Cadmium is a highly toxic heavy metal that damages multiple organ systems. However, the effects of cadmium on male reproductive function remain incompletely understood. The present work established a cadmium-exposed model of mouse testicular Sertoli cells (TM4 cells) to explore the effect of cadmium on ferroptosis in these cells and the underlying mechanisms involved. The experimental results showed that with increasing toxicant exposure, cell viability, intracellular glutathione (GSH) content, mitochondrial membrane potential, as well as Solute Carrier Family 7 Member 11 (SLC7A11) and Glutathione Peroxidase 4 (GPX4) expression were gradually decreased. In contrast, the endoplasmic reticulum stress marker Glucose-Regulated Protein 78 and proteins involved in the PERK-ATF4-CHOP pathway were significantly upregulated. Combined treatment with the PERK inhibitor GSK2656157 markedly reduced intracellular oxidative stress, elevated GSH levels and the expression of SLC7A11, GPX4 and Nuclear factor erythroid 2-related factor 2 (Nrf2), restored mitochondrial membrane potential, and downregulated key proteins in the PERK-ATF4-CHOP pathway. Similarly, combined treatment with the ferroptosis inhibitor Ferrostatin-1 significantly ameliorated cellular redox homeostasis, increased GSH content, upregulated the expression of SLC7A11, GPX4, Nrf2 and core ferroptosis regulators, and effectively recovered mitochondrial membrane potential. Therefore, our research indicates that cadmium can induce oxidative stress in TM4 cells, thereby activating the PERK-ATF4-CHOP signaling pathway. This leads to a disruption of the cells' ability to clear oxidative stress products, causing a significant accumulation of lipid peroxidation products within the cells. As a result, TM4 cells undergo ferroptosis, causing damage to the male (masculine) reproductive system functions.

Cadmium (Cd), an environmental toxicant, accumulates in the human body and damages the male reproductive system. To investigate the molecular mechanisms underlying Cd-induced reproductive toxicity, we used GC-2spd cells and treated them with CdCl2. Additionally, we added 2-APB (an inhibitor of the IP3R) and STF-083010 (an inhibitor of IRE1) to investigate whether they could ameliorate Cd-induced reproductive toxicity. Confocal microscopy and flow cytometry confirmed that CdCl2-treated GC-2spd cells displayed imbalance of calcium homeostasis, with upregulation of the expression of the IP3R, a key pathway for endoplasmic reticulum (ER) Ca2+ release. Furthermore, the ER stress (ERS) effector protein IRE1 expression was also increased, suggesting that Cd activated ERS and the IRE1 pathway by disrupting calcium homeostasis. Previous studies have shown that ERS induces autophagy. We performed the MDC assay to detect autophagosome formation, revealing increased expression of autophagy-related proteins LC3-II/LC3-I and Beclin-1 in response to Cd treatment. In contrast, treatment with 2-APB and STF-083010 inhibited autophagy and mitigated cell death. This inhibitory effect may be due to 2-APB blocking IP3R-mediated Ca2+ release, alleviating imbalance of calcium homeostasis, while STF-083010 inhibits IRE1, restoring ER homeostasis and reducing autophagy. These findings suggest that imbalance of calcium homeostasis activates the IRE1 pathway-mediated ERS, leading to excessive autophagy and male reproductive toxicity. Conversely, the addition of 2-APB and STF-083010 reversed these effects, synergistically restoring intracellular Ca2+ homeostasis and inhibiting ERS to promote cell health. This study provides a new therapeutic strategy for Cd-induced male reproductive disorders.

Effective instructional approaches for fostering students' competences in public health education remain to be explored. This study aimed to integrate the bridge-in, objective, pre-assessment, participatory learning, post-assessment, and summary (BOPPPS) framework with problem-based learning (PBL), team-based learning (TBL), and case-based learning (CBL) to develop a novel instructional model, termed the BOPPPS-integrated model (BIM), and to assess the influences of single and multiple BIM interventions on the competences of undergraduate public health students. A two-stage study was conducted by a quasi-experimental pilot study and a cross-sectional survey. First, the quasi-experiment compared a traditional lecture-based learning (LBL) group (n = 50) with a BIM group (n = 48) to evaluate the effect of a single BIM intervention. Second, a cross-sectional study was conducted to analyze the impacts of multiple BIM sessions across three groups: control (n = 96), basic intervention (1–2 times BIM, n = 66), and intensive intervention (≥ 3 times BIM, n = 62). All participants completed a self-administered questionnaire designed to evaluate seven competence dimensions: information literacy, summarization, expressive communication, critical thinking, self-directed learning, teamwork, and objective evaluation, which are essential for public health students to address complex public health challenges. Students who received single and multiple BIM instructional sessions scored significantly higher in information literacy, expressive communication, and teamwork than those who received LBL method (P < 0.05). Multiple BIM interventions further improved scores in summarization, self-directed learning, and objective evaluation (P < 0.05). The scores of six dimensions like information literacy, summarization, expressive communication, self-directed learning, teamwork, and objective evaluation showed an upward trend as the number of interventions increased (P for trend < 0.05). A single BIM intervention effectively improved students’ competences in information literacy, teamwork, and expressive communication. Additionally, multiple BIM interventions not only consolidated these competences but also fostered summarization, self-directed learning, and objective evaluation, thereby highlighting the importance of BIM in developing students’ competences in public health education.

Di-(2-ethylhexyl) phthalate (DEHP), a widely used plasticizer, could cause male reproductive toxicity by disrupting spermatogenesis. Piwi-interacting RNAs (piRNAs) are a small non-coding RNAs specifically highly expressed in the germline and interact with PIWI proteins to regulate spermatogenesis. Accumulating studies have confirmed that environmental poisons could induce male reproductive injury via altering piRNA expression. However, it remains unclear whether DEHP causes male reproductive dysfunction by perturbing piRNA expression levels. In this study, we conducted piRNA microarray expression analyses on testes of DEHP-exposed and control male rats and performed some in vitro and in vivo studies to explore the role of piRNA on DEHP-induced male reproductive toxicity. Our results showed that DEHP exposure leaded to changed expression profiles of piRNAs in pubertal male rat testes. And bioinformatics analyses revealed that down-regulated piR-rno-26751 probably targeted Insr mRNA expression regulation. Results from gene and protein expression tests demonstrated that DEHP caused decreased expression level of INSR mainly in spermatogonia. Moreover, MEHP, the main metabolite of DEHP resulted in cell apoptosis and down-regulation of INSR and its downstream p-IRS1, p-PI3K, p-AKT and p-FOXO1 in GC-1spg cells. Conversely, overexpression of INSR restored cell apoptosis and the down-regulation of the above proteins in GC-1spg cells. In conclusion, these findings suggest that DEHP-induced down-regulation of piR-rno-26751 targets the suppression of INSR, leading to apoptosis of spermatogonia in pubertal male rats.

Cadmium (Cd) is a harmful environmental pollutant that disrupts public health, including respiratory, digestive, and reproductive systems. In this study, male rats were exposed to CdCl2 at a dose of 3 mg/kg by oral for 28 days to investigate the impact on spermatogenesis. Testis tissue samples were collected after sacrifice, and piRNA expression levels were measured using piRNA microarray and qPCR. PiRNAs, specialized molecules involved in spermatogenesis, were examined. CdCl2 exposure led to disrupted piRNA expression, particularly in piRNADQ759395 in rats. This piRNA was found to have a binding site with p53, and a similar piRNA-DQ717867 was discovered in mice. In GC-2spd cells, CdCl2 exposure increased piRNA-DQ717867 expression, which resulted in cell cycle arrest and abnormal expression of cell cycle-related proteins. The activation of p53-related pathways and disruptions in cell cycle regulation were also observed. Antagomir-717867 transfections and PFT-a pretreatment in GC-2spd cells supported the involvement of piRNA-DQ717867 in regulating cell cycle-related proteins. This study suggests that Cd exposure induces abnormal expression of piRNA-DQ759395 in rat testis and that piRNA-DQ717867 may regulate p53, causing cell cycle abnormalities in GC-2spd cells. These findings help understand the mechanisms of male reproductive toxicity caused by Cd exposure and emphasize the role of piRNAs in cell cycle regulation and male reproductive health.

Graphene-based nanomaterials (GBNs) consist of a single or few layers of graphene sheets or modified graphene including pristine graphene, graphene nanosheets (GNS), graphene oxide (GO), reduced graphene oxide (rGO), as well as graphene modified with various functional groups or chemicals (e.g., hydroxyl, carboxyl, and polyethylene glycol), which are frequently used in industrial and biomedical applications owing to their exceptional physicochemical properties. Given the widespread production and extensive application of GBNs, they can be disseminated in a wide range of environmental mediums, such as air, water, food, and soil. GBNs can enter the human body through various routes such as inhalation, ingestion, dermal penetration, injection, and implantation in biomedical applications, and the majority of GBNs tend to accumulate in the respiratory system. GBNs inhaled and substantially deposited in the human respiratory tract may impair lung defenses and clearance, resulting in the formation of granulomas and pulmonary fibrosis. However, the specific toxicity of the respiratory system caused by different GBNs, their influencing factors, and the underlying mechanisms remain relatively scarce. This review summarizes recent advances in the exposure, metabolism, toxicity and potential mechanisms, current limitations, and future perspectives of various GBNs in the respiratory system.

OBJECTIVE:To study the effects of cadmium on autophagy in germ cells (GC-2 spd cells) through Ca2+ and IRE1 pathway.METHODS:The viability of GC-2 spd cells was determined using a CCK-8 assay to establish the concentration of cadmium treating . MDC staining was employed to assess autophagosome formation. Laser confocal microscopy and flow cytometry were utilized to measure cytoplasmic and endoplasmic reticulum (ER) Ca2+ levels. Western blot was conducted to evaluate the expression levels of proteins associated with the IRE1 signaling pathway and autophagy.RESULTS:As the concentration of cadmium increased, cell viability gradually decreased. The concentrations of cadmium were determined to be 2.5, 5, and 10 μmol/L. Compared with the control group, the IOD values of MDC fluorescence intensity within the cadmium group were all elevated (P<0.05), accompanied by elevated ratios of autophagy markers LC3-II/LC3-I and up-regulation of Beclin-1 protein expression (P<0.05). Cytoplasm Ca2+ levels gradually increased, while ER Ca2+ levels decreased (P<0.05). The expression of IP3R protein, the ER Ca2+ release pathway, was up-regulated (P<0.05). Additionally, the expressions of IRE1, XBP1s, CHOP, and GRP78 were up-regulated in the cadmium group (P<0.05).CONCLUSION:Cadmium exposure can induce dysregulation of calcium homeostasis in GC-2spd cells, activates the ER stress-induced IRE1 signaling pathway, and ultimately induces the occurrence of autophagy in GC-2spd cells.

Cadmium is one of the environmental and occupational pollutants and its potential adverse effects on human health have given rise to substantial concern. Cadmium causes damage to the male reproductive system via induction of germ-cell apoptosis; however, the underlying mechanism of cadmium-induced reproductive toxicity in Leydig cells remains unclear. In this study, twenty mice were divided randomly into four groups and exposed to CdCl2 at concentrations of 0, 0.5, 1.0 and 2.0 mg/kg/day for four consecutive weeks. Testicular injury, abnormal spermatogenesis and apoptosis of Leydig cells were observed in mice. In order to investigate the mechanism of cadmium-induced apoptosis of Leydig cells, a model of mouse Leydig cell line (i.e. TM3 cells) was subjected to treatment with various concentrations of CdCl2. It was found that mitochondrial function was disrupted by cadmium, which also caused a significant elevation in levels of mitochondrial superoxide and cellular ROS. Furthermore, while cadmium increased the expression of mitochondrial fission proteins (DRP1 and FIS1), it reduced the expression of mitochondrial fusion proteins (OPA1 and MFN1). This led to excessive mitochondrial fission, the release of cytochrome c and apoptosis. Conversely, cadmium-induced accumulation of mitochondrial superoxide was decreased by the inhibition of mitochondrial fission through the use of Mdivi-1 (an inhibitor of DRP1). Mdivi-1 also partially prevented the release of cytochrome c from mitochondria to cytosol and attenuated cell apoptosis. Finally, given the accumulation of LC3II and SQSTM1/p62 and the obstruction of Parkin recruitment into damaged mitochondria in TM3 cells, the autophagosome-lysosome fusion was probably inhibited by cadmium. Overall, these findings suggest that cadmium induces apoptosis of mouse Leydig cells via the induction of excessive mitochondrial fission and inhibition of mitophagy.

目的 研究镉对小鼠初级精母细胞(GC-2spd细胞)自噬和Bcl-2 蛋白表达的影响.方法 将处于对数生长期的GC-2spd细胞,加入 0(对照)～40 μmol/L氯化镉溶液染毒 24 h.采用CCK-8 法测定细胞的存活率,采用Western blotting法检测细胞Bcl-2的蛋白表达.结果 与对照组比较,各浓度氯化镉染毒组GC-2spd细胞的存活率均较低,差异有统计学意义(P＜0.01);且随着氯化镉染毒浓度的升高,细胞的存活率呈逐渐下降趋势.与对照组比较,5、10 μmol/L氯化镉染毒组GC-2spd细胞Bcl-2 蛋白表达水平较低,差异均有统计学意义(P＜0.05);且随着氯化镉染毒浓度的升高,GC-2spd细胞Bcl-2 蛋白的表达水平呈下降趋势.结论 氯化镉可能通过抑制生精细胞Bcl-2 蛋白表达,导致细胞自噬.

This study was designed to explore the mechanism of LncRNA-NBR2 on Bcl-2 and AMPK signaling pathway in breast cancer cells. The breast cancer cells were divided into blank group (MCF-7 cells were cultured without any treatment), NBR2 transfection group (MCF-7 cells were cultured after overexpression of LncRNA NBR2), and NC group (MCF-7 cells were transfected with negative mimics). The expression of LncRNA NBR2 mRNA in MCF10A and MCF-7 cells was detected by RT-PCR. MTT method was used to compare the proliferation of the three groups. Flow cytometry was used to compare the apoptosis of the three groups, Transwell chamber method was used to compare the invasion of the three groups of cells, and the expression of Bcl-2 and AMPK protein was compared by Western blot. Through the comparison of cell proliferation, invasion and apoptosis, it was found that the proliferation, apoptosis and invasion ability of blank group and NC group had no significant change (p > 0.05). Compared with the blank group and NC group, the proliferation and invasion ability of NBR2 group were significantly decreased (p < 0.05), and the apoptosis ability of breast cancer cells was significantly increased. Compared with the blank group and NC group, the expression of Bcl-2 and AMPK protein in NBR2 group was significantly lower (p < 0.05) than NC group. Overexpression of LncRNA-NBR2 can effectively inhibit the expression of Bcl-2 protein and promote the expression of AMPK protein in breast cancer cells. It is speculated that LncRNA NBR2 can regulate the proliferation and invasion of breast cancer cells by regulating Bcl-2 and AMPK proteins.

OBJECTIVE:To study the impact of cadmium (Cd) on the expressions of PIWI-interacting RNAs (piRNA) in the rat testis and its possible action mechanism.METHODS:Twelve 6-week-old SD rats were randomly divided into a Cd-exposure and a control group, the former gavaged with CdCl2 at 3 mg/kg/d and the latter with normal saline, all for 28 successive days. Then the testicular tissues were collected from the rats, sperm concentration and motility were obtained by computer-assisted sperm analysis (CASA), and piRNA sequencing was performed using the gene chip, followed by bioinformatics analysis of differentially expressed piRNAs.RESULTS:Compared with the controls, the rats in the Cd-exposure group showed significantly decreased sperm concentration and motility (P < 0.05). The expressions of 272 piRNAs were up-regulated and 402 down-regulated after 28 days of Cd exposure, and 4 of the up-regulated piRNAs were consistent with the results of gene chip verification. Bioinformatics analysis showed that the 4 up-regulated piRNA target genes were involved in 50 biological processes, such as negative regulation of apoptosis, positive regulation of gene expression and positive regulation of GTPase activity, and mainly concentrated in 13 signaling pathways including transcription dysregulation, calcium and mitogen-activated protein kinase signaling pathways in cancer. Among them, PIRNA-DQ765261 had a binding site with Bcl-2.CONCLUSION:Cadmium can induce changes in the expressions piRNAs in the rat testicular tissue, and some piRNAs may be involved in the autophagy and apoptosis of sperm. Bcl-2 may be the target of PIRNA-DQ765261.

目的 研究氧化应激在邻苯二甲酸单(2-乙基己基)酯(mono-2-ethylhexyl-phthalate,MEHP)诱导小鼠初级精母细胞(GC-2spd)毒性中的作用及机制.方法 将培养的GC-2spd细胞分为对照组(含0.1％二甲基亚砜的无血清培养基)、MEHP染毒组(1、10、100 μmol/L MEHP 3个不同剂量组)、N-乙酰半胱氨酸(N-acetylcysteine,NAC)预处理组(100 μmol/L NAC+100 μmol/L MEHP),MEHP 染毒24h,NAC预处理2h,NAC的预处理浓度(100 μmol/L)通过CCK-8实验确定.采用DCFH-DA探针法检测细胞内活性氧(reactive oxide species,ROS)水平,JC-1法检测线粒体膜电位,Western blot法检测细胞内线粒体凋亡通路相关蛋白和p-STAT3Tyr705、P53蛋白表达水平.结果 随着MEHP染毒剂量升高,细胞内代表活性氧水平的绿色荧光信号增多;不同剂量MEHP染毒组的线粒体膜电位均下降,表现为红绿荧光细胞比例比值减小,10和100μmol/L MEHP染毒组的红绿荧光细胞比例比值分别为5.15±1.68和4.09±1.72,明显低于对照组(7.91±1.24)(P＜0.05);促凋亡蛋白Bax与抗凋亡蛋白Bcl-2表达水平比值(Bax/Bcl-2)在1、10、100 μmol/L MEHP染毒组分别为 1.23±0.17、2.64±0.43和4.75±0.73,与对照组(0.52±0.11)相比明显增加(P＜0.05);cytochrome C 蛋白表达水平在 100 μmol/L MEHP 染毒组升高为0.83±0.09,cleaved caspase-9蛋白表达水平在10和100 μmol/L MEHP染毒组升高为0.41±0.03和0.52±0.09,cleaved caspase-3蛋白表达水平在 10和 100 μmol/L MEHP 染毒组升高为0.60±0.12和0.84±0.17,与对照组相比差异均具有统计学意义(P＜0.05);STAT3/p53通路中,p-STAT3Tyr705蛋白表达水平在10和100 μmol/L MEHP染毒组分别下降为0.70±0.14和0.41±0.04,P53蛋白表达水平在10和100 μmol/L MEHP染毒组分别升高为1.32±0.05和1.66±0.22,与对照组相比差异均具有统计学意义(P＜0.05);NAC预处理后,与100 μmol/L MEHP组相比,NAC预处理组ROS生成减少,线粒体膜电位升高为5.92±1.64,Bax/Bcl-2下降为 1.92±0.06,cytochrome C、cleaved caspase-9和 cleaved caspase-3蛋白表达水平分别下降为0.57±0.07、0.35±0.04和0.53±0.06,p-STAT3Tyr705蛋白表达水平升高为0.86±0.07,P53蛋白表达水平下降为1.01±0.06,差异均有统计学意义(P＜0.05).结论 MEHP诱导GC-2spd细胞凋亡可能与ROS介导的STAT3/p53通路调控线粒体凋亡通路有关.

Lung cancer is the leading cause of malignancy-related mortality and lung adenocarcinoma accounts for about 40% of lung malignancies. The aim of this study was to investigate the associations of intraflagellar transport protein 20 (IFT20) and Golgi matrix protein 130 (GM130) expression with clinicopathological features and survival in patients with lung adenocarcinoma. The expressions of IFT20 and GM130 protein in cancerous and matched adjacent lung tissues of 235 patients with lung adenocarcinoma were assessed by tissue microarray and immunohistochemistry, which were indicated by the mean optical density (IOD/area), the rate of positive staining cells and staining intensity score. The correlation between IFT20 and GM130 protein was assessed by Spearman’s rank correlation. Associations of IFT20 and GM130 protein expression with clinicopathological features of patients were analyzed by multivariate logistic regression models. The survival analysis of patients was performed by Cox proportional hazard regression models. With adjustment for multiple potential confounders, each one-point increase in IFT20 protein staining intensity score was significantly associated with 32% and 29% reduced risk for TNM stage in II ~ IV and lymphatic metastasis of patients, respectively (P < 0.05). And each one-point increase in GM130 protein staining intensity score was associated with a significant reduction in the risk of poor differentiation and tumors size > 7 cm by 29% and 38% for lung adenocarcinoma patients, respectively (P < 0.05). In stratified Cox model analysis, enhanced IFT20 staining intensity score was significantly decreased the risk of death by 16% for patients without distant metastasis. And elevated the IOD/area of GM130 expression significantly decreased the death risk of lung adenocarcinoma patients with tumor size > 7 cm or distant metastasis by 54% and 65%, respectively (P < 0.05). IFT20 and GM130 protein expressions were negatively associated with tumor differentiated types, size, TNM stage and lymphatic metastasis of lung adenocarcinoma. Both IFT20 and GM130 proteins have some protective effects on the survival of lung adenocarcinoma patients with specific clinicopathological features.

目的 调查汉川市不同人群对H7N9禽类流行性感冒(禽流感)疾病的知信行现状,为开展禽流感预防提供依据.方法 2019年6-8月,采用分层随机抽样的方法,选取汉川市农贸市场工作人员、医务人员、某校初中学生、1个城市街道和1个乡镇街道社区居民为调查对象,对居民H7N9禽流感的认知、行为和态度(24个条目)进行调查分析.结果 共发放问卷408份,回收有效问卷401份.在H7N9禽流感相关知识知晓情况中,医务人员的正确率最高,为58.75％,农村居民最低,仅为27.45％,87.03％的人群能够正确回答"接触禽类是否需要采取防护措施",而仅8.48％的人群可以正确回答"禽流感的多发季节";在不同人群对待H7N9禽流感的态度情况中,初中学生的正确率最高,为57.10％,农村居民最低,仅为46.78％,67.33％的人群认同"您觉得禽流感可怕吗",而仅28.18％的人群认同"您认为自己可能得禽流感吗";在H7N9禽流感预防行为情况中,初中学生的正确率最高,为73.63％,农贸市场工作人员最低,仅为54.00％,96.51％的人群认为接触禽类或禽类制品后应该洗手,仅有35.91％的人群接种过流行性感冒(流感)疫苗;在不同人群的H7N9禽流感防治知识获取途径中,医务人员各渠道获取信息途径比例最高,为59.25％,农贸市场工作人员最低,为26.50％,电视(69.33％)和网络(63.84％)在各人群的获取渠道中占比最高,差异均有统计学意义(均P＜0.05).结论 农贸市场工作人员和农村居民H7N9禽流感相关健康知识认知不足,存在一定的感染和传染风险.针对不同人群开展最有利的预防措施,有助于提升防治效率.

To investigate the potential associations between household renovation and allergic diseases among preschool children in Wuhan, we conducted a large cross-sectional questionnaire survey among 9455 preschool children aged 3-6 years in Wuhan during November to December 2019. Data on demographics, health status, and home decoration conditions were analysed based on a questionnaire. Compared with tiles/stone/cement floor covering, the use of composite floor significantly increased the risk of diagnosed rhinitis and eczema among children (rhinitis: AOR, 95% CI: 1.36, 1.06-1.73; eczema: AOR, 95% CI: 1.47, 1.17-1.85). Household renovation had significant associations with diagnosed eczema (within 1 year before pregnancy: AOR, 95% CI: 1.34, 1.20-1.50; during pregnancy: AOR, 95% CI: 1.25, 1.08-1.44). This study suggests that use of artificial synthetic materials in home renovation during early childhood and pregnancy may be potential risk factors for childhood asthma, allergic rhinitis, and eczema.

Cadmium (Cd) is a heavy metal that is widely present in modern industrial production. It is a known, highly toxic environmental endocrine disruptor. Long-term exposure to Cd can cause varying degrees of damage to the liver, kidney, and reproductive system of organisms, especially the male reproductive system. This study aimed to explore the mechanism of Cd toxicity in the male reproductive system during puberty. Eighteen healthy 6-week-old male Sprague-Dawley rats were randomly divided into three groups (control group, low-dose group, and high-dose group) according to their body weight, with six in each group. Cd (0, 1, and 3 mg/kg/day) was given by gavage for 28 consecutive days. The results showed that Cd exposure to each dose group caused a decrease in the testicular organ coefficient and sperm count, compared with the control group. Cd exposure resulted in significant changes in testicular morphology in the 3 mg/kg/day Cd group. In the 1 and 3 mg/kg/day Cd groups, serum testosterone decreased and apoptosis of testicular cells increased significantly (p < 0.05). In addition, compared with the control group, the activity of glutathione peroxidase and superoxide dismutase in each Cd exposure dose group decreased, but the content of malondialdehyde in the high-dose, 3 mg/kg/day Cd treatment group significantly increased (p < 0.05). Although Cd exposure caused an increase in the messenger RNA (mRNA) levels of Bcl-2, Caspase-3 and Caspase-9 in the testicular tissues (p < 0.05), Bcl-2 expression was unchanged (p > 0.05). The expression level of Akt mRNA in testicular tissue of rats in the high-dose 3 mg/kg/day Cd group was increased (p < 0.05). Our data suggest that Cd affected testosterone levels, and apoptosis was observed in spermatids.

[背景]职业人群的健康管理应贯穿生命全周期,职工健康问题不容忽视.[目的]评估武汉市某电子厂工人睡眠质量与抑郁情绪的分布特征和关联性.[方法]于2019年4—7月期间,采用整群抽样法选取武汉市某电子厂1500名工人,由经过统一培训的调查员采用面对面访谈方式进行问卷调查.采用匹兹堡睡眠量表(PSQI)和抑郁自评量表(SDS)对工人的睡眠质量和抑郁情绪进行评价.比较不同特征工人组间PSQI与SDS得分的差异,采用Spearman相关分析两量表得分的相关性,采用多元线性回归分析研究SDS得分可能的影响因素.[结果]回收有效问卷1440份,有效回收率为96.0％.工人PSQI平均得分为(2.67±2.03)分,睡眠障碍检出率为4.90％(71/1440);以性别、月收入、是否喜欢本职工作、是否被动吸烟和是否运动分组,工人的PSQI总分差异有统计学意义(P<0.05).工人SDS得分为(41.30±8.46)分,抑郁情绪检出率为15.60％(224/1440);以性别、年龄段、文化程度、月收入、是否喜欢本职工作、是否被动吸烟和是否运动分组,工人的SDS得分差异有统计学意义(P<0.05).PSQI总分和SDS得分呈正相关(r=0.249,P<0.001).多元线性回归分析显示,高的PSQI总分(b=0.891,P<0.001)和女性(b=1.403,P=0.013)与较高的SDS得分有关,喜欢本职工作(b=-2.425,P<0.001)、高学历(b=-2.200,P<0.001)、运动(b=-1.284,P=0.003)与较低的SDS得分有关.[结论]该电子厂工人的睡眠障碍和抑郁情绪检出率较低,睡眠障碍和抑郁情绪之间具有正相关关系.

Background: Emerging research suggested an association of early-life particulate air pollution exposure with development of asthma in childhood. However, the potentially differential effects of submicron particulate matter (PM; PM with aerodynamic diameter <= 1 mm [PM1]) remain largely unknown. Objective: This study primarily aimed to investigate associations of childhood asthma and wheezing with in utero and first-year exposures to size-specific particles. Methods: We conducted a large cross-sectional survey among 5788 preschool children aged 3 to 5 years in central China. In utero and first-year exposures to ambient PM1, PM with aerodynamic diameter less than or equal to 2.5 mu m, and PM with aerodynamic diameter less than or equal to 10 mu m at 1 x 1-km resolution were assessed using machine learning- based spatiotemporal models. A time-to-event analysis was performed to examine associations between residential PM exposures and childhood onset of asthma and wheezing. Results: Early-life size-specific PM exposures, particularly during pregnancy, were significantly associated with increased risk of asthma, whereas no evident PM-wheezing associations were observed. Each 10-mu g/m(3) increase in in utero and first-year PM1 exposure was accordingly associated with an asthma's hazard ratio in childhood of 1.618 (95% CI, 1.159-2.258; P = .005) and 1.543 (0.822-2.896; P = .177). Subgroup analyses suggest that short breast-feeding duration may aggravate PM associated risk of childhood asthma. Each 10-mu g/m(3) increase in in utero exposure to PM1, for instance, was associated with a hazard ratio of 2.260 (1.393-3.666) among children with 0 to 5 months' breast-feeding and 1.156 (0.721-1.853) among those longer breast-fed. Conclusions: Our study added comparative evidence for increased risk of childhood asthma in relation to early-life PM exposures, highlighting stronger associations with ambient PM1 than with PM with aerodynamic diameter less than or equal to 2.5 mu m and PM with aerodynamic diameter less than or equal to 10 mu m.

This study examined the prevalence of posttraumatic stress disorder (PTSD) symptoms and assessed mental illness via an online survey among healthcare workers (HCWs) at the Central Hospital of Wuhan after the peak of the COVID-19 outbreak. PTSD symptoms were measured using the PTSD Checklist Civilian Version (PCL-C), with a cutoff score of 50. Among the 642 HCWs, the prevalence of probable PTSD was 20.87%. Additionally, 88.88%, 82.09%, 100%, and 95.52% of HCWs with probable PTSD reported varying degrees of anxiety, depression, somatic symptoms, and insomnia, respectively. HCWs with probable PTSD scored higher on the Hospital Anxiety and Depression Scale (HADS), Patient Health questionnaire-15 (PHQ-15), and Insomnia Severity Index (ISI) than non-PTSD HCWs (all p < 0.05). Multivariate regression analysis revealed that HCWs with negative COVID-19 tests (OR, 0.35; 95% CI, 0.21-0.58; p < 0.00), those with high Social Support Self-Rating Scale (SSRS) scores (OR, 0.30; 95% CI, 0.17-0.52; p < 0.00), and HCWs whose family members tested negative (OR, 0.64; 95% CI, 0.42-0.96; p = 0.03) were less likely to have probable PTSD. This study found a high prevalence of probable PTSD and severe mental illness among local HCWs. Our finding emphasizes the need to provide mental health support for HCWs.

目的:探讨颈前路单枚空心螺钉内固定术对于治疗新鲜齿状突Ⅱ型骨折的临床疗效.方法:回顾性分析自2011年4月至2019年7月收治29例齿状突Ⅱ型骨折患者临床资料.结果:29例齿状突Ⅱ型骨折均获良好复位,患者手术切口一期愈合.随访结果显示骨折均愈合,螺钉位置良好,寰枢关节稳定且活动度良好.结论:颈前路单枚空心螺钉内固定术具有创伤小、恢复快等优点,是治疗新鲜齿状突Ⅱ型骨折较为理想的一种方法,但临床上应严格掌握手术适应证和禁忌症.