Cardiovascular and respiratory diseases, and several cancers resulting from tobacco smoking, are initially characterized by chronic systemic inflammation. Cytokine imbalances can result in inflammation, making it important to understand the pathological mechanisms behind cytokine production. In this study, we collected blood samples from 78 healthy male volunteers, including non-smokers (n = 30), current smokers (n = 30), and ex-smokers (n = 18), and utilized the liquid suspension chip technique to investigate and compare the expression levels of 17 cytokines and chemokines in the human serum of these volunteers. The results demonstrated that the expression levels of CXCL9/MIG and sIL-6R significantly increased after smoking, and continued to increase after quitting smoking. The expression levels of TARC, ITAC, and sVEGFR-3 increased after smoking but decreased after quitting smoking; the expression level of SAA significantly decreased after smoking and showed an upward trend after quitting smoking. Seven cytokines (IL-1β, BCA-1, TNF-α, CRP, ENA-78, MDC, and TNFRII) did not vary between the three groups, while four cytokines (IL-1α, IL-6, IL-8, and SCF) were not detected in any serum sample. In conclusion, this study assessed the physiological production of cytokines and chemokines, highlighting the differences in each due to smoking status. Our results could help evaluate the early development of smoking-related chronic diseases and cancers.

Accurate detection and timely treatment of component defects in substations is an important measure to ensure the safe operation of power systems. In this study, taking substation meters as an example, a dataset of common meter defects, such as a fuzzy or damaged dial on the meter and broken meter housing, is constructed from the images of manual inspection in power systems. There are several challenges involved in accurately detecting defects in substation meter images, such as the complex background, different meter sizes and large differences in the shapes of meter defects. Therefore, this paper proposes the PHAM-YOLO (Parallel Hybrid Attention Mechanism You Only Look Once) network for automatic detection of substation meter defects. In order to make the network pay attention to the key areas against the complex background of the meter defect images and the differences between different defect features, a Parallel Hybrid Attention Mechanism (PHAM) module is designed and added to the backbone of YOLOv5. PHAM integration of local and non-local correlation information can highlight these differences while remaining focused on the meter defect features. To improve the expressive ability of the feature map, a Spatial Pyramid Pooling Fast (SPPF) module is introduced, which pools the input feature map using a continuous fixed convolution kernel, fusing the feature maps of different receptive fields. Bounding box regression (BBR) is the key way to determine object positioning performance in defect detection. EIOU (Efficient Intersection over Union) is, therefore, introduced as a boundary loss function to solve the ambiguity of the CIOU (Complete Intersection Over Union) loss function, making the BBR regression more accurate. The experimental results show that the Average Precision Mean (mAP), Precision (P) and Recall (R) of the proposed PHAM-YOLO network in the dataset are 78.3%, 78.3%, and 79.9%, respectively, with mAP being improved by 2.7% compared to the original model and higher than SSD, Fast R-CNN, etc.

A simple and sensitive high performance liquid chromatography-tandem mass spectrometry (HPLC-ESI-MS-MS) method was developed and validated for the quantification of creatinine in human urine. The analysis was carried out on an Agilent Zorbax Eclipse XDB-C18 column (2.1×150 mm, 3.5 μm). The mobile phase was 0.1% formic acid in water and 0.1% formic acid in acetonitrile (50/50, v/v). Linear calibration curves were obtained in the concentration range of 1–2000.0 ng/mL, with a lower limit of quantification of 0.99 ng/mL. The intra- and interday precision (RSD) values were below 3%. The method was successfully applied to a bioequivalence study of creatinine in Chinese smokers and nonsmokers. The total cotinine in 24 h urine and cotinine : creatinine ratio were also positively associated (PearsonR=0.942,P<0.0001). However, cotinine : creatinine ratio varied significantly across smoking groups for the difference of individual. 24 h urinary cotinine was more appropriate for expressing correlation with tar than cotinine : creatinine ratio.

Cigarette smoke is a harmful air pollutant and nicotine dependence is the essential cause of the tobacco epidemic. Since mitochondrial abnormalities are associated with substance addiction, in this work we used mitochondrial DNA (mtDNA) copy number as an indicator of mitochondrial function to investigate whether nicotine addicts also exhibit mitochondrial abnormalities. We found significantly lower mtDNA copy number in the peripheral blood of healthy nicotine addicts than in non-smokers, indicating that long-term nicotine exposure through smoking has detrimental effects on mitochondria. We also examined the effects of nicotine on mtDNA levels in a rat conditioned place preference (CPP) model of addiction and in cultured neuron cells, which revealed that the mtDNA copy number was significantly reduced in the hippocampus of CPP rats, in human neuroblastoma SH-SY5Y cells, and in rat pheochromocytoma PC12 cells, suggesting that significantly reduced mtDNA copy number is a potential biomarker of nicotine addiction. In SH-SY5Y cells, nicotine treatment induced several mitochondrial defects, such as increased mtDNA damage, increased reactive oxygen species (ROS) levels, decreased mitochondrial membrane potential (△Ψm), and stimulation of autophagic flux via transcriptional up-regulation of several autophagy-related genes and elevated marker protein accumulation, although genes controlling mtDNA replication were unaffected. In addition, pretreatment with the autophagy inhibitor Bafilomycin A1 led to accumulation of microtubule-associated protein 1 light chain 3b-II (LC3B-II) and counteracted the nicotine-induced decrease in mtDNA copy number. These results were recapitulated in PC12 cells, which also showed significant down-regulation of the marker SQSTM1/P62, suggesting that the decrease in mtDNA copy number is mediated by autophagy. This study shows that prolonged nicotine exposure, such as that in nicotine addicts, leads to a decrease of mtDNA copy number in neurons due to enhanced induction of autophagy. CAPSULE: It was found that smoking or nicotine exposure decreased mtDNA copy number based on population, animal, and cell models, and these effects appear to be mediated by autophagy.