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Background Particulate matter (PM) refers to solid or liquid particles suspended in the atmosphere. These particles can be inhaled during normal respiration, leading to various respiratory diseases including upper respiratory tract infections (URTIs). We comprehensively evaluated the ambient particulate matter pollution-related disease burden. Methods Due to the particularity of Global Burden of Disease 2021 study (GBD 2021), this study only included data on URTIs attributed to PM, and the age limit was under 5 years old. We first assessed the global and subtype-specific mortality, disability-adjusted life years (DALYs), years lived with disability (YLDs), and years of life lost (YLLs) in 2021, along with their age-standardized rates. Additionally, linear regression models were employed to analyze temporal trends in disease burden. We will calculate the corresponding estimated annual percentage change (EAPC) based on the changes in the number of deaths, DALYs and the age-standardized data of both from 1990 to 2021. Cluster analysis was used to examine regional variations in disease burden across Global Burden of Disease study regions. Finally, ARIMA and exponential smoothing (ES) models were applied to forecast disease burden over the next 25 years. Results For indoor PM pollution, in 2021, there were 93.98 deaths per 100,000 population and 9,195.39 DALYs globally in children under 5 years of age. Females exhibited higher risks than males, and regions with a low sociodemographic index (SDI) faced elevated risks. Significant disparities in disease burden were observed across GBD regions and nations. Compared to 1990, mortality and DALYs per 100,000 population declined by 52.28% and 51.38%, respectively. ARIMA projections suggest continued declines in the absolute number of mortality and DALYs for both sexes by 2050, though age-standardized rates may increase for males while decreasing for females. For outdoor PM pollution, 2021 recorded 22.58 deaths per 100,000 population and 2,511.13 DALYs globallyin children under 5 years of age. Females and low-middle SDI regions were at higher risk. Mortality and DALYs per 100,000 population decreased by 55.10% and 48.37% compared to 1990. ARIMA forecasts indicate further reductions in mortality, DALYs, and age-standardized rates for both sexes by 2050. Conclusion Particulate pollutants, particularly indoor PM, pose a significant global public health threat. Tailored strategies based on national conditions are urgently needed to mitigate their impact.

Aging increases the risk for Alzheimer’s disease (AD), driving pathological changes like amyloid-β (Aβ) buildup, inflammation, and oxidative stress, especially in the prefrontal cortex (PFC). We present the first subcellular-resolution spatial transcriptome atlas of the human prefrontal cortex (PFC), generated with Stereo-seq from six male AD cases at varying neuropathological stages and six age-matched male controls. Our analyses revealed distinct transcriptional alterations across PFC layers, highlighted disruptions in laminar structure, and exposed AD-related shifts in layer-to-layer and cell-cell interactions. Notably, we identified genes highly upregulated in stressed neurons and nearby glial cells, where AD diminished stress-response interactions that promote Aβ clearance. Further, cell-type-specific co-expression analysis highlighted three neuronal modules linked to neuroprotection, protein dephosphorylation, and Aβ regulation, with all modules downregulated as AD progresses. We identified ZNF460 as a transcription factor regulating these modules, offering a potential therapeutic target. In summary, this spatial transcriptome atlas provides valuable insight into AD’s molecular mechanisms. Aging increases the risk for Alzheimer’s disease (AD). Here, the authors present a spatial transcriptome atlas of the human prefrontal cortex in AD, revealing distinct transcriptional alterations.

Parkinson's disease (PD) is characterized by age-dependent neurodegeneration and the accumulation of toxic phosphorylated α-synuclein (pS129-α-syn). The mechanisms underlying these crucial pathological changes remain unclear. Mutations in parkin RBR E3 ubiquitin protein ligase (PARK2), the gene encoding parkin that is phosphorylated by PTEN-induced putative kinase 1 (PINK1) to participate in mitophagy, cause early onset PD. However, current parkin-KO mouse and pig models do not exhibit neurodegeneration. In the current study, we utilized CRISPR/Cas9 technology to establish parkin-deficient monkey models at different ages. We found that parkin deficiency leads to substantia nigra neurodegeneration in adult monkey brains and that parkin phosphorylation decreases with aging, primarily due to increased insolubility of parkin. Phosphorylated parkin is important for neuroprotection and the reduction of pS129-α-syn. Consistently, overexpression of WT parkin, but not a mutant form that cannot be phosphorylated by PINK1, reduced the accumulation of pS129-α-syn. These findings identify parkin phosphorylation as a key factor in PD pathogenesis and suggest it as a promising target for therapeutic interventions.

In this paper, a room-temperature sulfur dioxide (SO2) gas sensor based on a TiO2/reduced graphene oxide/graphene (TiO2/rGO/G) composite structure was fabricated. The material was synthesized by a simple hydrothermal method, and X-ray photoelectron spectroscopy (XPS) characterization confirmed the successful preparation of TiO2 and the effective reduction of rGO. Under 365 nm ultraviolet light irradiation, the sensor exhibited rapid response characteristics to 200 ppm SO2 gas at room temperature, with response and recovery times of 147 seconds and 19 seconds, respectively, and a sensitivity of 63.84%. It also demonstrated excellent repeatability and long-term stability. The sensing mechanism can be attributed to the fact that graphene and reduced graphene oxide provide channels and adsorption sites for gas transmission, while TiO2 generates photogenerated carriers under ultraviolet light excitation, effectively regulating the interfacial charge distribution and surface reactivity, thereby enhancing the adsorption capacity for SO2 gas. This study provides a new approach for developing room-temperature SO2-sensitive materials with photo-enhanced response characteristics and high efficiency and low power consumption.

Currently, since the model of a driverless bus is not clear, it is difficult for most traditional path tracking methods to achieve a trade-off between accuracy and stability, especially in the case of driverless buses. In terms of solving this problem, a path-tracking controller based on a Fuzzy Pure Pursuit Control with a Front Axle Reference (FPPC-FAR) is proposed in this paper. Firstly, the reference point of Pure Pursuit is moved from the rear axle to the front axle. It relieves the influence caused by the ignorance of the bus’s lateral dynamic characteristics and improves the stability of Pure Pursuit. Secondly, a fuzzy parameter self-tuning method is applied to improve the accuracy and robustness of the path-tracking controller. Thirdly, a feedback-feedforward control algorithm is devised for velocity control, which enhances the velocity tracking efficiency. The proportional-integral (PI) controller is indicated for feedback control, and the gravity acceleration component in the car’s forward direction is used in feedforward control. Finally, a series of experiments is conducted to illustrate the excellent performances of proposed methods.

Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular disease that usually has a poor prognosis. Heat shock proteins (HSPs) have been implicated in the mechanisms of SAH-associated damage, including increased inflammation and reduced neurogenesis. The aim of this study was to investigate the effects of HSP90 inhibition on inflammation and neurogenesis in a mouse model of experimental SAH induced by endovascular surgery. Western blotting showed HSP90 levels to be decreased, while neurogenesis, evaluated by 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry, was decreased in the hippocampuses of SAH mice. SAH also induced pro-inflammatory factors such as interleukin-1β (IL-1β), capase-1 and the NLRP3 inflammasome. However, intraperitoneal administration of the specific HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) reduced the levels of HSP90, NLRP3, ASC, caspase-1 and IL-1β, while increasing the levels of brain-derived neurotrophic factor and doublecortin (DCX), as well as the number of BrdU-positive cells in SAH mice. In addition, 17-AGG improved short- and long-term neurobehavioral outcomes. The neuroprotective and anti-inflammatory effects of 17-AGG were reversed by recombinant HSP90 (rHSP90); this detrimental effect of HSP90 was inhibited by the specific P2X7 receptor (P2X7R) inhibitor A438079, indicating that SAH-induced inflammation and inhibition of neurogenesis were likely mediated by HSP90 and the P2X7R/NLRP3 inflammasome pathway. HSP90 inhibition by 17-AAG may be a promising therapeutic strategy for the treatment of SAH.

Background Alopecia areata (AA) is a common autoimmune hair loss disease with increasing incidence. Corticosteroids are the most widely used for hair loss treatment; however, long-term usage of hormonal drugs is associated with various side effects. Mesenchymal stem cells (MSCs) therapy has been studied extensively to curb autoimmune diseases without affecting immunity against diseases. Methods Hair follicle-derived MSCs (HF-MSCs) were harvested from the waste material of hair transplants, isolated and expanded. The therapeutic effect of HF-MSCs for AA treatment was investigated in vitro AA-like hair follicle organ model and in vivo C3H/HeJ AA mice model. Results AA-like hair follicle organ in vitro model was successfully established by pre-treatment of mouse vibrissa follicles by interferon-γ (IFN-γ). The AA-like symptoms were relieved when IFN-γ induced AA in vitro model was co-cultured with HF-MSC for 2 days. In addition, when skin grafted C3H/HeJ AA mice models were injected with 10 6 HF-MSCs once a week for 3 weeks, the transcription profiling and immunofluorescence analysis depicted that HF-MSCs treatment significantly decreased mouse hair loss and reduced inflammation around HF both in vitro and in vivo. Conclusions This study provides a new therapeutic approach for alopecia areata based on HF-MSCs toward its future clinical application.

A framework of path planning for autonomous electric bus is presented. ArcGIS platform is utilized for map-building and global path planning. Firstly, a high-precision map is built based on GPS in ArcGIS for global planning. Then the global optimal path is obtained by network analysis tool in ArcGIS. To facilitate local planning, WGS-84 coordinates in the map are converted to local coordinates. Secondly, a double-layer finite state machine (FSM) is devised to plan driving behavior under different driving scenarios, such as structured driving, lane changing, turning, and so on. Besides, local optimal trajectory is generated by cubic polynomial, which takes full account of the safety and kinetics of the electric bus. Finally, the simulation results show that the framework is reliable and feasible for driving behavior planning and trajectory generation. Furthermore, its validity is proven with an autonomous bus platform 12 m in length.

Microbial communities in sediments play an important role in alpine lake ecosystems. However, the microbial diversity and community composition of alpine lake sediments from the Hengduan Mountains remain largely unknown. Therefore, based on the Illumina MiSeq platform, high‐throughput sequencing analysis of the 16S rRNA gene was performed on 15 alpine lake sediments collected at different locations in the Hengduan Mountains. The abundance‐based coverage estimate (ACE), Chao1, and Shannon indices indicated that the microbial abundance and diversity of these sediments were high. There are some differences in the composition of microbial communities among sediments. However, in general, Proteobacteria accounted for the largest proportion of all sediments (22.3%–67.6%) and was the dominant phylum. Followed by Bacteroidetes, Acidobacteria, Chloroflexi, and Planctomycetes. In addition, the operational taxonomic unit (OTU) interactions network had modular structures and suggested more cooperation than competition in the microbial community. Besides, we also found that temperature has a significant contribution to the sample–environment relationship. This study revealed the diversity and composition of microbial communities in alpine lake sediments from the Hengduan Mountains, and describe the correlation between microbial community structure and different environmental variables. This study is the first to describe the microbial diversity and composition of sediments from 15 alpine lakes in the Hengduan Mountains. This study is a significant work, revealing the unknown bacterial communities in sediments of different alpine lakes, and interpreting the relationship between microbial diversity and composition and environmental variables.

There are no effective curative treatments for Alzheimer's disease (AD), the most prevalent form of dementia. Amyloid‐beta (Aβ) oligomers are considered key neurotoxic molecules that trigger AD. Recent studies have shown that direct antibody targeting of Aβ oligomers is beneficial for early AD patients; however, serious side effects (e.g., brain hemorrhage, edema, and shrinkage) persist. Considering that Aβ oligomers readily bind to other proteins, contributing to neurotoxicity and AD onset, those proteins could represent alternative therapeutic targets. However, proteins that bind to Aβ oligomers in the brains of AD patients have not yet been identified. In this study, we identified four proteins (DDX6, DSP, JUP, and HRNR) that bind to Aβ oligomers derived from the brains of AD patients. Intriguingly, among these four proteins, only the blockade of DEAD‐box helicase 6 (DDX6) in human‐derived Aβ oligomers attenuated their neurotoxicity both in vitro and in vivo. Mechanistic analysis revealed that DDX6 promotes the formation of Aβ oligomers, likely due to DDX6 bind to Aβ oligomers at four distinct sites. These findings suggest that DDX6 could serve as a potential therapeutic target to reduce the neurotoxicity of Aβ oligomers in the brain and prevent the progression of AD. We identified four proteins (DSP, JUP, HRNR, and DDX6) that bind to amyloid‐beta (Aβ) oligomers derived from the brains of Alzheimer's disease (AD) patients. Among these four proteins, only the blockade of DEAD‐box helicase 6 (DDX6) in AD brain‐derived Aβ oligomers attenuated their neurotoxicity. Mechanistic analysis showed that DDX6 promotes the formation of Aβ oligomers, likely due to DDX6 bind to Aβ oligomers at four distinct sites. Thus, DDX6 could serve as a therapeutic target for efforts to reduce the neurotoxicity of Aβ oligomers in the brain and prevent subsequent development of AD.