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Dense object detection is widely used in automatic driving, video surveillance, and other fields. This paper focuses on the challenging task of dense object detection. Currently, detection methods based on greedy algorithms, such as non-maximum suppression (NMS), often produce many repetitive predictions or missed detections in dense scenarios, which is a common problem faced by NMS-based algorithms. Through the end-to-end DETR (DEtection TRansformer), as a type of detector that can incorporate the post-processing de-duplication capability of NMS, etc., into the network, we found that homogeneous queries in the query-based detector lead to a reduction in the de-duplication capability of the network and the learning efficiency of the encoder, resulting in duplicate prediction and missed detection problems. To solve this problem, we propose learnable differentiated encoding to de-homogenize the queries, and at the same time, queries can communicate with each other via differentiated encoding information, replacing the previous self-attention among the queries. In addition, we used joint loss on the output of the encoder that considered both location and confidence prediction to give a higher-quality initialization for queries. Without cumbersome decoder stacking and guaranteeing accuracy, our proposed end-to-end detection framework was more concise and reduced the number of parameters by about 8% compared to deformable DETR. Our method achieved excellent results on the challenging CrowdHuman dataset with 93.6% average precision (AP), 39.2% MR−2, and 84.3% JI. The performance overperformed previous SOTA methods, such as Iter-E2EDet (Progressive End-to-End Object Detection) and MIP (One proposal, Multiple predictions). In addition, our method is more robust in various scenarios with different densities. [ABSTRACT FROM AUTHOR]

Solar photothermal utilization is the important aspect of solar energy utilization, among which the optical characteristics of nanofluids play a decisive role in the efficiency of solar photothermal utilization. ZnO nanoparticles with different morphologies were prepared by hydrothermal method, and then Au was successfully reduced to ZnO nanoparticles by sodium borohydride reduction method to prepare ZnO/Au composite nanomaterials. The morphology, structure and composition of ZnO and ZnO/Au nanoparticles were characterized by SEM and XRD. The UV/VIS/NIR absorption spectra show that ZnO/Au nanofluids significantly improve the absorption in the visible light band. Through the photothermal conversion experiment, the photothermal conversion performance of flower like ZnO nanofluids is better than that of rod like ZnO nanofluids. Due to the plasmon effect of Au, the photothermal conversion performance of ZnO/Au nanofluids is enhanced. When the concentration is 1.0 mg/mL, the photo thermal conversion efficiency of rod like ZnO/10% Au nanofluids is 59%, which is 16% higher than that of pure heat transfer oil nanofluids. When the concentration is 0.5 mg/mL, the photo thermal conversion efficiency of flower like ZnO/10% Au nanofluids is 71%, which is 28% higher than that of pure heat transfer oil nanofluids. [ABSTRACT FROM AUTHOR]

Glutamate transporters (also called excitatory amino acid transporters, EAAT) are important in extracellular homeostasis of glutamate, a major excitatory neurotransmitter. EAAT4, a neuronally expressed EAAT in cerebellum, has a large portion (~95% of the total L-aspartate-induced currents in human EAAT4) of substrate-gated [Cl.sup.-] currents, a distinct feature of this EAAT. We cloned EAAT4 from rat cerebellum. This molecule was predicted to have eight putative transmembrane domains. L-Glutamate induced an inward current in oocytes expressing this EAAT4 at a holding potential -60 mV. Phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, significantly increased the magnitude of L-glutamate-induced currents but did not affect the apparent affinity of EAAT4 for L-glutamate. This PMA-enhanced current had a reversal potential -17 mV at extracellular [Cl.sup.-] concentration ([Cl.sup.-]o) 104 mM with an ~60-mV shift per 10-fold change in [[Cl.sup.-]]o, properties consistent with [Cl.sup.-] -selective conductance. However, PMA did not change EAAT4 transport activity as measured by [[SUP.3]H]-L-glutamate. Thus PMA-enhanced [Cl.sup.-] currents via EAAT4 were not thermodynamically coupled to substrate transport. These PMA-enhanced [Cl.sup.-] currents were partially blocked by staurosporine, chelerythrine, and calphostin C, the three PKC inhibitors. Ro-31-8425, a PKC inhibitor that inhibits conventional PKC isozymes at low concentrations (nM level), partially inhibited the PMA-enhanced [Cl.sup.-] currents only at a high concentration (1 [micro]M). Intracellular injection of BAPTA, a [Ca.sup.2+]-chelating agent, did not affect the PMA-enhanced [Cl.sup.-] currents. 4[alpha]- Phorbol-12,13-didecanoate, an inactive analog of PMA, did not enhance glutamate-induced currents. These data suggest that PKC, possibly isozymes other than conventional ones, modulates the substrate-gated [Cl.sup.-] currents via rat EAAT4. Our results also suggest that substrate-gated ion channel activity and glutamate transport activity, two EAAT4 properties that could modulate neuronal excitability, can be regulated independently. oocytes; protein kinase C

Glutamate transporters may be important targets for anesthetic action in the central nervous system. The authors investigated the effects of the intravenous anesthetics, thiopental and ketamine, and the local anesthetics, lidocaine and bupivacaine, on the activity of glutamate transporter type 2, EAAT2. EAAT2 was expressed in Xenopus oocytes by injection of its mRNA. By using two-electrode voltage clamping, membrane currents were recorded after the application of l-glutamate (30 μM) in the presence or absence of various concentrations of anesthetics. Lidocaine and bupivacaine did not change glutamate-induced inward currents at the tested concentrations (1–1000 μM). Thiopental and ketamine also did not affect the activity of EAAT2 at the tested concentrations (0.3–300 μM). Our results suggest that the two commonly used local anesthetics (lidocaine and bupivacaine) and intravenous anesthetics (thiopental and ketamine) do not affect the activity of EAAT2 expressed in oocytes. EAAT2 may not be a target for these anesthetics. [Copyright &y& Elsevier]

The effect of rare earth oxides on the microstructure and corrosion behavior of laser-cladding coating on 316L stainless steel was investigated using hardness measurements, a polarization curve, electrochemical impedance spectroscopy (EIS), a salt spray test, X-ray diffraction, optical microscopy, and scanning electron microscopy (SEM). The results showed that the modification of rare earth oxides on the laser-cladding layer caused minor changes to its composition but refined the grains, leading to an increase in hardness. Electrochemical and salt spray studies indicated that the corrosion resistance of the 316L stainless steel could be improved by laser cladding, especially when rare earth oxides (i.e., CeO2 and La2O3) were added as a modifier. [ABSTRACT FROM AUTHOR]

Background: Long-term exposure to cadmium can induce renal toxicity in rats, leading to endoplasmic reticulum (ER) stress and iron death. Notably, in cadmium-exposed rats, there is an increased expression of UNC93B1 (unc-93 homolog B1). Consequently, our investigation aims to determine the impact of UNC93B1 on ER stress and iron death in cadmium-exposed rats by modulating the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) pathway., Methods: A cadmium-exposed rat model was established by intrabacally injecting chromium chloride (5 mg/kg, once a day for 4 weeks), and the levels of UCd (urine cadmium), UNAG (urine N -acetyl-β-D-glucosaminidase), and UCr (urine creatinine) in urine were assessed. A silent UNC93B1 lentivirus was constructed, and STING agonists were procured and administered to the rats. Subsequently, kidney tissues were extracted post-mortem, and pathological changes in renal tissue were observed through hematoxylin and eosin (HE) staining. The expression and mRNA levels of UNC93B1, cGAS, and STING were examined using western blot (WB) and polymerase chain reaction (PCR). Autophagy proteins (light chain 3 (LC3), Beclin-1, p62) were also assessed by WB. Additionally, iron concentration was determined using a kit, while oxidative stress markers (cytochrome oxidase subunit 2 (COX2), glutathione peroxidase 4 (GPX4), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH)) were measured through enzyme-linked immunosorbent assay (ELISA). Furthermore, endoplasmic reticulum stress proteins (protein kinase RNA-like ER kinase (PERK), CCAAT enhance-binding protein homologous protein (CHOP), activating transcription factor-4 (ATF4)) were analyzed by WB., Results: Wstaining, WB, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), ELISA, and HE staining collectively revealed a heightened expression of UNC93B1, cGAS, and STING, accompanied by increased levels of autophagy, oxidative stress, and ER stress in cadmium-exposed rats ( p < 0.05). Nephrotoxicity exhibited a reduction following the inhibition of UNC93B1, leading to decreased levels of oxidative stress, autophagy, and ER stress ( p < 0.05). Notably, this observed phenomenon was reversed upon the addition of STING agonists, suggesting that UNC93B1 might exert a nephroprotective effect in cadmium-exposed rats through modulation of the cGAS-STING pathway., Conclusions: The inhibition of UNC93B1 mitigates nephrotoxicity in cadmium-exposed rats, and this protective effect is mechanistically linked to the cGAS-STING pathway.

Pedestrian detection in crowded scenes is widely used in computer vision. However, it still has two difficulties: 1) eliminating repeated predictions (multiple predictions corresponding to the same object); 2) false detection and missing detection due to the high scene occlusion rate and the small visible area of detected pedestrians. This paper presents a detection framework based on DETR (detection transformer) to address the above problems, and the model is called AD-DETR (asymmetrical relation detection transformer). We find that the symmetry in a DETR framework causes synchronous prediction updates and duplicate predictions. Therefore, we propose an asymmetric relationship fusion mechanism and let each query asymmetrically fuse the relative relationships of surrounding predictions to learn to eliminate duplicate predictions. Then, we propose a decoupled cross-attention head that allows the model to learn to restrict the range of attention to focus more on visible regions and regions that contribute more to confidence. The method can reduce the noise information introduced by the occluded objects to reduce the false detection rate. Meanwhile, in our proposed asymmetric relations module, we establish a way to encode the relative relation between sets of attention points and improve the baseline. Without additional annotations, combined with the deformable-DETR with Res50 as the backbone, our method can achieve an average precision of 92.6%, MR$ ^{-2} $ of 40.0% and Jaccard index of 84.4% on the challenging CrowdHuman dataset. Our method exceeds previous methods, such as Iter-E2EDet (progressive end-to-end object detection), MIP (one proposal, multiple predictions), etc. Experiments show that our method can significantly improve the performance of the query-based model for crowded scenes, and it is highly robust for the crowded scene.

Glutamate transporters regulate extracellular concentrations of glutamate, an excitatory neurotransmitter in the central nervous system. We have shown that the commonly used anesthetic isoflurane increased the activity of glutamate transporter type 3 (excitatory amino acid transporter 3, EAAT3) possibly via a protein kinase C (PKC)-dependent pathway. In this study, we showed that isoflurane induced a time- and concentration-dependent redistribution of EAAT3 to the cell membrane in C6 glioma cells. This redistribution was inhibited by staurosporine, a pan PKC inhibitor, or by 12-(2-cyanoethyl)-6,7,12,13-tetrahydro-13-methyl-5-oxo-5H-indolo(2,3-a)pyrrolo(3,4-c)-carbazole (Go6976) at a concentration that selectively inhibits conventional PKC isozymes (PKC alpha, -beta, and -gamma). This isoflurane-induced EAAT3 redistribution was also blocked when the expression of PKC alpha but not PKC beta proteins was down-regulated by the respective antisense oligonucleotides. The isoflurane-induced increase of glutamate uptake by EAAT3 was abolished by the down-regulation of PKC alpha expression. Immunoprecipitation with an anti-EAAT3 antibody pulled down more PKC alpha in cells exposed to isoflurane than in control cells. Isoflurane also increased the phosphorylated EAAT3 and the redistribution of PKC alpha to the particulate fraction of cells. Consistent with the results in C6 cells, isoflurane also increased EAAT3 cell-surface expression and enhanced the association of PKC alpha with EAAT3 in rat hippocampal synaptosomes. Our results suggest that the isoflurane-induced increase in EAAT3 activity requires an increased amount of EAAT3 protein in the plasma membrane. These effects are PKC alpha-dependent and may rely on the formation of an EAAT3-PKC alpha complex. Together, these results suggest an important mechanism for the regulation of glutamate transporter functions and expand our understanding of isoflurane pharmacology at cellular and molecular levels.