Swin-Transformer -YOLOv5 for lightweight hot-rolled steel strips surface defect detection algorithm.

An essential industrial application is the examination of surface flaws in hot-rolled steel strips. While automatic visual inspection tools must meet strict real-time performance criteria for inspecting hot-rolled steel strips, their capabilities are constrained by the accuracy and processing speed of the algorithm used to identify defects. To solve the problems of poor detection accuracy, low detection efficiency, and unsuitability of low computing power platforms of the hot-rolled strip surface defect detection algorithm The Swin-Transformer-YOLOv5 model based on the improved one-stage detector is proposed. By employing GhostNet, the model's lightweight design, and guaranteed detection accuracy are both achieved. The C3 module introduces Swin-Transformer to address the issues of cluttered backdrops of defect photos and easily confused defect categories. With the addition of the CoordAttention module, the model's capacity to extract defective features is improved, and its performance keeps getting better. The issue of huge differences in different scales and poor detection of small flaws is resolved by employing BiFPN for feature fusion, and the detector's capacity to adapt to targets of different scales is improved. The experimental results demonstrate that the improved Swin-Transformer-Yolov5 model significantly outperforms the industry-standard target detection algorithms, and the model's mAP value still improves by 8.39% over the original model while reducing the number of parameters, GFLOPs, and weight by 36.6%, 40.0%, and 34.7%, respectively. The model is better suited for use on low-arithmetic platforms as a result.

A spark to the powder keg: Microneedle-based antitumor nanomedicine targeting reactive oxygen species accumulation for chemodynamic/photothermal/chemotherapy.

HYPOTHESIS: Chemodynamic therapy (CDT) can efficiently kill cancer cells by producing hydroxyl radical (•OH), a kind of high-toxic reactive oxygen species (ROS), via Fenton or Fenton-like reactions. This study involved a versatile nanomedicine, MSN@DOX/GA-Fe/PDA (M@DGP), delivered via microneedles, which was expected to combine chemodynamic/photothermal/chemotherapy and efficiently increase ROS accumulation to achieve significant therapeutic efficacy against melanoma. EXPERIMENTS: The composition of the synthesized nanoparticles was confirmed by a series of characterizations including transmission electron microscopy, Fourier transform infrared spectroscopy, and zeta potential. The photothermal properties of the nanomedicine was evaluated via infrared imaging, and •OH-producing ability was evaluated by UV-Vis and electron spin resonance. The mechanisms of ROS accumulation were studied in B16 cells by detecting intracellular •OH, glutathione, and ROS levels. The drug-loaded microneedles (M@DGP-MNs) were prepared, and their morphology and mechanical strength were characterized. The in vivo antimelanoma effect and biosafety evaluation of the nanomedicine were investigated in tumor-bearing C57 mice. FINDINGS: M@DGP was successfully prepared and could achieve ROS accumulation through a photothermal-enhanced Fenton reaction, polydopamine-induced glutathione consumption, and doxorubicin-mediated mitochondrial dysfunction which induced oxidative stress and apoptosis of tumor cells. M@DGP-MNs showed superior antitumor efficacy and good biosafety, providing a promising strategy for melanoma treatment.

Polymer Optical Waveguide Grating-Based Biosensor to Detect Effective Drug Concentrations of Ginkgolide A for Inhibition of PMVEC Apoptosis.

In this work, we successfully developed a fluorinated cross-linked polymer Bragg waveguide grating-based optical biosensor to detect effective drug concentrations of ginkgolide A for the inhibition of pulmonary microvascular endothelial cell (PMVEC) apoptosis. Fluorinated photosensitive polymer SU-8 (FSU-8) as the sensing core layer and polymethyl methacrylate (PMMA) as the sensing window cladding were synthesized. The effective drug concentration range (5-10 µg/mL) of ginkgolide A for inhibition of PMVEC apoptosis was analyzed and obtained by pharmacological studies. The structure of the device was optimized to be designed and fabricated by direct UV writing technology. The properties of the biosensor were simulated with various refractive indices of different drug concentrations. The actual sensitivity of the biosensor was measured as 1606.2 nm/RIU. The resolution and detection limit were characterized as 0.05 nm and 3 × 10-5 RIU, respectively. The technique is suitable for safe and accurate detection of effective organic drug dosages of Chinese herbal ingredients.

Ginsenoside Rh2-B1 stimulates cell proliferation and IFN-γ production by activating the p38 MAPK and ERK-dependent signaling pathways in CTLL-2 cells.

CONTEXT: Ginsenoside Rh2, an active component of ginseng, exhibits immunoregulatory and anti-inflammatory properties. Rh2-B1, a sulfated derivative, was prepared to enhance its water solubility. We studied the effect of Rh2-B1 on CTLL-2, a CD8⁺ cytotoxic T cell line that was known for protecting against viral infection. OBJECTIVE: We aimed to investigate the effect of Rh2-B1 on interferon (IFN)-γ production and cell proliferation and its possible mechanism. MATERIALS AND METHODS: Enzyme-linked immunosorbent assay (ELISA) was employed to analyze the IFN-γ concentration of the whole blood and the supernatant of CTLL-2 cell culture. Cell proliferation assay was conducted using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Western blots were used to evaluate changes in signal transduction pathways in CTLL-2 cells. RESULTS: Rh2-B1 was able to enhance IFN-γ production from whole blood culture of Balb/c mice. We then evaluated the effect of Rh2-B1 on a cytotoxic T cell line, CTLL-2 for cell proliferation, IFN-γ production and its molecular mechanism. Rh2-B1 promoted cell proliferation and IFN-γ production of CTLL-2 cells. It also induced activation of p38 mitogen-activated protein kinase (MAPK) and extracellular-signal-regulated kinases (ERK), but inhibited p56 Lck and transducer and activator of transcription 5 (STAT5) expression. The effect was blocked by the specific p38 MAPK inhibitor SB203580 and ERK inhibitor U0126. CONCLUSION: Rh2-B1 could stimulate cell proliferation and IFN-γ production by activating the p38 MAPK- and ERK-dependent signaling pathways in cytotoxic T cells. This may be a novel medicine for treatment of viral infections.

Peimine impairs pro-inflammatory cytokine secretion through the inhibition of the activation of NF-κB and MAPK in LPS-induced RAW264.7 macrophages.

In the previous study, we found that peimine has good anti-inflammatory effects in vivo. However, the anti-inflammatory mechanism of peimine remains unclear. We, therefore, assessed the effects of peimine on inflammatory cytokines in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We found that peimine (0-25 mg/L) significantly inhibited tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1ß, and increased IL-10 production. Furthermore, peimine significantly inhibited the phosphorylation of p38, ERK and c-jun N-terminal kinase (JNK) as well as decreased p65 and IκB. The present results indicate that peimine inhibits the production of inflammatory cytokines induced by LPS through blocking MAPKs and NF-κB signaling pathways.

Inhibitory effects of sulfated 20(S)-ginsenoside Rh2 on the release of pro-inflammatory mediators in LPS-induced RAW 264.7 cells.

Ginsenoside Rh2 is one of the most important ginsenosides in ginseng with anti-inflammatory and antitumor effects. However, the extremely poor oral bioavailability induced by its low water solubility greatly limits the potency of Rh2 in vivo. In the previous study, we sulfated 20(S)-ginsenoside Rh2 with chlorosulfonic acid and pyridine method, and got one novel derivative, Rh2-B1, with higher water solubility and greater immunologic enhancement than Rh2. However, the anti-inflammatory effect of Rh2-B1 remains unclear. We therefore investigated the effects of Rh2-B1 on lipopolysaccharide (LPS)-induced proinflammatory mediators in RAW 264.7 macrophages. We found that Rh2-B1 dramatically inhibited LPS-induced overproduction of nitric oxide, prostaglandin E2, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6. Consistently, the protein and mRNA expression levels of inducible nitric oxide synthase and cyclooxygenase-2 were remarkably decreased by Rh2-B1. In addition, Rh2-B1 significantly suppressed the phosphorylations of p38, c-Jun N-terminal kinase, and extracellular signal receptor-activated kinase 1/2 induced by LPS. Rh2-B1 was further shown to inhibit NF-κB p65 translocation into the nucleus by suppressing IκBα degradation. In conclusion, we demonstrate that Rh2-B1 inhibits the release of LPS-induced pro-inflammatory mediators through blocking mitogen-activated protein kinases and NF-κB signaling pathways, suggesting that sulfated ginsenosides could be potential agents for anti-inflammatory therapies.