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Background Parkinson’s disease (PD) is characterized by dopaminergic neuronal loss in the substantia nigra pars compacta and intracellular inclusions called Lewy bodies (LB). During the course of disease, misfolded α-synuclein, the major constituent of LB, spreads to different regions of the brain in a prion-like fashion, giving rise to successive non-motor and motor symptoms. Etiology is likely multifactorial, and involves interplay among aging, genetic susceptibility and environmental factors. Main body The prevalence of PD rises exponentially with age, and aging is associated with impairment of cellular pathways which increases susceptibility of dopaminergic neurons to cell death. However, the majority of those over the age of 80 do not have PD, thus other factors in addition to aging are needed to cause disease. Discovery of neurotoxins which can result in parkinsonism led to efforts in identifying environmental factors which may influence PD risk. Nevertheless, the causality of most environmental factors is not conclusively established, and alternative explanations such as reverse causality and recall bias cannot be excluded. The lack of geographic clusters and conjugal cases also go against environmental toxins as a major cause of PD. Rare mutations as well as common variants in genes such as SNCA, LRRK2 and GBA are associated with risk of PD, but Mendelian causes collectively only account for 5% of PD and common polymorphisms are associated with small increase in PD risk. Heritability of PD has been estimated to be around 30%. Thus, aging, genetics and environmental factors each alone is rarely sufficient to cause PD for most patients. Conclusion PD is a multifactorial disorder involving interplay of aging, genetics and environmental factors. This has implications on the development of appropriate animal models of PD which take all these factors into account. Common converging pathways likely include mitochondrial dysfunction, impaired autophagy, oxidative stress and neuroinflammation, which are associated with the accumulation and spread of misfolded α-synuclein and neurodegeneration. Understanding the mechanisms involved in the initiation and progression of PD may lead to potential therapeutic targets to prevent PD or modify its course.

An extended (3+1)-dimensional Kadomtsev–Petviashvili–Boussinesq equation is studied in this paper to construct periodic solution, n -soliton solution and folded localized excitation. Firstly, with the help of the Hirota’s bilinear method and ansatz, some periodic solutions have been derived. Secondly, taking Burgers equation as an auxiliary function, we have obtained n -soliton solution and n -shock wave. Lastly, we present a new variable separation method for (3+1)-dimensional and higher dimensional models, and use it to derive localized excitation solutions. To be specific, we have constructed various novel structures and discussed the interaction dynamics of folded solitary waves. Compared with the other methods, the variable separation solutions obtained in this paper not only directly give the analytical form of the solution u instead of its potential u y , but also provide us a straightforward approach to construct localized excitation for higher order dimensional nonlinear partial differential equation.

The dermal fibroblast is a crucial executor involved in wound healing, and lipopolysaccharide is a key factor in initiating the migration and proliferation of the dermal fibroblasts, followed by wound healing. However, the underlying molecular mechanism is still unknown. In this study, we demonstrated that stathmin increased concomitantly with p38/MAPK pathway activation by lipopolysaccharide stimulation of the human dermal fibroblast (HDF), which induced microtubule (MT) depolymerization followed by increased HDF migration and proliferation. In contrast, the application of taxol, the small interfering RNA transfection of stathmin, or the application of the p38/MAPK inhibitor SB203580 suppressed MT depolymerization and HDF migration and proliferation. Additionally, the overexpression of a MKK6(Glu) mutant, which constitutively activated p38/MAPK, resulted in MT depolymerization and, subsequently, promoted HDF migration and proliferation. Our data reveal a crucial role of stathmin in HDF migration and proliferation. These findings will provide new targets and strategies for clinical interventions in wound healing.

Nowadays, with the rapid development of consumer Unmanned Aerial Vehicles (UAVs), utilizing UAV platforms for visual surveillance has become very attractive, and a key part of this is remote vision-based pedestrian attribute recognition. Pedestrian Attribute Recognition (PAR) is dedicated to predicting multiple attribute labels of a single pedestrian image extracted from surveillance videos and aerial imagery, which presents significant challenges in the computer vision community due to factors such as poor imaging quality and substantial pose variations. Despite recent studies demonstrating impressive advancements in utilizing complicated architectures and exploring relations, most of them may fail to fully and systematically consider the inter-region, inter-attribute, and region-attribute mapping relations simultaneously and be stuck in the dilemma of information redundancy, leading to the degradation of recognition accuracy. To address the issues, we construct a novel Mask-Relation-Guided Transformer (MRG-T) framework that consists of three relation modeling modules to fully exploit spatial and semantic relations in the model learning process. Specifically, we first propose a Masked Region Relation Module (MRRM) to focus on precise spatial attention regions to extract more robust features with masked random patch training. To explore the semantic association of attributes, we further present a Masked Attribute Relation Module (MARM) to extract intrinsic and semantic inter-attribute relations with an attribute label masking strategy. Based on the cross-attention mechanism, we finally design a Region and Attribute Mapping Module (RAMM) to learn the cross-modal alignment between spatial regions and semantic attributes. We conduct comprehensive experiments on three public benchmarks such as PETA, PA-100K, and RAPv1, and conduct inference on a large-scale airborne person dataset named PRAI-1581. The extensive experimental results demonstrate the superior performance of our method compared to state-of-the-art approaches and validate the effectiveness of mask-relation-guided modeling in the remote vision-based PAR task.

Formyl peptide receptors (FPRs) are a group of G protein-coupled cell surface receptors that play important roles in host defense and inflammation. Owing to the ubiquitous expression of FPRs throughout different cell types and since they interact with structurally diverse chemotactic agonists, they have a dual function in inflammatory processes, depending on binding with different ligands so that accelerate or inhibit key intracellular kinase-based regulatory pathways. Neuroinflammation is closely associated with the pathogenesis of neurodegenerative diseases, neurogenic tumors and cerebrovascular diseases. From recent studies, it is clear that FPRs are important biomarkers for neurological diseases as they regulate inflammatory responses by monitoring glial activation, accelerating neural differentiation, regulating angiogenesis, and controlling blood brain barrier (BBB) permeability, thereby affecting neurological disease progression. Given the complex mechanisms of neurological diseases and the difficulty of healing, we are eager to find new and effective therapeutic targets. Here, we review recent research about various mechanisms of the effects generated after FPR binding to different ligands, role of FPRs in neuroinflammation as well as the development and prognosis of neurological diseases. We summarize that the FPR family has dual inflammatory functional properties in central nervous system. Emphasizing that FPR2 acts as a key molecule that mediates the active resolution of inflammation, which binds with corresponding receptors to reduce the expression and activation of pro-inflammatory composition, govern the transport of immune cells to inflammatory tissues, and restore the integrity of the BBB. Concurrently, FPR1 is essentially related to angiogenesis, cell proliferation and neurogenesis. Thus, treatment with FPRs-modulation may be effective for neurological diseases.

Exposure to ultraviolet light can cause oxidative damage and accelerate skin aging and is one of the main causes of skin aging. Peach gum polysaccharide (PG) is a natural edible plant component that has many biological activities, such as regulating blood glucose and blood lipids and improving colitis, as well as antioxidant and anticancer properties. However, there are few reports on the antiphotoaging effect of peach gum polysaccharide. Therefore, in this paper, we study the basic composition of the raw material peach gum polysaccharide and its ability to improve UVB-induced skin photoaging damage in vivo and in vitro. The results show that peach gum polysaccharide is mainly composed of mannose, glucuronic acid, galactose, xylose, and arabinose, and its molecular weight (Mw) is 4.10 × 106 g/mol. The results of the in vitro cell experiments show that PG could significantly alleviate UVB-induced apoptosis of human skin keratinocytes, promote cell growth repair, reduce the expression of intracellular oxidative factors and matrix metal collagenase, and improve the extent of oxidative stress repair. Moreover, the results from the in vivo animal experiments showed that PG could not only effectively improve the phenotype of UVB-induced photoaged skin in model mice but also significantly improve their oxidative stress status, regulate the contents of ROS and the levels of SOD and CAT, and repair the oxidative skin damage induced by UVB in vivo. In addition, PG improved UVB-induced photoaging-mediated collagen degradation in mice by inhibiting the secretion of matrix metalloproteinases. The above results indicate that peach gum polysaccharide has the ability to repair UVB-induced photoaging and may be used as a potential drug and antioxidant functional food to resist photoaging in the future.

This paper takes corporate social responsibility goodwill and consumers’ reference low-carbon level as endogenous variables of joint carbon emission reduction in the “supplier–manufacturer–retailer–consumer” supply chain system. The joint carbon emission reduction strategies of this four-tier system are analyzed from a dynamic perspective by considering random factors that affect the endogenous variables. Three stochastic differential games are proposed to examine the mechanism between each player, namely the cooperative model, Nash non-cooperative model, and Stackelberg master–slave model. Compared to the Nash non-cooperative game, the manufacturer/supplier-led Stackelberg master–slave game leads to Pareto improvement in the profits of the entire supply chain system and each player. The cooperative game demonstrates the highest expected emission reduction and corporate social responsibility goodwill, but also the highest variance. More importantly, the reference low-carbon level embraces consumers’ subjective initiative in the dynamic of carbon emission reduction. This level is an internal benchmark used to compare against the observed low-carbon level. This paper provides a theoretical foundation for strategic decision-making in emission reduction, contributing to sustainable development. By addressing environmental, economic, and social sustainability, it promotes climate action through carbon reduction strategies and offers policy recommendations aligned with the Sustainable Development Goals.

Anthocyanins and flavonols have vital roles in flower coloration, plant development, and defense. Because anthocyanins and flavonols share the same subcellular localization and common biosynthetic substrates, these pathways may compete for substrates. However, the mechanism regulating this potential competition remains unclear. Here, we identified GhMYB1a, an R2R3-MYB transcription factor involved in the regulation of anthocyanin and flavonol accumulation in gerbera ( Gerbera hybrida ). GhMYB1a shares high sequence similarity with that of other characterized regulators of flavonol biosynthesis. In addition, GhMYB1a is also phylogenetically grouped with these proteins. The overexpression of GhMYB1a in gerbera and tobacco ( Nicotiana tabacum ) resulted in decreased anthocyanin accumulation and increased accumulation of flavonols by upregulating the structural genes involved in flavonol biosynthesis. We further found that GhMYB1a functions as a homodimer instead of interacting with basic helix-loop-helix cofactors. These results suggest that GhMYB1a is involved in regulating the anthocyanin and flavonol metabolic pathways through precise regulation of gene expression. The functional characterization of GhMYB1a provides insight into the biosynthesis and regulation of flavonols and anthocyanins.

Cell expansion is a key determinant for the final size and shape of plant organ, and is regulated by various phytohormones. Zinc finger proteins (ZFPs) consist of a superfamily involved in multiple aspects of organ morphogenesis. However, little is known about WIP-type ZFP function in phytohormone-mediated organ growth. Using reverse genetics, RNA-seq and phytohormone quantification, we elucidated the role of a new WIP-type ZFP from Gerbera hybrida, GhWIP2, in controlling organ growth via regulation of cell expansion. GhWIP2 localizes to the nucleus and acts as a transcriptional repressor. Constitutive overexpression of GhWIP2 (GhWIP2OE) in both Gerbera and Arabidopsis thaliana caused major developmental defects associated with cell expansion, including dwarfism, short petals, scapes, and petioles. Furthermore, GhWIP2OE plants were hypersensitive to GA, but not to ABA, and showed a reduction in endogenous GA and auxin, but not ABA concentrations. Consistent with these observations, RNA-seq analysis revealed that genes involved in GA and auxin signaling were down-regulated, while those involved in ABA signaling were upregulated in GhWIP2OE plants. Our findings suggest that GhWIP2 acts as a transcriptional repressor, suppressing cell expansion during organ growth by modulating crosstalk between GA, ABA, and auxin.

Background Bulimia nervosa (BN) is a psychiatric disorder with unclear pathophysiology. Several studies have associated BN with structural and functional changes in the brain, but findings have been inconsistent. Here we explored this potential association in a small group of Chinese women with BN. Methods This retrospective study examined 34 women with BN and 34 age-matched healthy controls, all of whom underwent T1-weighted magnetic resonance imaging (MRI). Voxel-based morphometry was carried out to explore alterations in regional grey matter volume (GMV) that may be associated with BN. Results The BN group showed smaller GMV in the left medial superior frontal gyrus (SFGmed.L), right superior temporal gyrus (STG.R), right median cingulate and paracingulate gyri (DCG.R), left median cingulate and paracingulate gyri (DCG.L) and left dorsolateral superior frontal gyrus (SFGdor.L). No regions showing GMV increases in BN were identified. The GMV reduction did not correlate with body mass index, duration of illness, or patients’ self-esteem or overall self-evaluation. GMV reduction correlated negatively with age in the SFGmed. L (r = − 0.516, P  < 0.005), DCG. R (r = − 0.556, P < 0.005), DCG. L (r = − 0.576, P  < 0.05) and SFGdor. L (r = − 0.576, P < 0.005). Conclusions Women with BN show reduced GMV in several brain regions, but it is difficult to know whether these changes are the result of BN pathology or of binge-eating and compensatory behavior. These changes may be associated with impaired inhibitory control, body dissatisfaction and emotion dysregulation.