Background:Rheumatoid arthritis is a chronic autoimmune disease influenced by environmental exposures, including per- and polyfluoroalkyl substances (PFAS). Although previous studies have suggested links between PFAS and rheumatoid arthritis risk, none have used interpretable machine learning models for prediction. This study aimed to develop such a model to assess risk based on PFAS exposure. Methods:We analyzed data from 11,705 participants in the National Health and Nutrition Examination Survey (2003-2018). Twelve machine learning algorithms were evaluated using metrics including area under the curve (AUC), accuracy, sensitivity, specificity, and F1 score. Key predictors were identified using SHapley Additive exPlanations (SHAP). Partial dependence plots and locally weighted scatterplot smoothing (LOWESS) curves were used to examine non-linear associations and exposure thresholds. A web-based risk calculator was developed to enhance clinical and public health applicability. Results:CatBoost showed the best performance (AUC: 0.82; Accuracy: 74%; F1 score: 0.62) and was selected for further interpretation. SHAP analysis identified perfluorooctane sulfonic acid (PFOS) and 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (MPAH) as major contributors to risk prediction. PFOS exhibited a U-shaped relationship with increased risk above 15.10 ng/ml, while MPAH showed a risk transition at 0.22 ng/ml. Waterfall plots illustrated the contribution of individual exposures. The interactive web-based calculator allows users to input PFAS levels and receive personalized rheumatoid arthritis risk estimates. It is freely available on Hugging Face Spaces (https://huggingface.co/spaces/Machine199710/RA_ML). Conclusions:This study demonstrates the potential of machine learning to predict rheumatoid arthritis risk based on PFAS exposure. The identified non-linear patterns provide insights into environmental contributions to disease risk and may inform future prevention strategies.

Background: Previous studies have suggested that electromagnetic pulse (EMP) can induce openings in the blood–brain barrier (BBB). However, the temporal variation and spatial distribution of BBB permeability after EMP radiation are difficult to assess using conventional histopathological approaches. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) is a valuable tool for the in vivo evaluation of BBB permeability. The main purpose of this study was to investigate the temporal variation and spatial distribution of BBB permeability after EMP radiation in rats using DCE-MRI. Methods: The dose of EMP was estimated through simulations utilizing a digital rat model comprising 16 distinct brain regions. Then, the changes in BBB permeability of the different rat brain regions at different time points (3 h and 24 h) after EMP radiation were evaluated using quantitative DCE-MRI. Furthermore, the spatial difference in BBB permeability was assessed 3 h after exposure. Finally, the dose–effect relationship between the electric field strength and the BBB permeability was also investigated. Results: The results demonstrated that the changes in the values of volume transfer constant (ΔKtrans) significantly increased in several rat brain regions at 3 h after 400 kV/m EMP radiation. These changes vanished 24 h after exposure. Meanwhile, no significant spatial differences in BBB permeability were observed after EMP radiation. Moreover, Pearson’s correlation analysis showed that there was a significant positive linear relationship between BBB permeability and the electric field strength within an external electric field strength range of 0 to 400 kV/m at 3 h after EMP radiation. Conclusions: EMP radiation can induce a reversible increase in BBB permeability in rats. Moreover, no significant differences in BBB permeability were found across different brain regions. Additionally, the degree of BBB permeability was positively correlated with the regional electric field strength of EMP radiation within an external electric field strength range of 0 to 400 kV/m at 3 h after EMP radiation. These results indicate the promising potential of employing EMP for transient openings in the BBB, which could facilitate clinical pharmacological interventions via drug delivery into the brain.

OBJECTIVE:With the widespread utilization of S band (2 GHz ∼ 4 GHz) microwave (MW) in communication, its potential health risks have drawn significant attention. The purpose of this study was to investigate the impacts of acute 2.856 GHz MW exposure on recognition memory, its corresponding functional brain network, and the relationships between them in rats. METHODS:Novel object recognition (NOR) tests were conducted to examine the influence of 50 mW/cm2 acute 2.856 GHz MW on rat's recognition memory. Subsequently, resting state functional magnetic resonance imaging (rs-fMRI) was implemented to investigate the changes in the topological characteristics, long-range functional connectivity (FC), local FC assessed by regional homogeneity (ReHo), and fractional amplitude of low frequency fluctuation (fALFF) of rats' brain network related to recognition memory. Furthermore, the relationships between recognition memory and the potentially changed functional characteristics were investigated. RESULTS:Our findings revealed that the acute MW exposure induced recognition memory decline in rats. Though no significant alterations were detected in topological properties, long-range FCs, and fALFF within the brain network related to recognition memory, the local FCs of bilateral perirhinal cortex and right hippocampus in rats exhibited marginally significant increases following the MW exposure. Moreover, in the Sham group, the local FC of the left perirhinal cortex demonstrated a significantly positive linear correlation with recognition memory ability (p = 0.0193, r = 0.7182). However, this linear relationship was disrupted after the MW exposure. CONCLUSION:In conclusion, acute 2.856 GHz MW exposure can induce recognition memory impairments in rats. There is a positive linear relationship between recognition memory and the local FC of the left perirhinal cortex in normal rats. However, this relationship is disrupted after MW exposure, potentially due to maladaptive reorganization or failure of compensation within the brain region.

Terahertz (THz) waves, a novel type of radiation with quantum and electronic properties, have attracted increasing attention for their effects on the nervous system. Spatial working memory, a critical component of higher cognitive function, is coordinated by brain regions such as the infralimbic cortex (IL) region of the medial prefrontal cortex and the ventral cornu ammonis 1 (vCA1) of hippocampus. However, the regulatory effects of THz waves on spatial working memory and the underlying mechanisms remain unclear. In this study, the effects of 0.152 THz waves on glutamatergic neuronal activity and spatial working memory and the related mechanisms were investigated in cell, brain slice, and mouse models. Cellular experiments revealed that THz waves exposure for 60 min significantly increased the intrinsic excitability of primary hippocampal neurons, enhanced glutamatergic neuron activity, and upregulated the expression of molecules involved in glutamate metabolism. In brain slice experiments, THz waves markedly elevated neuronal activity, promoted synaptic plasticity, and increased glutamatergic synaptic transmission within the IL and vCA1 regions. Molecular dynamics simulations found that THz waves could inhibit the ion transport function of glutamate receptors. Moreover, Y-maze tests demonstrated that mice exposed to THz waves exhibited significantly improved spatial working memory. Multiomics analyses indicated that THz waves could induce changes in chromatin accessibility and increase the proportion of excitatory neurons. These findings suggested that exposure to 0.152 THz waves increased glutamatergic neuronal activity, promoted synaptic plasticity, and improved spatial working memory, potentially through modifications in chromatin accessibility and excitatory neuron proportions.

The mechanisms underlying the negative health effects of microwave exposure on male reproduction remain unclear. Thus, this study aimed to explore the role and regulatory mechanisms of ferroptosis in microwave-induced reproductive damage. The exposure of male C57 mice to 2.856 GHz of microwave radiation at 0, 10 and 20 mW/cm² for 30 min decreased sperm motility, induced morphological changes, damaged testicular tissue and mitochondrial morphology, increased malondialdehyde (MDA) contents and decreased the GSH/GSSG ratio. Simultaneously, the Fe²⁺ levels increased and SLC7A11 and GPX4 protein expressions decreased, causing oxidative stress. After 30 min of mouse spermatocyte (GC-2) irradiation, the cell viability of the Fer-1 inhibitor group and the GSH/GSSG ratio increased, while the reactive oxygen species, MDA and ferrous iron contents decreased. Furthermore, the depolarisation of membrane potential improved. Western blotting revealed that Nrf2, Keap1, SLC7A11, GPX4 and HO-1 expressions were down-regulated by microwave exposure and significantly up-regulated following the addition of the Fer-1 inhibitor. The results confirmed that the Nrf2 signalling pathway can regulate ferroptosis of oxidative stress. This study demonstrates that microwave exposure affects mouse reproductive function by enhancing oxidative stress, inducing ferroptosis by inhibiting the Nrf2 signalling pathway and reducing SLC7A11 and GPX4 protein expressions.

The anxieties and concerns about health hazards caused by microwave has been growing recently. Previous studies have reported microwave induced structural and functional injuries to brain. However, the biological effects caused by compound microwave were largely unexplored. In this study, we investigated the biological effects on rat’s hippocampus after sequentially exposure to 2.8 GHz and 9.3 GHz at average power density of 10 mW/cm2. Morris water maze (MWM) navigation tests showed that microwave exposure significantly extended the average escape latency (AEL) at 1d and 3d after exposure, suggesting reduced learning and memory ability. Importantly, compound microwave produced strongest responses at 3 d after exposure. Moreover, microwave also could induce abnormal electroencephalogram (EEG), such as increasing the power of θ wave and δ wave, suggesting brain damage or dysfunction. Histopathological analysis suggested that microwave resulted in obvious structural injuries in hippocampus at 7 d after exposure, and most serious injuries were observed in compound microwave exposed rats. Moreover, disorder of mitochondria and reduced Nissl bodies in hippocampus might contribute to the decrease of cognitive function. However, both the cognitive function and hippocampal structure restored to normal at 28 d after exposure, which might be attributed to self-recovery mechanisms. Gene ontology (GO) and Protein-protein interaction (PPI) analyses of differential expressed genes (DEGs) in peripheral blood suggested that Htt and Bdnf might be potential indicators to predict microwave. In conclusion, compound microwave of 2.8 GHz and 9.3 GHz could elicit reversible structural injuries to hippocampus, which could decrease the cognitive function of rats.

The study aims to explore the new mechanism of human induced pluripotent stem cell-derived myocardial cells (iPSC-CMs) damage caused by microwave exposure, focusing on the changes in inflammatory factors, and to clarify the association between the dynamic sensing network and electrophysiological disorders. In this study, iPSC-CMs were exposed to 60 W/kg S-band microwaves for 30 min. The damage effects and mechanisms were investigated 1 h, 3 h, and 6 h after radiation. Using techniques such as flow cytometry, transmission electron microscopy, calcium transient, Olink proteomics, and immunofluorescence, the activity, ultrastructure, calcium signal changes, and expression of inflammatory factors of iPSC-CMs after microwave radiation were detected. Results: After microwave radiation, the activity of iPSC-CMs significantly decreased, the mitochondrial cristae were broken, the Ca2 + activation time and activation speed were abnormal, the amplitude of calcium transient changed significantly, and the action potential repolarization was abnormal. The dynamic changes of inflammatory factors were as follows: 1 h after microwave radiation, IL-6 drove acute inflammatory response, 3 h when the NF-κB pathway integrated inflammatory signals through IL-8, and 6 h after, CXCL11 dominated the repair program, and VEGFA expression rebounded to synergistically promote generation. Microwave radiation activated the classical NF-κB pathway and regulated the inflammatory balance. This study found that microwave radiation caused structural and functional damage to iPSC-CMs, and the temporal inflammatory regulation is a new mechanism of injury.

The annual increase of microwave exposure in human environments continues to fuel debates regarding its potential health impacts. This study monitored the EEG and ECG responses of three Cynomolgus monkeys before and at 0, 3, 7, 14, and 30 days after exposure to 50 mW/cm² microwave radiation for 15 min. The findings revealed no significant differences in the power spectral densities (PSDs) of the whole brain, frontal, and temporal lobes across various frequency bands (δ, θ, α, β, low-γ, and high-γ) immediately and up to 30 days postexposure. Notable alterations were observed primarily at 14 days in the PSDs of the parietal lobe, prefrontal cortex, central zone, and occipital lobe, particularly in the θ and α bands. By Day 30, these values returned to normal ranges. ECG alterations were characterized by changes in T-wave shape and amplitude. One monkey exhibited bidirectional spikes at 7 and 14 days that normalized by Day 30. Another showed similar patterns with reduced amplitude, and a third monkey displayed a towering forward wave at 14 days that persisted at 30 days. In conclusion, the administration of L-band microwave radiation at the specified dose did not result in immediate alterations to EEG and ECG, but it induced transient modifications in brain electrical activity and normalized after 30 days, which contributed to evaluate the health implications of microwave exposure in humans.

Terahertz (THz) waves,also known as T-rays,encompass frequencies ranging from 0.1 to 10 THz and possess unique properties that render them applicable in various biomedical domains,particularly in neurobiology[1]. Synaptic transmission,the process through which signals propagate between neurons at synapses,is pivotal for brain function and information processing.

Researches have shown that microwave radiation could cause oxidative stress injury in male reproductive system, and blueberry anthocyanins had excellent oxidation resistance. Our study aimed to investigate the protective effect of blueberry anthocyanins (100, 200 and 400 mg/kg/d) on testicular tissue damage in Wistar rats exposed to 2.856 GHz microwave and the optimal dose. We found that blueberry anthocyanins could ameliorate the decrease of sperm motility and sex hormone levels and testicular tissue structure damage caused by microwave radiation, increase SIRT1 expression and decrease FoxO1 expression, increase GSH/GSSG, SOD and inhibit MDA. The LDH, SDH and ATP synthase were increased, and Caspase-3 expression was decreased, and the high-dose of blueberry anthocyanins (400 mg/kg/d) had the best protective effect. These results suggested that blueberry anthocyanins could inhibit oxidative stress injury induced by 2.856 GHz microwave radiation in rat testicular tissue by regulating SIRT1/FoxO1 pathway, enhance energy metabolism and reduce cell apoptosis.

The effect of multi-frequency electromagnetic environments on male reproduction has attracted the medical community's interest. Studies have investigated the effects and mechanisms of single-frequency microwave exposure on male reproduction, but comparative research on high-power microwave (HPM) composite and single exposure remains scarce. This study aimed to examine the effects and mechanisms of combined 1.5 GHz and 4.3 GHz microwave exposure on male reproduction. Male Wistar rats were exposed to 1.5 GHz (L-band) and 4.3 GHz (C-band) electromagnetic radiation for 15 minutes. The four groups were: sham, 10 mW/cm² L-band, 10 mW/cm² C-band, and 5 mW/cm² L-band and 5 mW/cm² C-band compound. Assessments were made on the pathological structures of testes, sperm viability, serum sex hormones, oxidative stress, and energy metabolism levels after radiation. Exposure to 1.5 GHz and 4.3 GHz microwaves individually resulted in testicular tissue damage and reduced sperm quality. There was little difference between the damage caused by HPM composite and single exposure. The exposed groups showed histological and ultrastructural changes, with reduced spermatozoa viability, motility parameters, and serum testosterone, luteinizing hormone, follicle-stimulating hormone, and serum inhibin-B on days 1 and 7 after exposure. These tended to recover partially by day 14. Adenosine triphosphate content and lactate dehydrogenase and succinate dehydrogenase activities in the exposed testicular tissue decreased, corresponding to decreased superoxide dismutase activity and increased malondialdehyde content. Both single and combined exposure to L- and C-band HPM affect the male reproductive system. Exposure to single and compound HPM shows no significant difference in risks, with oxidative stress and energy metabolism disturbances playing key roles.

The brain is complex and metabolically active, and the detection of metabolites plays an important role in brain development and diseases. Currently, there is a lack of research on the metabolic spectrum changes in learning and memory impairment, and hippocampal damage induced by microwave radiation from the metabolic perspective. Aiming to provide sensitive indicators for microwave radiation-induced brain damage and establish a foundation for understanding its injury mechanisms, this study employed non-targeted metabolomics to investigate metabolic fluctuations and key metabolic pathway alterations in rats’ hippocampal tissue after microwave radiation. The memory and spatial exploration abilities of rats decreased after radiation. The postsynaptic densities were thickened in the MW group. The cholesterol sulfate, SM(d16:1/24:1(15Z)), and linoelaidylcarnitine were significantly increased after radiation, whereas etrahydrocorticosterone, L-phenylalanine, and histamine were significantly decreased after radiation. These metabolites were enriched in signaling pathways related to the inflammatory mediator regulation of transient receptor potential (TRP) channels, neuroactive ligand–receptor interaction, steroid hormone biosynthesis, and phenylalanine, tyrosine, and tryptophan biosynthesis. These findings indicate that microwave radiation causes spatial learning and memory dysfunction in rats and structural damage to hippocampal tissue.

Excessive noise exposure presents significant health risks to humans, affecting not just the auditory system but also the cardiovascular and central nervous systems. This study focused on three male macaque monkeys as subjects. 90 dB sound pressure level (SPL) pure tone exposure (frequency: 500Hz, repetition rate: 40Hz, 1 min per day, continuously exposed for 5 days) was administered. Assessments were performed before exposure, during exposure, immediately after exposure, and at 7-, 14-, and 28-days post-exposure, employing auditory brainstem response (ABR) tests, electrocardiograms (ECG), and electroencephalograms (EEG). The study found that the average threshold for the Ⅴ wave in the right ear increased by around 30 dB SPL right after exposure (P < 0.01) compared to pre-exposure. This elevation returned to normal within 7 days. The ECG results indicated that one of the macaque monkeys exhibited an RS-type QRS wave, and inverted T waves from immediately after exposure to 14 days, which normalized at 28 days. The other two monkeys showed no significant changes in their ECG parameters. Changes in EEG parameters demonstrated that main brain regions exhibited significant activation at 40Hz during noise exposure. After noise exposure, the power spectral density (PSD) in main brain regions, particularly those represented by the temporal lobe, exhibited a decreasing trend across all frequency bands, with no clear recovery over time. In summary, exposure to 90 dB SPL noise results in impaired auditory systems, aberrant brain functionality, and abnormal electrocardiographic indicators, albeit with individual variations. It has implications for establishing noise protection standards, although the precise mechanisms require further exploration by integrating pathological and behavioral indicators.

Background. Coronary artery disease (CAD) is a type of cardiovascular disease which is one of the leading causes of death around the world. The presence of coronary stenosis is considered a pivotal indicator in the diagnosis of various CADs. The main purpose of this paper was to investigate the feasibility of an anchor‐free deep learning (DL) method, fully convolutional one‐stage object detection (FCOS), in coronary artery stenosis automatic detection. Methods. First, 2786 invasive coronary angiography (ICA) images from 130 patients were randomly divided into training, validation, and testing datasets using the 10‐fold cross‐validation approach. Then, FCOS was compared with other three widely used anchor‐based DL models: single shot multibox detector (SSD), faster region‐based convolutional network (Faster R‐CNN), and you only look once (YOLOv3), in terms of precision, recall, F1 score, average precision (AP), and average recall (AR). Finally, the performances of different models in the detection of stenosis were compared in either single or multiple lesion scenarios using statistical tests. Results. FCOS achieved significantly superior precision (96.14% ± 0.53%), recall (94.36% ± 0.79%), F1 score (95.22% ± 0.56%), AP0.50 (93.36% ± 0.93%), AR0.50:0.95 (64.73% ± 1.46%), APsmall (55.04 ± 0.96%), APmedium (59.97 ± 1.13%), and APlarge (68.09 ± 5.18%) compared to Faster R‐CNN and YOLOv3. Moreover, FCOS demonstrated significantly higher AR0.50:0.95 and APsmall compared to SSD. Regardless of the presence of single or multiple coronary stenoses in ICA images, FCOS also outperformed Faster R‐CNN and YOLOv3. Furthermore, it showed significantly higher AR0.50:0.95 compared to SSD when in the multiple stenosis scenario. Conclusions. It is feasible to use the anchor‐free DL model FCOS in detecting coronary stenosis based on ICA images.

To investigate the dynamic changes in hippocampal metabolism after microwave radiation using liquid chromatography in tandem with mass spectrometry/mass spectrometry (LC–MS/MS) and to identify potential biomarkers. Wistar rats were randomly assigned to a sham group and a microwave radiation group. The rats in the microwave radiation group were exposed to 2.856 GHz for 15 min for three times, with 5 min intervals. The rats in the sham group were not exposed. Transmission electron microscope revealed blurring of the synaptic cleft and postsynaptic dense thickening in hippocampal neurons after microwave radiation. Metabolomic analysis revealed 38, 24, and 39 differentially abundant metabolites at 3, 7, and 14 days after radiation, respectively, and the abundance of 9 metabolites, such as argininosuccinic acid, was continuously decreased. After microwave radiation, the abundance of metabolites such as argininosuccinic acid was successively decreased, indicating that these metabolites could be potential biomarkers for hippocampal tissue injury.

Shortwave radiation has been reported to have harmful effects on several organs in humans and animals. However, the biological effects of 27 MHz shortwave on the reproductive system are not clear. In this study, we investigated the effects of shortwave whole-body exposure at a frequency of 27 MHz on structural and functional changes in the testis. Male Wistar rats were exposed to 27 MHz continuous shortwaves at average power densities of 0, 5, 10, or 30 mW/cm2 for 6 min. The levels of insulin-like factor 3 (INSL3) and anti-sperm antibodies (AsAb) in the peripheral serum, sperm motility, sperm malformation rate, and testicular tissue structure of rats were analyzed. Furthermore, the activity of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) content, calpain, and Cdk5 expression were analyzed at 1, 7, 14, and 28 days after exposure. We observed that the rats after radiation had decreased serum INSL3 levels (p < 0.01), increased AsAb levels (p < 0.05), decreased percentage of class A+B sperm (p < 0.01 or p < 0.05), increased sperm malformation (p < 0.01 or p < 0.05), injured testicular tissue structure, decreased SOD and CAT activities (p < 0.01 or p < 0.05), increased MDA content (p < 0.01), and testicular tissue expressions of calpain1, calpain2, and Cdk5 were increased (p < 0.01 or p < 0.05). In conclusion, Shortwave radiation caused functional and structural damage to the reproductive organs of male rats. Furthermore, oxidative stress and key molecules in the calpain/Cdk5 pathway are likely involved in this process.

Electromagnetic waves are widely used in both military and civilian fields, which could cause long-term and high-power exposure to certain populations and may pose a health hazard. The aim of this study was to simulate the long-term and high-power working environment of workers using special electromagnetic radiation occupations to clarify the radiation-induced stress response and cardiac damage and thus gain insights into the mechanisms of injuries caused by electromagnetic radiation. In this study, the combination of microwave and stress was an innovative point, aiming to broaden the research direction with regard to the effect and mechanism of cardiac injury caused by radiation. The myocardial structure was observed by optical and transmission electron microscope, mitochondrial function was detected by flow cytometry, oxidative-stress markers were detected by microplate reader, serum stress hormone was detected by radioimmunoassay, and heart rate variability (HRV) was analyzed by multichannel-physiological recorder. The rats were weighed and subjected to an open field experiment. Western blot (WB) and immunofluorescence (IF) were used to detect the expressions and distributions of JNK (c-Jun N-terminal kinase), p-JNK (phosphorylated c-Jun N-terminal kinase), HSF1 (heat shock factor), and NFATc4 (nuclear factor of activated T-cell 4). This study found that radiation could lead to the disorganization, fragmentation, and dissolution of myocardial fibers, severe mitochondrial cavitation, mitochondrial dysfunction, oxidative-stress injury in myocardium, increase to stress hormone in serum, significant changes in HRV, and a slow gain in weight. The open field experiment indicated that the rats experienced anxiety and depression and had decreased exercise capacity after radiation. The expressions of JNK, p-JNK, HSF1, and NFATc4 in myocardial tissue were all increased. The above results suggested that 30 mW/cm2 of S-band microwave radiation for 35 min could cause both physiological and psychological stress damage in rats; the damage was related to the activation of the JNK pathway, which provided new ideas for research on protection from radiation.

Microwave (MW) and electromagnetic pulse (EMP) are considered environmental pollutants, both of which can induce learning and memory impairments. However, the bioeffects of combined exposure to MW and EMP have never been explored. This paper aimed to investigate the effects of combined exposure to MW and EMP on the learning and memory of rats as well as its association with ferroptosis in the hippocampus. In this study, rats were exposed to EMP, MW, or EMP and MW combined radiation. After exposure, impairment of learning and memory, alterations in brain electrophysiological activity, and damage to hippocampal neurons were observed in rats. Moreover, we also found alterations in ferroptosis hallmarks, including increased levels of iron, lipid peroxidation, and prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA, as well as downregulation of glutathione peroxidase 4 (GPX4) protein in the rat hippocampus after exposure. Our results suggested that either single or combined exposure to MW and EMP radiation could impair learning and memory and damage hippocampal neurons in rats. Moreover, the adverse effects caused by the combined exposure were more severe than the single exposures, which might be due to cumulative effects rather than synergistic effects. Furthermore, ferroptosis in the hippocampus might be a common underlying mechanism of learning and memory impairment induced by both single and combined MW and EMP exposure.

目的 探讨S波段和X波段微波长期复合暴露对大鼠免疫功能的影响.方法 96只二级雄性Wistar大鼠随机分为4组:假辐射组(Sham)、S波段微波辐射组(S10)、X波段微波辐射组(X10)和复合辐射组(SX10),每组24只.分别采用平均功率密度为10 mW/cm2的S波段和X波段微波辐射6 min,1次/d,连续辐射30 d,复合组采用先S波段后X波段微波暴露.于辐射后6 h、7 d、14 d和28 d,采用血细胞计数仪分析外周血细胞数量;酶联免疫吸附法检测血清免疫球蛋白(IgA、IgM和IgG)和补体(C3和C4)含量;多功能液相芯片分析平台检测细胞因子水平,包括白细胞介素-2(IL-2)、IL-4、IL-10、IL-12p70、IL-13、IL-17A、肿瘤坏死因子α(TNF-α)和γ干扰素(IFN-γ).苏木素伊红染色和光镜观察脾脏和胸腺组织结构;透射电子显微镜观察脾脏和胸腺超微结构.结果 与Sham组相比,SX10组外周血白细胞和淋巴细胞数量于辐射后6 h显著下降(P<0.01或P<0.001),分别于辐射后7 d和14 d恢复;S10和X10组则无显著变化.SX10组血清免疫球蛋白IgM、补体C3和C4于辐射后6 h显著下降(P<0.05或P<0.01),分别于辐射后7 d或14 d恢复.辐射后6 h,SX10组血清IL-2、IL-4、IL-10、IL-12p70、IL-13和TNF-α等含量显著升高(P<0.05,P<0.01或P<0.001),于辐射后7 d恢复.辐射后6 h和7 d,各辐射组大鼠胸腺和脾脏组织淋巴细胞核碎裂,至辐射后28 d恢复.辐射后7 d,各辐射组胸腺和脾脏组织淋巴细胞线粒体空化、嵴断裂等,其中X10组和SX10组溶酶体增多.结论 10 mW/cm2 S波段和X波段微波长期复合暴露可致外周血细胞、免疫球蛋白和补体抑制,胸腺和脾脏组织结构损伤.