AFTR: A Robustness Multi-Sensor Fusion Model for 3D Object Detection Based on Adaptive Fusion Transformer.

Multi-modal sensors are the key to ensuring the robust and accurate operation of autonomous driving systems, where LiDAR and cameras are important on-board sensors. However, current fusion methods face challenges due to inconsistent multi-sensor data representations and the misalignment of dynamic scenes. Specifically, current fusion methods either explicitly correlate multi-sensor data features by calibrating parameters, ignoring the feature blurring problems caused by misalignment, or find correlated features between multi-sensor data through global attention, causing rapidly escalating computational costs. On this basis, we propose a transformer-based end-to-end multi-sensor fusion framework named the adaptive fusion transformer (AFTR). The proposed AFTR consists of the adaptive spatial cross-attention (ASCA) mechanism and the spatial temporal self-attention (STSA) mechanism. Specifically, ASCA adaptively associates and interacts with multi-sensor data features in 3D space through learnable local attention, alleviating the problem of the misalignment of geometric information and reducing computational costs, and STSA interacts with cross-temporal information using learnable offsets in deformable attention, mitigating displacements due to dynamic scenes. We show through numerous experiments that the AFTR obtains SOTA performance in the nuScenes 3D object detection task (74.9% NDS and 73.2% mAP) and demonstrates strong robustness to misalignment (only a 0.2% NDS drop with slight noise). At the same time, we demonstrate the effectiveness of the AFTR components through ablation studies. In summary, the proposed AFTR is an accurate, efficient, and robust multi-sensor data fusion framework.

Inhibition of the Occurrence and Development of Inflammation-Related Colorectal Cancer by Fucoidan Extracted from Sargassum fusiforme.

Fucoidan has many biological activities, including the inhibitory effect on the development of various cancer types. This study showed that lipopolysaccharide-induced inflammation in FHC cells (normal human colonic epithelial cells) could be reversed using fucoidan at different concentrations. The fucoidan-induced anti-inflammatory effect was also confirmed through in vivo experiments in mice. Compared to the mice of the model group, the ratio of Firmicutes/Bacteroidetes in feces increased and the diversity of gut microbial composition was restored in mice after fucoidan intervention. In colorectal cancer (CRC) cells DLD-1 and SW480, fucoidan inhibited cell proliferation and promoted cell apoptosis. It also blocked the cell cycle of DLD-1 and SW480 at the G0/G1 phase. The animal model of inflammation-related CRC showed that the incidence of tumors in mice was significantly reduced by fucoidan intervention. Furthermore, the administration of fucoidan decreased the expression levels of inflammatory factors such as TNF-α IL-6 and IL-1ß in the colonic tissues. Therefore, fucoidan can effectively prevent the development of colitis-associated CRC.

Fusobacterium nucleatum Affects Cell Apoptosis by Regulating Intestinal Flora and Metabolites to Promote the Development of Colorectal Cancer.

Background/Aims: Intestinal flora, especially Fusobacterium nucleatum (Fn), can affect the development of colorectal cancer (CRC). In this study, we examined the composition of intestinal flora and their metabolites in the tissues, serum and feces of CRC patients. Materials and Methods: CRC tissues, adjacent normal colonic tissues, fecal and serum samples were collected from CRC patients who received surgical treatment between January 2018 and January 2020. Fecal and serum samples were collected from healthy individuals for comparison. In addition, fecal samples were collected from BALB/c female mice. SW480, a human CRC cell line, was utilized for in vitro studies. The experiments involved 1H-NMR-based metabolomics analysis, targeted and untargeted mass spectrometry analysis, and intestinal flora 16S rDNA V4 region sequencing. Results: The abundance of Bacteroides and propionic acid concentration were decreased and that of Lactobacillus and lactic acid concentration were increased in CRC tissues. In addition, the abundances of Ruminococcus, Prevotella, and Sutterell were decreased in CRC patients. The levels of leucine and isoleucine were decreased in the serum and tumor tissues of CRC patients. Aspartate, glutamate and glutathione levels were elevated in the tissues of CRC patients only. The serum glutamine, tyrosine, valine, alanine, and histidine levels were decreased significantly. Lactic acid inhibited and propionic acid promoted apoptosis among SW480 CRC cells. Conclusion: Fn affected the apoptosis of CRC cells and promoted the progression of CRC by affecting the distribution of intestinal flora, which altered the concentrations of metabolites such as lactic acid, propionic acid. Intestinal flora could regulate amino acid metabolism.

The correlation between dysfunctional intestinal flora and pathology feature of patients with pulmonary tuberculosis.

Introduction: Recent studies have provided insights into the important contribution of gut microbiota in the development of Pulmonary Tuberculosis (PTB). As a chronic consumptive infectious disease, PTB involves many pathological characteristics. At present, research on intestinal flora and clinical pathological Index of PTB is still rare. Methods: We performed a cross-sectional study in 63 healthy controls (HCs) and 69 patients with untreated active PTB to assess the differences in their microbiota in feces via 16S rRNA gene sequencing. Results: Significant alteration of microbial taxonomic and functional capacity was observed in PTB as compared to the HCs. The results showed that the alpha diversity indexes of the PTB patients were lower than the HCs (P<0.05). Beta diversity showed differences between the two groups (P<0.05). At the genus level, the relative abundance of Bacteroides, Parabacteroides and Veillonella increased, while Faecalibacterium, Bifidobacterium, Agathobacter and CAG-352 decreased significantly in the PTB group, when compared with the HCs. The six combined genera, including Lactobacillus, Faecalibacterium, Roseburia, Dorea, Monnoglobus and [Eubacterium]_ventriosum_group might be a set of diagnostic biomarkers for PTB (AUC=0.90). Besides, the predicted bacterial functional pathway had a significant difference between the two groups (P<0.05), which was mainly related to the nutrient metabolism pathway. Significant alterations in the biochemical index were associated with changes in the relative abundance of specific bacteria, the short chain fatty acid (SCFA)-producing bacteria enriched in HCs had a positively correlated with most of the biochemical indexes. Discussion: Our study indicated that the gut microbiota in PTB patients was significantly different from HCs as characterized by the composition and metabolic pathway, which related to the change of biochemical indexes in the PTB group. It was hypothesized that the abovementioned changes in the gut microbiota could exert an impact on the clinical characteristics of PTB through the regulation of the nutrient utilization pathway of the host by way of the gut-lung axis.

Fecal microbiota transplantation alleviated Alzheimer's disease-like pathogenesis in APP/PS1 transgenic mice.

Alzheimer's disease (AD) is the most common dementia in the elderly. Treatment for AD is still a difficult task in clinic. AD is associated with abnormal gut microbiota. However, little is known about the role of fecal microbiota transplantation (FMT) in AD. Here, we evaluated the efficacy of FMT for the treatment of AD. We used an APPswe/PS1dE9 transgenic (Tg) mouse model. Cognitive deficits, brain deposits of amyloid-ß (Aß) and phosphorylation of tau, synaptic plasticity as well as neuroinflammation were assessed. Gut microbiota and its metabolites short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and 1H nuclear magnetic resonance (NMR). Our results showed that FMT treatment could improve cognitive deficits and reduce the brain deposition of amyloid-ß (Aß) in APPswe/PS1dE9 transgenic (Tg) mice. These improvements were accompanied by decreased phosphorylation of tau protein and the levels of Aß40 and Aß42. We observed an increases in synaptic plasticity in the Tg mice, showing that postsynaptic density protein 95 (PSD-95) and synapsin I expression were increased after FMT. We also observed the decrease of COX-2 and CD11b levels in Tg mice after FMT. We also found that FMT treatment reversed the changes of gut microbiota and SCFAs. Thus, FMT may be a potential therapeutic strategy for AD.

Fructooligosaccharides Ameliorating Cognitive Deficits and Neurodegeneration in APP/PS1 Transgenic Mice through Modulating Gut Microbiota.

Alzheimer's disease (AD) is closely related to gut microbial alteration. Prebiotic fructooligosaccharides (FOS) play major roles by regulating gut microbiota. The present study aimed to explore the effect and mechanism of FOS protection against AD via regulating gut microbiota. Male Apse/PSEN 1dE9 (APP/PS1) transgenic (Tg) mice were administrated with FOS for 6 weeks. Cognitive deficits and amyloid deposition were evaluated. The levels of synaptic plasticity markers including postsynaptic density protein 95 (PSD-95) and synapsin I, as well as phosphorylation of c-Jun N-terminal kinase (JNK), were determined. The intestinal microbial constituent was detected by 16S rRNA sequencing. Moreover, the levels of glucagon-like peptide-1 (GLP-1) in the gut and GLP-1 receptor (GLP-1R) in the brain were measured. The results indicated that FOS treatment ameliorated cognitive deficits and pathological changes in the Tg mice. FOS significantly upregulated the expression levels of synapsin I and PSD-95, as well as decreased phosphorylated level of JNK. The sequencing results showed that FOS reversed the altered microbial composition. Furthermore, FOS increased the level of GLP-1 and decreased the level of GLP-1R in the Tg mice. These findings indicated that FOS exerted beneficial effects against AD via regulating the gut microbiota-GLP-1/GLP-1R pathway.

A novel training-free externally-regulated neurofeedback (ER-NF) system using phase-guided visual stimulation for alpha modulation.

The efficacy of neurofeedback is a point of great controversy, because a certain proportion of users cannot properly regulate their brain activities and thereby fail to benefit from neurofeedback. To address the neurofeedback inefficacy problem, the present study is aimed to design and implement a new neurofeedback system that can more effectively and consistently regulate users' brain activities than the conventional way of training users to voluntarily regulate brain activities. The new neurofeedback system delivers external visual stimuli continuously at a specific alpha phase, which is real-time decoded from ongoing alpha wave, to regulate the alpha wave. Experimental results show that the proposed training-free externally-regulated neurofeedback (ER-NF) system can achieve consistent (effective in almost all sessions for almost all users), flexible (either increasing or decreasing peak alpha frequency and alpha power), and immediate (taking or losing effect immediately after stimulation is on or off) modulation effects on alpha wave. Therefore, the ER-NF system holds great potential to be able to more reliably and flexibly modulate cognition and behavior.