics of the phase selection of the 12 kV fast vacuum circuit breaker, the variation laws of mechanical dispersion and the influence factors such as ambient temperature, capacitance voltage, capacitance degradation, mechanical wear, and conductive rod deformation were obtained by simulation and experiment. The results showed that the ambient temperature and capacitance voltage had a great influence on the switching time of the fast circuit breaker, while other factors had a small influence. Again, the pre-breakdown characteristics of the 12 kV fast vacuum circuit breaker were obtained by experiments. The results showed that the influence of contact opening distance and pre-breakdown voltage was a linear relationship, and the pre-breakdown slope was 30 kV/mm. According to the pre-breakdown closing characteristic curve, the pre-breakdown time of the fast circuit breaker was 0.45 ms at most. The feedforward compensation mechanism based on a neural network was proposed to compensate for the action characteristics of the fast circuit breaker and aimed to improve the phase selection accuracy. Finally, two rounds of capacitive current switching tests of 12 kV fast vacuum circuit breakers with C2 level were carried out in a third-party test station. The accuracy of phase closing is within the ±0.5 ms closing window, effectively preventing the occurrence of closing inrush current.

Chronic infusion of the tryptophan metabolite kynurenine increases mean arterial pressure in male Sprague-Dawley rats.

Chronic kidney disease is the loss of renal function that can occur from aging or through a myriad of other disease states. Rising serum concentrations of kynurenine, a tryptophan metabolite, have been shown to correlate with increasing severity of chronic kidney disease. This study used chronic intravenous infusion in conscious male Sprague-Dawley rats to test the hypothesis that kynurenine can induce renal damage and promote alterations in blood pressure, heart rate, and decreased renal function. We found that kynurenine infusion increased mean arterial pressure, increased the maximum and minimum range of heart rate, decreased glomerular filtration rate, and induced kidney damage in a dose-dependent manner. This study shows that kynurenine infusion can promote kidney disease in healthy, young rats, implying that the increase in kynurenine levels associated with chronic kidney disease may establish a feed-forward mechanism that exacerbates the loss of renal function.NEW & NOTEWORTHY In humans, an elevated serum concentration of kynurenine has long been associated with negative outcomes in various disease states as well as in aging. However, it has been unknown whether these increased kynurenine levels are mediating the disorders or simply associated with them. This study shows that chronically infusing kynurenine can contribute to the development of hypertension and kidney impairment. The mechanism of this action remains to be determined in future studies.

Positive feed-forward regulation of nitrate uptake by rice roots and its molecular mechanism

To investigate the positive feed-forward regulatory mechanism of nitrate uptake by rice, its responses to various light and carbohydrates were compared. In order to measure nitrate uptake in real time, the non-invasive method was used. The results showed that net nitrate uptake increased in the light and decreased in the dark, and finally reached a steady state after about 5 h. Based on it, carbohydrates effects could be investigated without considering light effects. After sucrose addition for 2 h, net nitrate uptake increased by about 80% without a lag, while glucose, fructose and raffinose had a slight effect with a lag and other sugars had no effect. It provided an evidence that sucrose was a positive feed-forward signal molecule of nitrate uptake by rice roots. To further analyze the effect of sucrose on the expression of high affinity nitrate transporter genes OsNRT2.1, OsNRT2.2, OsNRT2.3a and OsNRT2.3b, qRT-PCR was used to further verify after treated with 10 mM sucrose. The results revealed that these genes expression was immediately up-regulated, which indicated that these genes were post transcriptionally regulated. Further, 15N exchange dynamics analyzed N transport. It is benefit for increasing nitrate uptake by rice and improving its yield.

Enhancing the load ramp-up capability of the subcritical CFB power unit by considering the evolution of internal stored energy

The substantial inertia of the boiler restricts the flexibility of circulating fluidized bed (CFB) power units. To enhance the load ramp-up capability of the CFB power unit, we proposed a novel control strategy considering the spatial-temporal evolution of its internal stored energy. A dynamic model of the subcritical CFB power unit with a capacity of 300 MW was developed, incorporating the mechanism and control modules. By analyzing the spatial-temporal evolution of the stored energy in bed material, flue gases, refractory materials, economizer, evaporation subsystem, superheater subsystem, reheater subsystem, and turbine subsystem, we identified that the over-utilization of chemical and thermal stored energy in the bed materials is the primary factor restricting load ramp-up, while the thermal stored energy of the economizer is suitable for further utilization. Under the optimized control strategy that utilizes deviations of stored energy per mass of bed materials as a feedforward mechanism, the deviations of the key operating parameters during the load ramp-up process are significantly reduced, and the load ramp-up rate of the subcritical CFB power unit can be improved from 2.0 % Pe/min to 3.0 % Pe/min.

Act1 drives chemoresistance via regulation of antioxidant RNA metabolism and redox homeostasis.

The IL-17 receptor adaptor molecule Act1, an RNA-binding protein, plays a critical role in IL-17-mediated cancer progression. Here, we report a novel mechanism of how IL-17/Act1 induces chemoresistance by modulating redox homeostasis through epitranscriptomic regulation of antioxidant RNA metabolism. Transcriptome-wide mapping of direct Act1-RNA interactions revealed that Act1 binds to the 5'UTR of antioxidant mRNAs and Wilms' tumor 1-associating protein (WTAP), a key regulator in m6A methyltransferase complex. Strikingly, Act1's binding sites are located in proximity to m6A modification sites, which allows Act1 to promote the recruitment of elF3G for cap-independent translation. Loss of Act1's RNA binding activity or Wtap knockdown abolished IL-17-induced m6A modification and translation of Wtap and antioxidant mRNAs, indicating a feedforward mechanism of the Act1-WTAP loop. We then developed antisense oligonucleotides (Wtap ASO) that specifically disrupt Act1's binding to Wtap mRNA, abolishing IL-17/Act1-WTAP-mediated antioxidant protein production during chemotherapy. Wtap ASO substantially increased the antitumor efficacy of cisplatin, demonstrating a potential therapeutic strategy for chemoresistance.

Unveiling the neural dynamics of conscious perception in rapid object recognition

Our brain excels at recognizing objects, even when they flash by in a rapid sequence. However, the neural processes determining whether a target image in a rapid sequence can be recognized or not remains elusive. We used electroencephalography (EEG) to investigate the temporal dynamics of brain processes that shape perceptual outcomes in these challenging viewing conditions. Using naturalistic images and advanced multivariate pattern analysis (MVPA) techniques, we probed the brain dynamics governing conscious object recognition. Our results show that although initially similar, the processes for when an object can or cannot be recognized diverge around 180 ms post-appearance, coinciding with feedback neural processes. Decoding analyses indicate that gist perception (partial conscious perception) can occur at ∼120 ms through feedforward mechanisms. In contrast, object identification (full conscious perception of the image) is resolved at ∼190 ms after target onset, suggesting involvement of recurrent processing. These findings underscore the importance of recurrent neural connections in object recognition and awareness in rapid visual presentations.

Neuronal activity-driven O-GlcNAcylation promotes mitochondrial plasticity

Neuronal activity is an energy-intensive process that is largely sustained by instantaneous fuel utilization and ATP synthesis. However, how neurons couple ATP synthesis rate to fuel availability is largely unknown. Here, we demonstrate that the metabolic sensor enzyme O-linked N-acetyl glucosamine (O-GlcNAc) transferase regulates neuronal activity-driven mitochondrial bioenergetics in hippocampal and cortical neurons. We show that neuronal activity upregulates O-GlcNAcylation in mitochondria. Mitochondrial O-GlcNAcylation is promoted by activity-driven glucose consumption, which allows neurons to compensate for high energy expenditure based on fuel availability. To determine the proteins that are responsible for these adjustments, we mapped the mitochondrial O-GlcNAcome of neurons. Finally, we determine that neurons fail to meet activity-driven metabolic demand when O-GlcNAcylation dynamics are prevented. Our findings suggest that O-GlcNAcylation provides a fuel-dependent feedforward control mechanism in neurons to optimize mitochondrial performance based on neuronal activity. This mechanism thereby couples neuronal metabolism to mitochondrial bioenergetics and plays a key role in sustaining energy homeostasis.

Cortical responses to looming sources are explained away by the auditory periphery

A wealth of behavioral evidence indicate that sounds with increasing intensity (i.e. appear to be looming towards the listener) are processed with increased attentional and physiological resources compared to receding sounds. However, the neurophysiological mechanism responsible for such cognitive amplification remains elusive. Here, we show that the large differences seen between cortical responses to looming and receding sounds are in fact almost entirely explained away by nonlinear encoding at the level of the auditory periphery. We collected electroencephalography (EEG) data during an oddball paradigm to elicit mismatch negativity (MMN) and others Event Related Potentials (EPRs), in response to deviant stimuli with both dynamic (looming and receding) and constant level (flat) differences to the standard in the same participants. We then combined a computational model of the auditory periphery with generative EEG methods (temporal response functions, TRFs) to model the single-participant ERPs responses to flat deviants, and used them to predict the effect of the same mechanism on looming and receding stimuli. The flat model explained 45% variance of the looming response, and 33% of the receding response. This provide striking evidence that difference wave responses to looming and receding sounds result from the same cortical mechanism that generate responses to constant-level deviants: all such differences are the sole consequence of their particular physical morphology getting amplified and integrated by peripheral auditory mechanisms. Thus, not all effects seen cortically proceed from top-down modulations by high-level decision variables, but can rather be performed early and efficiently by feed-forward peripheral mechanisms that evolved precisely to sparing subsequent networks with the necessity to implement such mechanisms.

Schwann cell TRPA1 elicits reserpine-induced fibromyalgia pain in mice.

Fibromyalgia is a complex clinical disorder with an unknown aetiology, characterized by generalized pain and co-morbid symptoms such as anxiety and depression. An imbalance of oxidants and antioxidants is proposed to play a pivotal role in the pathogenesis of fibromyalgia symptoms. However, the precise mechanisms by which oxidative stress contributes to fibromyalgia-induced pain remain unclear. The transient receptor potential ankyrin 1 (TRPA1) channel, known as both a pain sensor and an oxidative stress sensor, has been implicated in various painful conditions. The feed-forward mechanism that implicates reactive oxygen species (ROS) driven by TRPA1 was investigated in a reserpine-induced fibromyalgia model in C57BL/6J mice employing pharmacological interventions and genetic approaches. Reserpine-treated mice developed pain-like behaviours (mechanical/cold hypersensitivity) and early anxiety-depressive-like disorders, accompanied by increased levels of oxidative stress markers in the sciatic nerve tissues. These effects were not observed upon pharmacological blockade or global genetic deletion of the TRPA1 channel and macrophage depletion. Furthermore, we demonstrated that selective silencing of TRPA1 in Schwann cells reduced reserpine-induced neuroinflammation (NADPH oxidase 1-dependent ROS generation and macrophage increase in the sciatic nerve) and attenuated fibromyalgia-like behaviours. Activated Schwann cells expressing TRPA1 promote an intracellular pathway culminating in the release of ROS and recruitment of macrophages in the mouse sciatic nerve. These cellular and molecular events sustain mechanical and cold hypersensitivity in the reserpine-evoked fibromyalgia model. Targeting TRPA1 channels on Schwann cells could offer a novel therapeutic approach for managing fibromyalgia-related behaviours.

Nonuniform and pathway-specific laminar processing of spatial frequencies in the primary visual cortex of primates

The neocortex comprises six cortical layers that play a crucial role in information processing; however, it remains unclear whether laminar processing is consistent across all regions within a single cortex. In this study, we demonstrate diverse laminar response patterns in the primary visual cortex (V1) of three male macaque monkeys when exposed to visual stimuli at different spatial frequencies (SFs). These response patterns can be categorized into two groups. One group exhibit suppressed responses in the output layers for all SFs, while the other type shows amplified responses specifically at high SFs. Further analysis suggests that both magnocellular (M) and parvocellular (P) pathways contribute to the suppressive effect through feedforward mechanisms, whereas amplification is specific to local recurrent mechanisms within the parvocellular pathway. These findings highlight the non-uniform distribution of neural mechanisms involved in laminar processing and emphasize how pathway-specific amplification selectively enhances representations of high-SF information in primate V1.

Enhancing Soil Moisture Forecasting Accuracy with REDF-LSTM: Integrating Residual En-Decoding and Feature Attention Mechanisms

This study introduces an innovative deep learning model, Residual-EnDecode-Feedforward Attention Mechanism-Long Short-Term Memory (REDF-LSTM), designed to overcome the high uncertainty challenges faced by traditional soil moisture prediction methods. The REDF-LSTM model, by integrating a residual learning encoder–decoder LSTM layer, enhanced LSTM layers, and feedforward attention, not only captures the deep features of time series data but also optimizes the model’s ability to identify key influencing factors, including land surface features, atmospheric conditions, and other static environmental variables. Unlike existing methods, the innovation of this model lies in its first-time combination of the residual learning encoder–decoder and feedforward attention mechanisms in the soil moisture prediction field. It delves into the complex patterns of time series through the encoder–decoder structure and accurately locates key influencing factors through the feedforward attention mechanism, significantly improving predictive performance. The choice to combine the feedforward attention mechanism and encoder–decoder with the LSTM model is to fully leverage their advantages in processing complex data sequences and enhancing the model’s focus on important features, aiming for more accurate soil moisture prediction. After comparison with current advanced models such as EDLSTM, FAMLSTM, and GANBiLSTM, our REDF-LSTM demonstrated the best performance. Compared to traditional LSTM models, it achieved an average improvement of 13.07% in R2, 20.98% in RMSE, 24.86% in BIAS, and 11.1% in KGE key performance indicators, fully proving its superior predictive capability and potential application value in precision agriculture and ecosystem management.