LiDAR Point Cloud Object Recognition Method via Intensity Image Compensation

LiDAR point cloud object recognition plays an important role in robotics, remote sensing, and automatic driving. However, it is difficult to fully represent the object feature information only by using the point cloud information. To address this challenge, we proposed a point cloud object recognition method that uses intensity image compensation, which is highly descriptive and computationally efficient. First, we constructed the local reference frame for the point cloud. Second, we proposed a method to calculate the deviation angle between the normal vector and local reference frame in the local neighborhood of the point cloud. Third, we extracted the contour information of the object from the intensity image corresponding to the point cloud, carried out Discrete Fourier Transform on the distance sequence between the barycenter of the contour and each point of the contour, and took the obtained result as Discrete Fourier Transform contour feature of the object. Finally, we repeated the above steps for the existing prior data and marked the obtained results as the feature information of the corresponding object to build a model library. We can recognize an unknown object by calculating the feature information of the object to be recognized and matching the feature information with the model library. We rigorously tested the proposed method with avalanche photon diode array LiDAR data and compared the results with those of four other methods. The experimental results show that the proposed method is superior to the comparison method in terms of description and computational efficiency and that it can meet the needs of practical applications

Molecular Cluster Mining of Adrenocortical Carcinoma via Multi-Omics Data Analysis Aids Precise Clinical Therapy

Adrenocortical carcinoma (ACC) is a malignancy of the endocrine system. We collected clinical and pathological features, genomic mutations, DNA methylation profiles, and mRNA, lncRNA, microRNA, and somatic mutations in ACC patients from the TCGA, GSE19750, GSE33371, and GSE49278 cohorts. Based on the MOVICS algorithm, the patients were divided into ACC1-3 subtypes by comprehensive multi-omics data analysis. We found that immune-related pathways were more activated, and drug metabolism pathways were enriched in ACC1 subtype patients. Furthermore, ACC1 patients were sensitive to PD-1 immunotherapy and had the lowest sensitivity to chemotherapeutic drugs. Patients with the ACC2 subtype had the worst survival prognosis and the highest tumor-mutation rate. Meanwhile, cell-cycle-related pathways, amino-acid-synthesis pathways, and immunosuppressive cells were enriched in ACC2 patients. Steroid and cholesterol biosynthetic pathways were enriched in patients with the ACC3 subtype. DNA-repair-related pathways were enriched in subtypes ACC2 and ACC3. The sensitivity of the ACC2 subtype to cisplatin, doxorubicin, gemcitabine, and etoposide was better than that of the other two subtypes. For 5-fluorouracil, there was no significant difference in sensitivity to paclitaxel between the three groups. A comprehensive analysis of multi-omics data will provide new clues for the prognosis and treatment of patients with ACC

Levels of oxidative stress in patients with neoadjuvant chemotherapy for gastric cancer: correlation with treatment response

ObjectiveThe intent of this study was to investigate the relationship between oxidative stress and treatment response in gastric cancer patients undergoing neoadjuvant chemotherapy.MethodsBlood samples from 108 patients and 108 healthy subjects were collected, and all patients were enrolled in SOX chemotherapy. The patients received four cycles of neoadjuvant chemotherapy. Blood samples were collected to determine oxidative stress levels at baseline prior to beginning chemotherapy, and at the end of cycles 2 and 4. The patients receiving neoadjuvant chemotherapy were followed up for several months to years. A survival curve was created according to the follow-up information from the patients. In addition, the correlation between oxidative stress level and treatment effect was evaluated and ROC curves were plotted according to the final collected data.ResultsCompared with the normal group, the levels of the antioxidant index decreased while the peroxide index increased in the patients. Conversely, when patients were compared before and after chemotherapy, the antioxidant index increased but the peroxide index decreased. Furthermore, the antioxidant index increased in the response group while the peroxide index decreased in the non-response group.ConclusionPatients with an increased antioxidant index after chemotherapy have good treatment responsiveness. These indicators can also be used as predictors to judge the patients’ response to chemotherapy

Changes in gut microbiota linked to a prevention of cardiac remodeling induced by hypertension in spontaneously hypertensive rats fed a pawpaw fruit diet

Objective: Dietary intake of fruit is associated with lower incidence of hypertension and cardiovascular risk. Papaya is a kind of delicious fruit and reported has dietary therapeutic effects, such as digestive stimulation and hypotensive efficacy. However, the mechanism of pawpaw involved have not been elucidated. Here, we illustrate that the effect of pawpaw on the gut microbiota and the prevention of cardiac remodeling. Methods: Gut microbiome, cardiac structure/function, and blood pressure were examined in SHR and WKY groups. The intestinal barrier was tested with histopathologic; immunostaining and Western blot were used to measure the tight junction protein level; Gpr41 was tested by RT-PCR, and inflammatory factors were detected with ELISA. Results: We observed a significant decrease in microbial richness, diversity, and evenness is the spontaneously hypertensive rat (SHR), in addition to an increased Firmicutes/Bacteroidetes (F/B) ratio. These changes were accompanied by decreased in acetate and butyrate-producing bacteria. Compared with SHR, treatment with pawpaw at the dosage of 10 g/kg for 12 weeks significantly reduced the blood pressure, cardiac fibrosis and cardiac hypertrophy, while the ratio of F/B decreased. We also found that the concentration of short-chain fatty acids (SCFAs) was increased in SHR fed with pawpaw compared with that in control group, while the gut barrier was restored and level of proinflammatory cytokines in the serum were decreased. Conclusions: Pawpaw, rich of high fiber, led to changes in the gut microbiota that played a protective role in the development of cardiac remodeling. The potential mechanism of pawpaw may explained by the generation of one of the main metabolites of the gut microbiota, the short-chain fatty acid acetate, increasing tight junction protein level occluding to enhance the gut barrier for less releasing the inflammation cytokines, and upregulating G-protein-coupled receptor 41 (GPR41) to reduce blood pressure

An Orally Active Allosteric GLP-1 Receptor Agonist Is Neuroprotective in Cellular and Rodent Models of Stroke.

Diabetes is a major risk factor for the development of stroke. Glucagon-like peptide-1 receptor (GLP-1R) agonists have been in clinical use for the treatment of diabetes and also been reported to be neuroprotective in ischemic stroke. The quinoxaline 6,7-dichloro-2-methylsulfonyl-3-N-tert- butylaminoquinoxaline (DMB) is an agonist and allosteric modulator of the GLP-1R with the potential to increase the affinity of GLP-1 for its receptor. The aim of this study was to evaluate the neuroprotective effects of DMB on transient focal cerebral ischemia. In cultured cortical neurons, DMB activated the GLP-1R, leading to increased intracellular cAMP levels with an EC50 value about 100 fold that of exendin-4. Pretreatment of neurons with DMB protected against necrotic and apoptotic cell death was induced by oxygen-glucose deprivation (OGD). The neuroprotective effects of DMB were blocked by GLP-1R knockdown with shRNA but not by GLP-1R antagonism. In C57BL/6 mice, DMB was orally administered 30 min prior to middle cerebral artery occlusion (MCAO) surgery. DMB markedly reduced the cerebral infarct size and neurological deficits caused by MCAO and reperfusion. The neuroprotective effects were mediated by activation of the GLP-1R through the cAMP-PKA-CREB signaling pathway. DMB exhibited anti-apoptotic effects by modulating Bcl-2 family members. These results provide evidence that DMB, a small molecular GLP-1R agonist, attenuates transient focal cerebral ischemia injury and inhibits neuronal apoptosis induced by MCAO. Taken together, these data suggest that DMB is a potential neuroprotective agent against cerebral ischemia

Effects of DMB on the cAMP-PKA-CREB signaling pathway after MCAO.

<p>(A) Western blot analysis of PKA, p-CREB and CREB in ipsilateral ischemic penumbra 24 h post MCAO or sham operation. (B-D) Bar graphs reflect PKA, p-CREB and CREB proteins in each group. Data are expressed as a percentage of sham. n = 6. ** <i>p</i> < 0.01.</p

DMB activates the GLP-1 receptor in cortical neurons.

<p>(A) Western blot showing GLP-1R expression in neurons and β-cells. (B) Bar graph reflecting the GLP-1R expression in each group. Data are presented as percentage of β-cells. n = 5 (C) cAMP stimulation by DMB (1 μM) in neurons and detected 0–30 min after incubation. Data are expressed as percentage of 0 min. n = 6.</p

DMB treatment improved neurological deficit and decreased infarct volume 24 h after MCAO.

<p>(A) Neurological deficit scores. n = 8. (B) Photographs of brain slices stained with TTC. (C) Quantitative analysis of infarct volume. n = 6. * <i>p</i> < 0.05, ** <i>p</i> < 0.01.</p

Structure of DMB, molecular formula C₁₃H₁₅Cl₂N₃O₂S.

<p>Structure of DMB, molecular formula C₁₃H₁₅Cl₂N₃O₂S.</p