OBJECTIVE：As a carcinogen classified as Group 2A by the International Agency for Research on Cancer (IARC)，glycidyl methacrylate (GMA) is widely used in the synthesis and modification of various composite materials. However，the specific carcinogenic mechanism of GMA remains unclear. This study aimed to investigate whether the key molecular mechanisms underlying the malignant transformation of 16HBE cells induced by GMA are associated with the expression of aldehyde dehydrogenase 3A1 (ALDH3A1). METHODS：The transient transfection technique was used to overexpress ALDH3A1 in the GMA-induced malignant transformed 16HBE cells，which was established by our research group in previous work. qPCR and Western blot techniques were used to analyze the gene and protein expression levels of IL-6/signal transducer and activator of transcription 3 (STAT3) pathway and epithelial-mesenchymal transition (EMT) markers，including E-cadherin，Vimentin，matrix metalloproteinase 3 (MMP3) and Snail protein and mRNA expression. RESULTS：The qPCR and Western blot results showed that，compared to the control group，the ALDH3A1 overexpression group upregulation of E-cadherin expression，and downregulation of IL-6，STAT3，p-STAT3，MMP3 and Snail expression (P<0.05). Additionally，the transcription levels of MMP3，Snail，and Vimentin were downregulated (P<0.05). The results indicated that ALDH3A1 reduced the expression of several key proteins involved in the EMT process in GMA-induced malignant transformed 16HBE cells by inhibiting the activation of the IL6/STAT3 pathway. CONCLUSION：ALDH3A1 is closely associated with the GMA-induced malignant transformation process in 16HBE cells，and it inhibits the activation of the IL-6/STAT3 pathway，thereby attenuating the expression of multiple key proteins involved in the EMT process. These findings contribute to elucidating the carcinogenic mechanism of GMA and provide potential biomarkers for the assessment of health effects of GMA exposure.

OBJECTIVE：To investigate the expression of tonsoku-like DNA repair protein (TONSL) in esophageal carcinoma and its effect and mechanism on the proliferation of esophageal squamous cell carcinoma. METHODS：Databases such as cBioPortal，GEPIA and PRIDE were used to analyze changes in TONSL genome copy number and its transcription and translation levels in esophageal cancer. The expression of TONSL in esophageal squamous cell carcinoma and normal esophageal tissues was detected by immunohistochemistry. Small interfering RNA (siRNA) was used to construct a TONSL knockdown esophageal squamous cell model. The effect of TONSL knockdown on the proliferation of esophageal squamous cell carcinoma cells was studied by colony formation assay and EdU assay，while the changes of phosphorylated activation levels of ATM serine/threonine kinase (ATM) and checkpoint kinase 2 (CHK2)，two DNA damage repair related marker proteins in esophageal squamous cell carcinoma cells was detected by Western blot. RESULTS：Compared with normal esophageal tissue，copy number amplification of TONSL was common in esophageal cancer，and its mRNA and protein levels in esophageal cancer were up-regulated compared with those in normal esophageal tissues (P<0.05)，and high TONSL expression was associated with poor prognosis of patients with esophageal carcinoma (P<0.05). The results of immunohistochemistry also showed that TONSL was up-regulated in esophageal squamous cell carcinoma. The results of colony formation assay and EdU assay showed that knockdown of TONSL inhibited the proliferation of esophageal squamous cell carcinoma cells (P<0.05). Moreover，TONSL knockdown induced up-regulation of the phosphorylation of ATM serine/threonine kinase (ATM) and checkpoint kinase 2 (CHK2) in esophageal squamous cell carcinoma cells. CONCLUSION：TONSL was up-regulated in esophageal squamous cell carcinoma and promoted the proliferation of esophageal squamous cell carcinoma by participating in DNA damage repair.

OBJECTIVE：To investigate effects of low dose (≤30 Gy) ionizing radiation on antioxidant enzyme and photosynthesis activities in Brassica napus L. (B. napus) seedlings. METHODS：B. napus seedlings were obtained through soil culture，with each dose group consisted of 5 rapeseed plants. Intermittent ¹³⁷Cs irradiation instead of chronic irradiation was used. The irradiation was conducted 5 days per week for 7 hours per day at doses of 0 (control group)，5，10，15，20，25，and 30 Gy，with an irradiation dose rate of 8.28 mGy/min. The activities of superoxide dismutase (SOD)，catalase (CAT)，peroxidase (POD)，content of chlorophyll a，b，a+b，carotenoid in leaves，and expression of genes related to photosynthesis (psb A，psb D，psb C，and LOD106434505) in the leaves of the seedlings after irradiation were detected and analyzed. RESULTS：Compared with the control group，the activities of SOD and CAT increased with the increase of irradiation dose (P<0.05)，but there is no significant trend in POD activity (P>0.05). As the irradiation dose increased，the chlorophyll a and b contents of the seedlings first increased，reaching the highest in the 10 Gy dose group (P<0.05)，and then decreased. There was no significant trend in changes in chlorophyll a+b content and carotenoid content，with the highest in the 5 Gy dose group (P<0.05). After irradiation，the expression level of gene psb C was downregulated (except for the 15 Gy dose group，P<0.05). The expression of LOC106434505 was significantly upregulated with increasing irradiation (P<0.05)，while the expression changes of psb A and psb D were not significant. CONCLUSION：Low dose (≤30 Gy) ¹³⁷Cs irradiation enhanced the antioxidant enzyme activities of rapeseed seedlings，and affected photosynthesis by perturbing chlorophyll content，photoelectron transport，and energy capture and transfer.

OBJECTIVE：To investigate expression of the transmembrane protein 79(TMEM79) in hepatocellular carcinoma(HCC)，and to analyze its correlations with clinicopathological characteristics and prognosis of the patients. METHODS：From May 2011 to August 2017，clinicopathological data of 95 patients in the Meizhou People--s Hospital with HCC who received radical surgical treatment were collected. Expression levels of TMEM79 were evaluated using immunohistochemistry. Relationships between TMEM79 expressions and clinicopathological factors were analyzed using the χ² test. Kaplan-Meier method and Log-rank test were performed to analyze the survival time. Cox proportional risk regression model was used to analyze prognostic factors. RESULTS：The expression levels of TMEM79 in HCC was significantly correlated with the differentiation degree of HCC (χ²=8.902；P<0.05). The overall survival times (OS) and the progression-free survival times (PFS) of the negative expression group was significantly prolonged comparing with the positive expression group (P<0.01). Positive expression of TMEM79 was a risk factor for postoperative recurrences and metastases in patients with stage Ⅰa-Ⅱa [HR=2.001，95%CI (1.152，3.476)，P<0.05]. Histological morphology with mass form predominantly [HR=3.090，95%CI(1.317，7.273)，P<0.05] and the positive expression levels of TMEM79 [HR=3.323，95%CI (1.652，6.683)，P<0.05] were independent factors affecting postoperative PFS and OS in HC C patients with stageⅠa-Ⅱa(P<0.05). CONCLUSION：Expression of the TMEM79 protein in HCC tissue was related to the degrees of HCC differentiation. The positive expression levels of TMEM79 were related to poor prognosis. Positive expression levels of TMEM79 protein can possibly be used as a predictive factor for postoperative HCC patients with stage Ⅰa-Ⅱa.

OBJECTIVE：To investigate the acute and sub-chronic toxicity of tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) in rats. METHODS：In the acute toxicity test，50 SD rats at SPF level were randomly divided into 5 groups，with 10 rats per group，equally male and female，and given a single oral dose of 464，1 000，2 150，4 640，and 10 000 mg/kg. In the sub-chronic toxicity test，80 SD rats at the SPF level were randomly divided into 4 groups of 20 rats per group，equally divided between males and females，and orally administered a dose of 0，13.3，40，and 120 (high dose) mg/kg per day for 112 consecutive days. Organs were harvested and weighed，and the organ coefficient was calculated. Blood routine and blood biochemical indices were examined. HE staining was performed to analyze histopathological changes. Representative indicators were selected for toxic effects using the baseline dose BMD method to assess exposure levels at specific risk levels，compared with the NOAEL method reference values to analyze relatively more specific and sensitive dose limits. RESULTS：The LD₅₀ of TDCIPP in acute oral toxicity test in SD rats was 2 000-2 300 mg/kg. Compared with the control group，the 120 mg/(kg·d) sub-chronic exposure dose significantly affected the body mass growth of female rats；the organ coefficients of the liver and kidney of rats in the 40 and 120 mg/(kg·d) dose of TDCIPP group were significantly elevated (P<0.05)；and the leukocyte counts，lymphocyte counts，and monocyte counts of male rats in the 40 mg/(kg·d) dose of TDCIPP group were significantly elevated (P<0.05). The mean values of white blood cell count，lymphocyte count，monocyte count and eosinophil count in male rats dosed with 40 mg/(kg·d) were significantly higher than those in the control group (P<0.05). The mean values of AST in male rats were significantly lower than those in the control group in the 40 mg/(kg·d) dose group；the mean values of ALT and AST in female rats in the 40 mg/(kg·d) dose group were significantly lower than those in the control group (P<0.05)；and HE staining of the 40 and 120 mg/(kg·d) dose groups showed significant renal pathology damage. The highest NOAEL of 13.3 mg/(kg·d) was assessed based on the no-observed-adverse-effects level (NOAEL). The benchmark dose method (BMD)，which uses blood creatinine as an indicator of renal function，determined the reference dose in the risk assessment with a limit of 2.696 mg/(kg·d). CONCLUSION：The livers and kidneys were the main target organs of TDCIPP in rats.

OBJECTIVE：To investigate sub-acute toxicity of the ionic liquid，1-heptyl-3-methy- limidazolium chloride，(C₇[MIM]Cl) in mice. METHODS：According to the median lethal dose (LD₅₀) of C₇[MIM]Cl to mice as 119.00 mg/kg， Kunming mice (n=24) were randomly divided into blank control group and low，middle and high dose (1/50 LD₅₀，1/20 LD₅₀ and 1/10 LD₅₀) groups (n=6 per group). Mice were treated with C₇[MIM]Cl once a day by gavage for 28 days. The control group was given an equal volume of normal saline by gavage. The changes of food intake and body mass of mice were recorded；organ coefficients were calculated；serum biochemical indexes were detected；and the pathological changes of each organ were observed by H&E staining. RESULTS：The food intake in middle exposure group was lower than the control group (P=0.05). Serum biochemical indices showed that the activities of alanine aminotransferase (ALT) in the liver of the low exposure group was significantly increased (P=0.049). The total bilirubin (TBIL)，UREA，uric acid (UA) and cholesterol (CHO) in the serum of the middle exposure group was significantly lower than the control (P<0.05). The glucose (GLU) level in the high dose group was significantly decreased (P<0.05). The observation of tissue section showed that different exposure doses induced a certain degree of damage to liver，spleen，lung，kidney and ovary. Especially，damages to the liver and kidney were more obvious. CONCLUSION：With sub-acute exposure of C₇[MIM]Cl，liver and kidney were important target organs for damage from C7[MIM]Cl.

OBJECTIVE：To construct esophageal squamous cell carcinoma (ESCC) cell lines with ANXA2 gene knockdown using CRISPR/Cas9 system，and to study the effect of ANXA2 on cell phenotype and downstream molecules. METHODS：The guide RNAs (gRNAs) of ANXA2 and control were searched in the public database，and the recombinant plasmids expressing the gRNAs were constructed using CRISPR/Cas9 vector，which was transferred into HEK293FT cells to prepare CRISPR/Cas9 lentivirus. After ESCC cells KYSE30 and KYSE150 were infected with the lentivirus，positive cells were screened with purinomycin and expanded in culture. The Western blot assay was used to detect expressions of the ANXA2 protein and its downstream molecule MYC，RT-qPCR assay for the expression of ANXA2 mRNA，and the colony formation and The transwell assays for the changes of colonies as well as migration and invasion abilities，respectively. RESULTS：CRISPR/Cas9 plasmids were successfully constructed. Based on the Sanger sequencing results， the ANXA2 gene knockdown plasmids and the control plasmid were successfully constructed. After virus infection，Western blotting showed that the levels of ANXA2 protein and its downstream MYC protein were significantly decreased in KYSE30 infected with two gRNA target viruses (P<0.05). The RT-qPCR results confirmed that the above two targets significantly down-regulated the mRNA expression level of ANXA2 (P<0.05). Cell phenotype experiments showed that invasion and migration as well as cell colony formation abilities were significantly weakened after knockdown of ANXA2 (P<0.05). CONCLUSION：ANXA2 gene knockdown significantly inhibited the malignant phenotype of ESCC cells，which provides a cell model and experimental basis for further study on mechanisms of ANXA2 in promoting the malignant phenotype of ESCC cells.

OBJECTIVE：To analyze the usefulness of determining chromosome copy numbers in fetuses with different NT values. METHODS：From January 2017 to May 2022，514 pregnant women who met the inclusion criteria were recruited from the Foshan Women and Children Hospital.They were divided into the elderly group (Group A)，the 2.5 mm≤NT<3.0 mm group (Group B) and the NT≥3.0 mm group (Group C). Karyotype analysis and next generation sequencing on fetal villi or amniotic fluid were performed simultaneously. RESULTS：From our analysis，there were 42 cases (8.17%) of aneuploidy，8 cases (1.56%) of pathogenic copy number variants (CNVs)，and 10 cases (1.95%) of uncertain significance. There was no significant different in aneuploidy frequencies between Group A (2.63%) and Group B (4.72%)，P>0.05. The aneuploidy frequencies in Group C (17.22%) was significantly higher than that in Groups A and B (P<0.05). For the detection of clinically significant CNVs，there was no statistically significant difference between Group B (0) and Group A (3.51%)，but Group C (5.56%) was significantly higher than that in Group B (0) (P<0.05). CONCLUSION：For pregnant women with only NT value thickening，further testing recommendations should be based on the NT values. CNVs is not necessary for pregnant women with 2.5 mm≤NT<3.0 mm but patients should be informed of residual risk. For pregnant women with NT≥3.0 mm，both karyotype analysis and CNVs are necessary.

OBJECTIVE：To investigate the usefulness for combined detection of serum miRNA-183 and carbohydrate antigen 199 (CA199) in the diagnosis and prognosis of gastric cancer. METHODS：From January 2017 to December 2021，fifty-two patients with gastric cancer，who were diagnosed in the Affiliated Chuzhou Hospital of Anhui Medical University were selected and their case data were used as the gastric cancer group. In addition，40 patients with benign stomach lesions were included as the non-gastric cancer group. Their levels of serum miRNA-183 and CA199 were determined. RESULTS：Differences in the levels of serum miRNA-183 between the gastric cancer and the non-gastric cancer groups were statistically significant (P<0.05). Expression levels of the serum miRNA-183 in patients with histopathologic classification of low-undifferentiated，T3-T4 and TNM stage III-IV were significantly higher than that in patients with histopathologic classification of medium-highly differentiated，T1-T2 and TNM stage I-II， (P<0.05). Expression levels of the serum CA199 in patients with histopathologic classification of low-undifferentiated and TNM stage III-IV were significantly higher than that in patients with histopathologic classification of medium-highly differentiated and TNM stage I-II， (P<0.05). Using the ROC curve analysis，the optimal cutoff value of the relative expression level of serum miRNA-183 was 4.11. The sensitivity and specificity were 67.31% and 80%，respectively. The area under the curve (AUC) was 0.771. The optimal cutoff value of the relative expression level of serum CA199 was 46.17 U/mL. The sensitivity and specificity were 53.8% and 87.5%，respectively. The area under the curve (AUC) was 0.724. The sensitivity and specificity of combined detection of serum miRNA-183 and CA199 in the diagnosis of gastric cancer were 76.92% and 87.5%，respectively，and the AUC was 0.882. The AUC of miRNA-183 combined with CA199 in diagnosis of gastric cancer was greater than that of miRNA-183 and CA199 independently. Kaplan-Meier analysis showed that the prognosis of patients with high expression of miRNA-183 was worse than that of patients with low expression，and the prognosis of patients with double high expression of miRNA-183 and CA199 was worse than that of patients without double high expression (P<0.05). CONCLUSION：There was a significant increase in the expression of miRNA-183 in serums of the patients with gastric cancer. Moreover，the expression levels of miRNA-183 were related to T stage，TNM stage and histological grading of tumor. Combined detection of serum miRNA-183 and CA199 improved the diagnostic efficiency of gastric cancer and predicted the prognosis of these patients.

OBJECTIVE：To investigate correlations of serum miR-146a with tumor necrosis factor α (TNF-α) and T-regulatory cells (Treg) in patients with non-small cell lung cancer (NSCLC) and prognostic valuesa in the patients. METHODS：From June 2020 to November 2021，a total of 162 patients with advanced NSCLC who were treated in Cangzhou Central Hospital were selected for our study. Levels of miR-146a in patients were detected using fluorescence quantitative PCR ELISA，serum levels of miR-146a and TNF-α were detected using enzyme-linked immunoassay，and Treg levels were detected using flow cytometry. Pearson correlation was used to analyze correlations among miR-146a expressions， TNF-α concentrations and Treg proportion. Multi-factor logistic regression was used to analyze whether the relative expression levels of miR-146a was a prognostic risk factor for the patients. ROC curve was used to compare the predictive efficacy of miR-146a on prognosis. RESULTS：The relative expression levels of miR-146a was positively correlated with the concentrations of TNF-α (r=0.651，P<0.01)，and negatively correlated with the proportions of Treg (r=-0.676，P<0.01). The relative expression levels of miR-146a and the concentrations of TNF-α were prognostic risk factors (OR=1.95 and 1.39，respectively；P<0.01). Treg was a prognostic protective factor for death in NSCLC patients (OR=0.53；P<0.01). The AUC of miR-146a was 0.959 and 95%CI (0.934，0.985)，P<0.01. CONCLUSION：Serum miR-146a in NSCLC patients was positively correlated with TNF-α and negatively correlated with Treg，which was shown to be a risk factor for death in NSCLC patients and to have high prognostic value for NSCLC.

OBJECTIVE：To investigate expression of DNAJB4 in non-small cell lung cancer (NSCLC) and its association with immune cell infiltration levels and prognosis. METHODS：Differences in expression of DNAJB4 mRNA in cancer tissues of NSCLC patients and normal tissues adjacent to the cancers were evaluated based on GEPIA database analysis. Real-time quantitative PCR and immunohistochemical methods were used to detect expressions of DNAJB4 mRNA and protein in NSCLC tissues. The TIMER database was used to analyze correlations between the expression of DNAJB4 and the level of immune cells (B cells，CD4⁺T cells，CD8⁺T cells，neutrophils，macrophages，dendritic cells) infiltration in NSCLC，and to explore the prognosis of NSCLC patients with immune cell infiltration. Relationships between expression levels of DNAJB4 and prognosis of NSCLC were evaluated using the Kaplan Meier plot database. RESULTS：Expression of DNAJB4 in NSCLC tissues was lower than that of normal tissues. The low expression was associated with the infiltration levels of immune cells. In lung adenocarcinoma，copy number variations of DNAJB4 had a significant impact on the infiltration levels of immune cells (P<0.05). In addition，B cells served as independent prognostic factors for LUAD. In lung squamous cell carcinoma (LUSC)，DNAJB4 copy number variations had a significant impact on immune cell infiltration levels except for CD8⁺ T cells (P<0.05). Survival analysis showed a significant correlation between low expression of DNAJB4 and poor prognosis in NSCLC patients (P<0.05). CONCLUSION：DNAJB4 expression in NSCLC tissues was downregulated，involved in immune cell infiltration into cancer tissues，impacted on the balance of immune microenvironment，and adversely affected prognosis of the patients. DNAJB4 may be useful as a biological marker for immune cell infiltration and prognosis in NSCLC.