MC-YOLOv5: A Multi-Class Small Object Detection Algorithm.

The detection of multi-class small objects poses a significant challenge in the field of computer vision. While the original YOLOv5 algorithm is more suited for detecting full-scale objects, it may not perform optimally for this specific task. To address this issue, we proposed MC-YOLOv5, an algorithm specifically designed for multi-class small object detection. Our approach incorporates three key innovations: (1) the application of an improved CB module during feature extraction to capture edge information that may be less apparent in small objects, thereby enhancing detection precision; (2) the introduction of a new shallow network optimization strategy (SNO) to expand the receptive field of convolutional layers and reduce missed detections in dense small object scenarios; and (3) the utilization of an anchor frame-based decoupled head to expedite training and improve overall efficiency. Extensive evaluations on VisDrone2019, Tinyperson, and RSOD datasets demonstrate the feasibility of MC-YOLOv5 in detecting multi-class small objects. Taking VisDrone2019 dataset as an example, our algorithm outperforms the original YOLOv5L with improvements observed across various metrics: mAP50 increased by 8.2%, mAP50-95 improved by 5.3%, F1 score increased by 7%, inference time accelerated by 1.8 ms, and computational requirements reduced by 35.3%. Similar performance gains were also achieved on other datasets. Overall, our findings validate MC-YOLOv5 as a viable solution for accurate multi-class small object detection.

UN-YOLOv5s: A UAV-Based Aerial Photography Detection Algorithm.

With the progress of science and technology, artificial intelligence is widely used in various disciplines and has produced amazing results. The research of the target detection algorithm has significantly improved the performance and role of unmanned aerial vehicles (UAVs), and plays an irreplaceable role in preventing forest fires, evacuating crowded people, surveying and rescuing explorers. At this stage, the target detection algorithm deployed in UAVs has been applied to production and life, but making the detection accuracy higher and better adaptability is still the motivation for researchers to continue to study. In aerial images, due to the high shooting height, small size, low resolution and few features, it is difficult to be detected by conventional target detection algorithms. In this paper, the UN-YOLOv5s algorithm can solve the difficult problem of small target detection excellently. The more accurate small target detection (MASD) mechanism is used to greatly improve the detection accuracy of small and medium targets, The multi-scale feature fusion (MCF) path is combined to fuse the semantic information and location information of the image to improve the expression ability of the novel model. The new convolution SimAM residual (CSR) module is introduced to make the network more stable and focused. On the VisDrone dataset, the mean average precision (mAP) of UAV necessity you only look once v5s(UN-YOLOv5s) is 8.4% higher than that of the original algorithm. Compared with the same version, YOLOv5l, the mAP is increased by 2.2%, and the Giga Floating-point Operations Per Second (GFLOPs) is reduced by 65.3%. Compared with the same series of YOLOv3, the mAP is increased by 1.8%, and GFLOPs is reduced by 75.8%. Compared with the same series of YOLOv8s, the detection accuracy of the mAP is improved by 1.1%.

A new detection algorithm for alien intrusion on highway.

In recent years, highway accidents occur frequently, the main reason is that there is always foreign body invasion on the highway, which makes people unable to respond to emergencies in time. In order to reduce the occurrence of highway incidents, an object detection algorithm for highway intrusion was proposed in this paper. Firstly, a new feature extraction module was proposed to better preserve the main information. Secondly, a new feature fusion method was proposed to improve the accuracy of object detection. Finally, a lightweight method was proposed to reduce the computational complexity. We compare the algorithm in this paper with existing algorithms, the experimental results showed that: On the Visdrone dataset (small size targets), (a) the CS-YOLO was 3.6% more accurate than the YOLO v8. (b) The CS-YOLO was 1.2% more accurate than the YOLO v8 on the Tinypersons dataset (minimal size targets). (c) CS-YOLO was 1.4% more accurate than YOLO v8 on VOC2007 data set (normal size).

Improved GBS-YOLOv5 algorithm based on YOLOv5 applied to UAV intelligent traffic.

As the road traffic situation becomes complex, the task of traffic management takes on an increasingly heavy load. The air-to-ground traffic administration network of drones has become an important tool to promote the high quality of traffic police work in many places. Drones can be used instead of a large number of human beings to perform daily tasks, as: traffic offense detection, daily crowd detection, etc. Drones are aerial operations and shoot small targets. So the detection accuracy of drones is less. To address the problem of low accuracy of Unmanned Aerial Vehicles (UAVs) in detecting small targets, we designed a more suitable algorithm for UAV detection and called GBS-YOLOv5. It was an improvement on the original YOLOv5 model. Firstly, in the default model, there was a problem of serious loss of small target information and insufficient utilization of shallow feature information as the depth of the feature extraction network deepened. We designed the efficient spatio-temporal interaction module to replace the residual network structure in the original network. The role of this module was to increase the network depth for feature extraction. Then, we added the spatial pyramid convolution module on top of YOLOv5. Its function was to mine small target information and act as a detection head for small size targets. Finally, to better preserve the detailed information of small targets in the shallow features, we proposed the shallow bottleneck. And the introduction of recursive gated convolution in the feature fusion section enabled better interaction of higher-order spatial semantic information. The GBS-YOLOv5 algorithm conducted experiments showing that the value of mAP@0.5 was 35.3[Formula: see text] and the mAP@0.5:0.95 was 20.0[Formula: see text]. Compared to the default YOLOv5 algorithm was boosted by 4.0[Formula: see text] and 3.5[Formula: see text], respectively.

Lightweight aerial image object detection algorithm based on improved YOLOv5s.

YOLOv5 is one of the most popular object detection algorithms, which is divided into multiple series according to the control of network depth and width. To realize the deployment of mobile devices or embedded devices, the paper proposes a lightweight aerial image object detection algorithm (LAI-YOLOv5s) based on the improvement of YOLOv5s with a relatively small amount of calculation and parameter and relatively fast reasoning speed. Firstly, to better detect small objects, the paper replaces the minimum detection head with the maximum detection head and proposes a new feature fusion method, DFM-CPFN(Deep Feature Map Cross Path Fusion Network), to enrich the semantic information of deep features. Secondly, the paper designs a new module based on VoVNet to improve the feature extraction ability of the backbone network. Finally, based on the idea of ShuffleNetV2, the paper makes the network more lightweight without affecting detection accuracy. Based on the VisDrone2019 dataset, the detection accuracy of LAI-YOLOv5s on the mAP@0.5 index is 8.3% higher than that of the original algorithm. Compared with other series of YOLOv5 and YOLOv3 algorithms, LAI-YOLOv5s has the advantages of low computational cost and high detection accuracy.

Astragalus polysaccharides affects multidrug resistance gene 1 and P-glycoprotein 170 in adriamycin nephropathy rats via regulating microRNA-16/NF-κB axis. / 黄芪多糖调控微RNA-16/NF-κBè½´å¯¹é˜¿éœ‰ç´ è‚¾ç— å¤§é¼ å¤šè¯è€è¯åŸºå› 1和P-糖蛋白170的影响.

OBJECTIVES: Nephrotic syndrome is a common disease of the urinary system. The aim of this study is to explore the effect of astragalus polysaccharides (APS) on multidrug resistance gene 1 (MDR1) and P-glycoprotein 170 (P-gp170) in adriamycin nephropathy rats and the underlying mechanisms. METHODS: A total of 72 male Wistar rats were divided into a control group, a model group, an APS low-dose group, an APS high-dose group, an APS+micro RNA (miR)-16 antagomir group and an APS+miR-16 antagomir control group, with 12 rats in each group. Urine protein (UP) was detected by urine analyzer, and serum cholesterol (CHOL), albumin (ALB), blood urea nitrogen (BUN), and creatinine (SCr) were detected by automatic biochemical analyzer; serum interleukin-6 (IL-6), IL-1ß, tumor necrosis factor α (TNF-α) levels were detected by ELISA kit; the morphological changes of kidney tissues were observed by HE staining; the levels of miR-16 and MDR1 mRNA in kidney tissues were detected by real-time RT-PCR; the expression levels of NF-κB p65, p-NF-κB p65, and P-gp170 protein in kidney tissues were detected by Western blotting; and dual luciferase was used to verify the relationship between miR-16 and NF-κB. RESULTS: The renal tissue structure of rats in the control group was normal without inflammatory cell infiltration. The renal glomeruli of rats in the model group were mildly congested, capillary stenosis or occlusion, and inflammatory cell infiltration was obvious. The rats in the low-dose and high-dose APS groups had no obvious glomerular congestion, the proliferation of mesangial cells was significantly reduced, and the inflammatory cells were reduced. Compared with the high-dose APS group and the APS+miR-16 antagomir control group, there were more severe renal tissue structure damages in the APS + miR-16 antagomir group. Compared with the control group, the levels of UP, CHOL, BUN, SCr, IL-6, IL-1ß, TNF-α, and MDR1 mRNA, and the protein levels of p-NF-κB p65 and P-gp170 in the model group were significantly increased (all P<0.05); the levels of ALB and miR-16 were significantly decreased (both P<0.05). Compared with the model group, the levels of UP, CHOL, BUN, SCr, IL-6, IL-1ß, TNF-α, and MDR1 mRNA, and the protein levels of pNF-κB p65 and P-gp170 in the low-dose and high-dose APS groups were significant decreased (all P<0.05); and the levels of ALB and miR-16 were significantly increased (both P<0.05). Compared with APS+miR-16 antagomir control group, the UP, CHOL, BUN, SCr, IL-6, IL-1ß, and TNF-α levels, MDR1 mRNA, and the protein levels of p-NF-κB p65 and P-gp170 were significantly increased (all P<0.05). The levels of ALB and miR-16 were significantly decreased in the APS+miR-16 antagomir group compared with the APS+miR-16 antagomir control group (both P<0.05). CONCLUSIONS: APS can regulate the miR-16/NF-κB signaling pathway, thereby affecting the levels of MDR1 and P-gp170, and reducing the inflammation in the kidney tissues in the adriamycin nephropathy rats.

Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis / Isoflurano fornece neuroproteção em lesão cerebral hipóxico-isquêmica neonatal por inibição da apoptose

Abstract Background and objectives: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. Methods: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. Results: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. Conclusions: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.

Resumo Justificativa e objetivos: Isoflurano é um éter volátil halogenado usado para anestesia por via inalatória. É amplamente usado na clínica como um anestésico para inalação. A lesão hipóxico-isquêmica neonatal ocorre no cérebro imaturo e resulta em morte celular tardia via excitotoxicidade e estresse oxidativo. Isoflurano mostrou ter propriedades neuroprotetoras que formam uma base benéfica para o seu uso tanto em cultura de células quanto em modelos animais, incluindo vários modelos de lesão cerebral. Nosso objetivo foi determinar o efeito neuroprotetor de isoflurano em hipóxia cerebral e elucidar o mecanismo subjacente. Métodos: Fatias de hipocampo, em fluido cerebrospinal artificial (CSFA) com glicose e privação de oxigênio, foram usadas como um modelo in vitro de hipóxia cerebral. O pico de população ortodrômica (PPO) e o potencial de lesão hipóxica (PLH) foram registrados nas regiões CA1 e CA3. A concentração de neurotransmissores de aminoácidos na solução de perfusão das fatias de hipocampo foi medida. Resultados: O tratamento com isoflurano retardou a eliminação do PPO e melhorou a recuperação do PPO; diminuiu a frequência do PLH, retardou o início do PLH e aumentou a duração do PLH. O tratamento com isoflurano também diminuiu a liberação de neurotransmissores de aminoácidos induzida pela hipóxia, como aspartato, glutamato e glicina, mas os níveis de ácido γ-aminobutírico (GABA) estavam elevados. Estudos morfológicos mostram que o tratamento de edema com isoflurano atenuou o edema de neurônios piramidais na região CA1. Também reduziu a apoptose, como mostrado pela expressão reduzida da caspase-3 e genes PARP. Conclusões: Isoflurano mostrou um efeito neuroprotetor na lesão neuronal no hipocampo induzida por hipóxia através da supressão de apoptose.

Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis.

BACKGROUND AND OBJECTIVES: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. METHODS: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. RESULTS: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. CONCLUSIONS: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.

[Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis]. / Isoflurano fornece neuroproteção em lesão cerebral hipóxico­isquêmica neonatal por inibição da apoptose.

BACKGROUND AND OBJECTIVES: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. METHODS: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. RESULTS: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. CONCLUSIONS: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.

Effect of bone marrow stem cell mobilisation on the expression levels of cellular growth factors in a rat model of acute tubular necrosis.

The aim of the present study was to observe the mobilisation effects of stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) on bone marrow stem cells (BMSCs) in rats with renal ischaemia-reperfusion injury. In addition, the effects of the BMSCs on the expression levels of hepatocyte growth factor (HGF) and epidermal growth factor (EGF) were investigated, with the aim to further the understanding of the protective mechanisms of SCF and G-CSF in renal ischaemia-reperfusion injury. The model and treatment groups were established using a model of unilateral renal ischaemia-reperfusion injury, in which the treatment group and the treatment control group were subcutaneously injected once a day with 200 µg/kg SCF and 50 µg/kg G-CSF, 24 h after the modelling, for five consecutive days. The CD34+ cell count was measured in the peripheral blood using flow cytometry. The mRNA expression levels of HGF and EGF were determined using polymerase chain reaction analysis, while the protein expression levels of HGF and EGF were detected using immunohistochemistry. The CD34+ cell count in the peripheral blood of the treatment and treatment control groups was significantly higher compared with that in the model group (P<0.05). However, CD34 expression levels in the cells from the renal tissues of the model and treatment groups were significantly higher compared with that of the control and treatment control groups (P<0.05), with the greatest increase observed in the treatment group. The mRNA and protein expression levels of HGF and EGF in the treatment group were significantly higher compared with the model group (P<0.05). Therefore, the results indicated that a combination of SCF and G-CSF can promote the repair of acute tubular necrosis. This combination, which can mobilise sufficient numbers of BMSCs to migrate back to the injured site, is a key factor in promoting the repair of renal tubular injury. Upregulation of HGF and EGF was also shown to promote the repair of renal tubular injury.

Effects of autologous bone marrow-derived stem cell mobilization on acute tubular necrosis and cell apoptosis in rats.

The aim of this study was to investigate the effects of stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) on bone marrow-derived stem cell (BMSC) mobilization in rat models of renal ischemia/reperfusion (I/R) injury. In addition, the effects of SCF and G-CSF on cellular apoptosis were explored in order to determine the protective mechanism of the two factors against renal I/R injury. A unilateral renal I/R injury model was established for the model and treatment groups. The treatment and treatment control groups were subcutaneously injected with SCF (200 µg/kg/day) and G-CSF (50 µg/kg/day) 24 h after the establishment of the model for five consecutive days. The total number of leukocytes in the peripheral blood and the cellular percentages of cluster of differentiation (CD)34+, renal CD34+ and apoptotic cells were detected. The total number of leukocytes in the peripheral blood and the percentages of CD34+ cells in the treatment and treatment control groups reached maximum levels on the fifth postoperative day and were significantly higher than those in the normal control and model groups. The number of renal CD34+ cells in the treatment group was significantly increased compared with that in the treatment control and model groups. The apoptotic indices (AIs) of the model and treatment groups were higher than those of the normal control and treatment control groups. The AI of the model group was significantly higher than that of the treatment group. In conclusion, the combined application of SCF and G-CSF can mobilize sufficient numbers of BMSCs and cause cellular 'homing' to the injured site, thus inhibiting apoptosis and promoting the repair of renal tubular injury.

Erythropoietin protects lipopolysaccharide-induced renal mesangial cells from autophagy.

The aim of this study was to investigate the effects of erythropoietin (EPO) on the impairment of autophagy induced by lipopolysaccharide (LPS) in primary cultured rat glomerular mesangial cells (GMCs). Rat GMCs were isolated and cultured in normal glucose, high-glucose, LPS or LPS + EPO medium. At 24 and 72 h of culture, the cells were examined for expression levels of the autophagy markers LC3 and p62/sequestosome-1 (SQSTM1) using western blot analysis. At 24 h, no significant difference in the expression of LC3 and p62/SQSTM1 was observed among the groups; however, the cells exposed to high-glucose medium for 72 h showed downregulated LC3 expression and upregulated p62/SQSTM1 expression. The cells exposed to LPS (10 ng/ml) for 72 h showed upregulated LC3 expression and upregulated p62/SQSTM1 expression. These changes were reversed in the LPS + EPO group at 72 h. In conclusion, EPO can inhibit LPS-induced autophagy in rat GMCs.

Formononetin induces apoptosis in PC-3 prostate cancer cells through enhancing the Bax/Bcl-2 ratios and regulating the p38/Akt pathway.

Formononetin (FN), a bioactive component extracted from the red clover (Trifolium pratense L.), has been long used for treating carcinomas in China. In the present study, we aim to investigate the potential therapeutical effects of FN on cell line of prostatic adenocarcinoma (PC-3) and human prostate epithelial cells (RWPE1). These findings indicated that FN significantly inhibited the cell growth of PC-3 in a dose-dependent manner, but no such effect was observed in RWPE1 cells. The apoptotic counts were effectively increased following the treatments as shown in flow cytometry. The results from Western blotting assay suggested that FN treatment contributed to the reduced Bcl-2 protein level and the elevated Bax expression in PC-3 cells, thereby resulting in the increasing Bax/Bcl-2 ratios. Furthermore, the phosphorylated level of p38 in PC-3 cells was activated through the FN treatment, whereas the endogenous Akt phosphorylation was blocked. Collectively, our findings demonstrate that FN exerts the anticarcinogenic effect on prostate cancer in vitro, in which the underlying mechanisms are associated with enhancing the Bax/Bcl-2 ratios and regulating the p38/Akt pathway, thus triggering apoptosis in tumor cells.

Formononetin induces the mitochondrial apoptosis pathway in prostate cancer cells via downregulation of the IGF-1/IGF-1R signaling pathway.

Abstract Context: Formononetin, an isoflavone, can inhibit the proliferation of cancer cells, including those of the prostate. However, its antitumor mechanism remains unclear. Aim: To investigate whether the insulin-like growth factor 1 (IGF-1)/insulin-like growth factor 1 receptor (IGF-1 R) signaling pathway mediates the formononetin antitumor effect on prostate cancer cells. Materials and methods: The viability of PC-3 cells was measured by MTT assay 48 h after formononetin treatment (25, 50 and 100 µM). Formononetin-induced cell apoptosis was measured by Hoechst 33258 staining and flow cytometry. Expression of Bax mRNA was detected by real-time PCR, and the expression levels of Bax and IGF-1 R proteins were detected by western blots. Results: At concentrations >12.5 µM, formononetin significantly inhibited the proliferation of human prostate cancer cells. Formononetin increased Bax mRNA and protein expression levels and decreased the expression levels of pIGF-1 R protein in a dose-dependent manner. Conclusion: High concentrations of formononetin-induced apoptosis in androgen-independent prostate cancer cells through inhibition of the IGF-1/IGF-1 R pathway.