To investigate the transcription of neutrophils (Neu) expressing high levels of Csf3r^hiCD14^hiNeu in C3H/HeN mouse lung tissues before and after irradiation.

Twelve C3H/HeN mice were randomly divided into an irradiation group and a control group before being exposed to a single dose of 20 Gy chest irradiation. Twenty-four weeks after irradiation, two Neu subsets, Csf3r^hiCD14^hiNeu and Csf3r^lowCD14^hiNeu, were selected from lung tissues of irradiated and non-irradiated mice by flow cytometry. Transcriptomic sequencing (RNA-Seq) was performed on the two types of cells. Differentially expressed genes (DEGs) were identified using the DESeq2 package. Functional enrichment analysis and gene set enrichment analysis (GSEA) were performed using the gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) databases.

At 24 weeks post-irradiation, the alveolar space was significantly reduced, collagen deposition increased, and fibrosis localized in C3H/HeN mice. RNA-seq analysis suggested that there were 1499 DEGs in Csf3r^hiCD14^hiNeu compared with Csf3r^lowCD14^hiNeu in the irradiated group, 179 of which were upregulated and 1320 downregulated. In the control group, there were 701 significantly upregulated and 431 downregulated genes in Csf3r^hiCD14^hiNeu compared with Csf3r^lowCD14^hiNeu. Compared with non-irradiated Csf3r^lowCD14^hiNeu, there were 1319 upregulated and 219 downregulated genes in the irradiated group. Compared with non-irradiated Csf3r^hiCD14^hiNeu, the irradiated group had 202 upregulated and 540 downregulated genes. GO enrichment analysis indicated that these DEGs were involved in immune response, Wnt signaling pathway, and cytokine production. KEGG pathway analysis pointed to significant enrichment in the TGF-β signaling pathway, cytokine-cytokine receptor interactions, and Jak-STAT signaling pathway. GSEA revealed significant alterations in non-canonical NF-κB signaling, PD-1 signaling, and laminin interaction-related pathways.

Thoracic γ-ray irradiation can cause pulmonary fibrosis in C3H/HeN mice, with marked transcriptomic differences between Csf3r^hiCD14^hi and Csf3r^lowCD14^hiNeu subsets in lung tissue post-irradiation.

To investigate the real-time biological effects of 2650 MHz radiofrequency radiation (RFR) on learning and memory as well as calcium activity patterns of hippocampal CA1 pyramidal neurons of mice.

Adult male C57BL/6N mice were randomly assigned to control (CON) and RFR groups before being exposed to 2650 MHz RFR for 3 hours in an electromagnetic reverberation chamber. Within 1 hour after exposure, changes in learning and memory were assessed using novel object recognition (NOR), object location recognition (OLR), and temporal order recognition (TOR) tests. Calcium activity of CA1 pyramidal neurons was monitored before, during, and after exposure using genetically encoded calcium imaging combined with fiber photometry. Neuronal activation was evaluated by c-Fos immunofluorescence staining.

Compared with the CON group, RFR-exposed mice showed significantly reduced preference indices for target objects in the NOR (P < 0.001), OLR (P < 0.01), and TOR (P < 0.01) tests within 1 hour post-exposure. During RFR exposure, neuronal calcium signals exhibited an abnormal high-frequency but low-amplitude pattern, characterized by increased event frequency (P < 0.05) and decreased single-event amplitude (P < 0.05). Furthermore, the immunofluorescence intensity of c-Fos in the hippocampal CA1 region was significantly reduced (P < 0.05).

2650 MHz radiofrequency radiation exposure can induce immediate effects, such as abnormalities in calcium signaling patterns and suppressed excitability of pyramidal neurons in the hippocampal CA1 region, ultimately leading to impaired learning and memory functions.

To investigate the impact of myeloid cell-specific knockout of the granulocyte colony-stimulating factor receptor (G-CSFR) on the progression of acute radiation pneumonitis.

Myeloid cell-specific G-CSFR knockout (G-CSFR^{-/-, Lyz2-cre}) mice were constructed. G-CSFR^{-/-, Lyz2-cre} and C57BL/6N mice underwent a single whole-body irradiation with 6.5 Gy of ⁶⁰Co γ-rays to establish a model of radiation injury. The lung function of mice was assessed using a mouse lung function test system at 3, 7 and 14-days post γ-ray irradiation. Pathological changes in the lung tissue were analyzed via hematoxylin and eosin (HE) staining of paraffin sections. Tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) levels were measured via radioimmunoassay. IL-8 and its receptor CXCR2 were quantified using enzyme-linked immunosorbent assay (ELISA). The infiltration of neutrophils in lung tissue was evaluated by immunohistochemical detection of myeloperoxidase.

At 3-, 7- and 14-days post-irradiation with 6.5 Gy of ⁶⁰Co γ-rays, there were no significant differences observed in lung function or interstitial inflammatory lesions between G-CSFR^{-/-, Lyz2-cre} mice and C57BL/6N mice. However, the infiltration of neutrophils in lung tissue of G-CSFR^{-/-, Lyz2-cre} mice was significantly reduced (P＜0.01), and the levels of IL-8, CXCR2 and TNF-α in lung tissues were markedly lower than in C57BL/6N mice (P＜0.05).

The myeloid cell-specific knockout of G-CSFR can effectively diminish neutrophil infiltration as well as inflammatory cytokine levels in lung tissues following radiation exposure.

To investigate the functional changes of oligodendrocytes in a mouse model of cognitive impairment induced by microwave radiation and the mechanism.

C57 BL/6N male mice were exposed to S-band microwave at 2.856 GHz and 8 mW/cm² for 15 min. The rectal temperature of mice was monitored by an optical fiber thermometer during microwave radiation. The changes of autonomous exploration behavior and learning and memory ability of mice on the 1 st and 7 th days after microwave radiation were detected via the open field test and novel object recognition test. Immunofluorescence was used to detect the expression and distribution of neuroglia-2 proteoglycan (NG2) and myelin basic protein (MBP) in the hippocampus of mice on the 1 st and 7 th days after radiation. Clemastine fumarate, a drug that promoted the maturation of oligodendrocyte precursor cells was administered by gavage, and the expression levels of brain-derived neurotrophic factor (BDNF) and fibroblast growth factor 2 (FGF2) in hippocampal tissues were detected by radioimmunoassay at 1 and 7 days after radiation. The changes of myelin sheath structure an 1 and 7 days after radiation were observed by transmission electron microscopy. The effects of clemastine fumarate on learning and memory impairment induced by microwave exposure in mice were assessed via open field and new object recognition experiments.

Under the experimental conditions, the rectal temperature in mice caused by microwave radiation increased by less than1 ℃, which was within the thermal safety range of the body. The open field test showed that compared with the control group, the microwave radiation group didn’t change significant in terms of movement speedon the 1 st and 7 th days, but the time spent exploring in the central area was significantly reducedon the 1 st day after radiation (P＜0.05) . In the novel object recognition test, the indexes of the mice on the 1 st day were significantly reduced (P＜0.05) , indicating that the anxiety like behavior and cognitive function of the mice were impaired after microwave radiation. Compared with the control group, the proportion of NG2⁺ area in the hippocampus was significantly decreased (P＜0.05) in the microwave radiation group, while that of MBP⁺ area hardly changed on the 1 st day after microwave radiation (P＞0.05) . The expression level of oligodendrocyte related BDNF in the hippocampus was significantly decreased (P＜0.05) . The myelin of the corpus callosum was broken, and the myelin g ratio was significantly increased (P＜0.05) , suggesting that microwave radiation could reduce the number of oligodendrocyte precursors and damage the secretion and myelin function of oligodendrocyte. Compared with the radiation group, the expression levels of BNDF and FGF2 in the radiation combined with clemastine fumarate group were up-regulated, the myelin g ratio was significantly decreased on the 1 st day after radiation (P＜0.05) , and the novel object recognition index was significantly increased (P＜0.05) .

Pulsed microwave radiation below the body’s fever threshold can cause cognitive dysfunction and other brain damage in mice. The impaired secretion and myelin function of oligodendrocytes and the decreased self-repair ability are the important mechanisms of cognitive dysfunction induced by microwave radiation.