Objective:To investigate the association between magnesium sulfate exposure within 24 h before birth and short-term outcomes in preterm infants under 34 weeks' gestation.Methods:This retrospective cohort study analyzed data from preterm infants under 34 weeks admitted to the neonatal intensive care unit of the Affiliated Hospital of Qingdao University between June 1, 2020, and December 31, 2024. Infants were categorized into the exposure and the control groups based on magnesium sulfate administration within 24 hours before delivery. Maternal characteristics, birth parameters, and neonatal outcomes were compared using independent t-tests or Chi square tests (Fisher's exact test), with logistic regression assessing magnesium sulfate's effect on non-cerebral palsy outcomes. Results:The cohort comprised 384 preterm infants (24-33 +6 weeks), with 290 (75.5%) in the exposure group and 94 (24.5%) in the control group. (1) Baseline characteristics showed no significant differences in maternal hypertensive disorders, antenatal corticosteroids administration, premature rupture of membranes, delivery mode, or male infant proportion (all P>0.05). The exposure group had lower birth weight [(1 583±451) vs. (1 744±473) g; t=2.97] and gestational age [(31.3±2.1) vs.(31.8±2.4) weeks; t=2.20; both P<0.05)]. (2) The exposure group demonstrated reduced incidence of in-hospital mortality [0.3% (1/290) vs. 6.4% (6/94); Fisher's exact test], grade Ⅲ-Ⅳ intracranial hemorrhage [1.7% (5/290) vs. 9.6% (9/94); χ2=12.86], and white matter injury [2.1% (6/290) vs. 9.1% (8/94); χ2=9.08] (all P<0.01). (3) Univariate logistic regression identified antenatal magnesium sulfate as protective against grade Ⅲ-Ⅳ intracranial hemorrhage ( OR=0.20, 95% CI: 0.04-0.96), white matter injury ( OR=0.11, 95% CI: 0.01-0.91), and in-hospital mortality ( OR=0.93, 95% CI: 0.88-0.99). (4) Multivariate analysis confirmed the independent protective effect of antenatal exposure of magnesium sulfate against intracranial hemorrhage in preterm infants under 34 weeks ( OR=0.19, 95% CI: 0.04-0.95), particularly pronounced in infants <32 weeks ( OR=0.11, 95% CI: 0.01-0.96). (5) No significant differences emerged in secondary outcomes including 5-minute Apgar scores, respiratory distress syndrome, surfactant administration, mechanical ventilation, bronchopulmonary dysplasia, hemodynamically significant patent ductus arteriosus, necrotizing enterocolitis, early-onset sepsis, retinopathy of prematurity, metabolic bone disease, or hospitalization duration (all P>0.05). Conclusions:Magnesium sulfate exposure within 24 hours before delivery reduces grade Ⅲ-Ⅳ intracranial hemorrhage risk in preterm infants under 34 weeks, with enhanced protection in those <32 weeks, without increasing adverse effects in other organ systems.

Objective:The association between air pollutants and the risk of sudden cardiac death (SCD) remains controversial. This study aimed to investigate the relationship between five air pollutants—PM 2.5, PM 2.5–10, PM 10, NO 2, and NO?—and the risk of SCD. Methods:We analyzed data from 460 862 participants in the UK Biobank cohort, all enrolled between 2006 and 2010, with no baseline SCD. Follow-up continued until the study endpoint. Annual average concentrations of the five pollutants were assessed. Associations between pollutants and SCD were evaluated using Cox proportional hazards models, followed by Mendelian randomization (MR) to assess causality.Results:Over a mean follow-up of 12.4 years, 2 662 SCD cases were recorded. After adjusting for confounders, no significant associations were found between air pollutants and SCD risk: PM 2.5 ( HR 1.03, 95% CI 0.99–1.07, P = 0.14), PM 2.5–10 ( HR 1.04, 95% CI 1.00–1.08, P = 0.08), PM 10 ( HR 1.01, 95% CI 0.99–1.03, P = 0.26), NO? ( HR 1.00, 95% CI 0.99–1.00, P = 0.26), and NO x ( HR 1.00, 95% CI 1.00–1.01, P = 0.19). MR analysis further supported the absence of causal relationships: PM 2.5 ( β = -0.149, P = 0.90), PM 2.5–10 ( β = 0.387, P = 0.62), PM 10 ( β = -0.994, P = 0.62), NO? ( β = –0.005, P = 0.99), and NO 2 ( β = –0.827, P = 0.25). Conclusions:This study found no evidence linking PM 2.5, PM 2.5–10, PM 10, NO?, or NO 2 to an increased risk of SCD. Mendelian randomization confirmed the lack of causal associations between these pollutants and SCD.

Objective:To investigate the association between magnesium sulfate exposure within 24 h before birth and short-term outcomes in preterm infants under 34 weeks' gestation.Methods:This retrospective cohort study analyzed data from preterm infants under 34 weeks admitted to the neonatal intensive care unit of the Affiliated Hospital of Qingdao University between June 1, 2020, and December 31, 2024. Infants were categorized into the exposure and the control groups based on magnesium sulfate administration within 24 hours before delivery. Maternal characteristics, birth parameters, and neonatal outcomes were compared using independent t-tests or Chi square tests (Fisher's exact test), with logistic regression assessing magnesium sulfate's effect on non-cerebral palsy outcomes. Results:The cohort comprised 384 preterm infants (24-33 +6 weeks), with 290 (75.5%) in the exposure group and 94 (24.5%) in the control group. (1) Baseline characteristics showed no significant differences in maternal hypertensive disorders, antenatal corticosteroids administration, premature rupture of membranes, delivery mode, or male infant proportion (all P>0.05). The exposure group had lower birth weight [(1 583±451) vs. (1 744±473) g; t=2.97] and gestational age [(31.3±2.1) vs.(31.8±2.4) weeks; t=2.20; both P<0.05)]. (2) The exposure group demonstrated reduced incidence of in-hospital mortality [0.3% (1/290) vs. 6.4% (6/94); Fisher's exact test], grade Ⅲ-Ⅳ intracranial hemorrhage [1.7% (5/290) vs. 9.6% (9/94); χ2=12.86], and white matter injury [2.1% (6/290) vs. 9.1% (8/94); χ2=9.08] (all P<0.01). (3) Univariate logistic regression identified antenatal magnesium sulfate as protective against grade Ⅲ-Ⅳ intracranial hemorrhage ( OR=0.20, 95% CI: 0.04-0.96), white matter injury ( OR=0.11, 95% CI: 0.01-0.91), and in-hospital mortality ( OR=0.93, 95% CI: 0.88-0.99). (4) Multivariate analysis confirmed the independent protective effect of antenatal exposure of magnesium sulfate against intracranial hemorrhage in preterm infants under 34 weeks ( OR=0.19, 95% CI: 0.04-0.95), particularly pronounced in infants <32 weeks ( OR=0.11, 95% CI: 0.01-0.96). (5) No significant differences emerged in secondary outcomes including 5-minute Apgar scores, respiratory distress syndrome, surfactant administration, mechanical ventilation, bronchopulmonary dysplasia, hemodynamically significant patent ductus arteriosus, necrotizing enterocolitis, early-onset sepsis, retinopathy of prematurity, metabolic bone disease, or hospitalization duration (all P>0.05). Conclusions:Magnesium sulfate exposure within 24 hours before delivery reduces grade Ⅲ-Ⅳ intracranial hemorrhage risk in preterm infants under 34 weeks, with enhanced protection in those <32 weeks, without increasing adverse effects in other organ systems.

Objective:To explore the effect and molecular mechanism of circ_0000263 on HeLa cell activity, apoptosis, telomerase activity, and radiosensitivity.Methods:The Hela cells were divided into si-NC, si-circ, vector, circ_0000263, anti-NC, anti-miR-338-3p, miR-NC, miR-338-3p, si-circ+anti-NC, si-circ+ anti-miR-338-3p, si-circ+vector, si-circ+TERT, sh-NC, sh-circ groups. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of circ_0000263 and miR-338-3p. Cell clone formation array was used to detect cell survival; cell counting kit-8 (CCK-8) to detect cell proliferation; flow cytometry to detect apoptosis; western blot method to detect the expressions of proliferating cell nuclear antigen (PCNA), Cleaved-casp3, telomerase reverse transcriptase (TERT) proteins; double luciferase assay to detect the targeting relationships of circ_0000263 and miR-338-3p, miR-338-3p and TERT; telomere repeat amplification enzyme linked immunosorbent assay (TRAR-ELISA) to detect telomerase activity.Results:Circ_0000263 was highly expressed in Hela cells, miR-338-3p was low expressed, and TERT was highly expressed; circ_0000263 was also highly expressed in Hela cells treated with radiation ( P＜0.05). Knockdown of circ_0000263 inhibited the clone formation and cell proliferation ability of HeLa cells, and enhanced the radiosensitivity and apoptosis of HeLa cells. In contrast, knockdown of circ_0000263 decreased PCNA protein expression level and enhanced Cleaved-casp3 protein expression level in HeLa cells ( P＜0.05). The apoptosis rate in the si-circ group was (13.19±1.12)%, which was higher than (6.80±0.62)% of si-NC group ( P＜0.05). The apoptosis rate in the si-circ+4 Gy group was (24.82±1.57)%, which was higher than (17.00±0.96)% of si-NC+4 Gy group ( P＜0.05). Circ_0000263 targeted regulated miR-338-3p, and miR-338-3p targeted regulated TERT. MiR-338-3p was lowly expressed in HeLa cells, and knockdown of circ_0000263 elevated miR-338-3p expression level in HeLa cells. Circ_0000263 regulated TERT expression and inhibited telomerase activity through miR-338-3p. MiR-338-3p/TERT can restore the effect of circ_0000263 on the radiosensitivity of Hela cells. The apoptosis rate in the si-circ+anti-NC group was (27.37±0.89)%, which was higher than (18.22±1.18)% of the si-circ+anti-miR-338-3p group ( P＜0.05). The apoptosis rate in the si-circ+vector group was (27.55±0.48)%, which was higher than (20.10±0.68)% of si-circ+TERT group ( P＜0.05). After 72 hours of radiation by 4 Gy, the cell survival fraction of si-circ+anti-NC group was 0.41±0.02, which was lower than 0.66±0.03 of the si-circ+anti-miR-338-3p group ( P＜0.05); the cell survival fraction of si-circ+vector group was 0.42±0.05, which was lower than 0.70±0.03 of si-circ+TERT group ( P＜0.05). Conclusion:Inhibiting the expression of circ_0000263 supresses the proliferation of Hela cells by regulating miR-338-3p/TERT, promotes apoptosis, inhibits telomerase activity, increases the radiosensitivity of cancer cells, and provides a theoretical basis for improving the radiosensitivity of Hela cells.

Objective:To explore the effect and molecular mechanism of circ_0000263 on HeLa cell activity, apoptosis, telomerase activity, and radiosensitivity.Methods:The Hela cells were divided into si-NC, si-circ, vector, circ_0000263, anti-NC, anti-miR-338-3p, miR-NC, miR-338-3p, si-circ+anti-NC, si-circ+ anti-miR-338-3p, si-circ+vector, si-circ+TERT, sh-NC, sh-circ groups. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of circ_0000263 and miR-338-3p. Cell clone formation array was used to detect cell survival; cell counting kit-8 (CCK-8) to detect cell proliferation; flow cytometry to detect apoptosis; western blot method to detect the expressions of proliferating cell nuclear antigen (PCNA), Cleaved-casp3, telomerase reverse transcriptase (TERT) proteins; double luciferase assay to detect the targeting relationships of circ_0000263 and miR-338-3p, miR-338-3p and TERT; telomere repeat amplification enzyme linked immunosorbent assay (TRAR-ELISA) to detect telomerase activity.Results:Circ_0000263 was highly expressed in Hela cells, miR-338-3p was low expressed, and TERT was highly expressed; circ_0000263 was also highly expressed in Hela cells treated with radiation ( P＜0.05). Knockdown of circ_0000263 inhibited the clone formation and cell proliferation ability of HeLa cells, and enhanced the radiosensitivity and apoptosis of HeLa cells. In contrast, knockdown of circ_0000263 decreased PCNA protein expression level and enhanced Cleaved-casp3 protein expression level in HeLa cells ( P＜0.05). The apoptosis rate in the si-circ group was (13.19±1.12)%, which was higher than (6.80±0.62)% of si-NC group ( P＜0.05). The apoptosis rate in the si-circ+4 Gy group was (24.82±1.57)%, which was higher than (17.00±0.96)% of si-NC+4 Gy group ( P＜0.05). Circ_0000263 targeted regulated miR-338-3p, and miR-338-3p targeted regulated TERT. MiR-338-3p was lowly expressed in HeLa cells, and knockdown of circ_0000263 elevated miR-338-3p expression level in HeLa cells. Circ_0000263 regulated TERT expression and inhibited telomerase activity through miR-338-3p. MiR-338-3p/TERT can restore the effect of circ_0000263 on the radiosensitivity of Hela cells. The apoptosis rate in the si-circ+anti-NC group was (27.37±0.89)%, which was higher than (18.22±1.18)% of the si-circ+anti-miR-338-3p group ( P＜0.05). The apoptosis rate in the si-circ+vector group was (27.55±0.48)%, which was higher than (20.10±0.68)% of si-circ+TERT group ( P＜0.05). After 72 hours of radiation by 4 Gy, the cell survival fraction of si-circ+anti-NC group was 0.41±0.02, which was lower than 0.66±0.03 of the si-circ+anti-miR-338-3p group ( P＜0.05); the cell survival fraction of si-circ+vector group was 0.42±0.05, which was lower than 0.70±0.03 of si-circ+TERT group ( P＜0.05). Conclusion:Inhibiting the expression of circ_0000263 supresses the proliferation of Hela cells by regulating miR-338-3p/TERT, promotes apoptosis, inhibits telomerase activity, increases the radiosensitivity of cancer cells, and provides a theoretical basis for improving the radiosensitivity of Hela cells.

Neonatal hypoxic-ischemic encephalopathy often causes long-term adverse effect on neurological system or even death in near-term or full-term infants, but no effective treatment is available currently. Studies have shown that xenon can reduce brain injury caused by hypoxia-ischemia and is promising in clinical practice. The possible mechanisms include antagonism to glutamic acid receptors, anti-apoptosis, promotion of cell repair and xenon preconditioning. This article reviews the mechanism and research progress on neuroprotection effect of xenon in the treatment of neonatal hypoxic-ischemic encephalopathy.

Objective:To analyze the phenotypic and genomic characteristics of Salmonella isolates recovered from meat products in Beijing wholesale markets. Methods:A total of 336 Salmonella strains from meat products collected from wholesale markets in Beijing were tested for antimicrobial resistance to 25 antimicrobial compounds by micro-broth dilution method; whole genome data were sequenced, followed by the serotype and ST type prediction by Seqsero2 and SISTR software, and the drug resistance genes and virulence factors were also predicted with CARD and VFDB databases of Abricate software; Salmonella serotyping assay kit and serum agglutination method were used for serotype confirmation of some isolates with different genome prediction results. Results:The resistance rates to Nalidixic acid and Ampicillin were 62.5% (210/336) and 55.1% (185/336), respectively, and all isolates were susceptible to Tigecyclin, Cefoxitin and Carbapenem antimicrobial compounds; 207 isolates (61.6%, 207/336) were multi-drug resistant, some could even be resistant to ten categories of drugs at the same time, and the most common antimicrobial resistance spectrum was NAL-AMP-SAM. A total of 24 serotypes were detected with predominant serotypes of Enteritidis (34.5%, 116/336), Derby (17.3%, 58/336) and Indiana (10.4%, 35/336). A total of 27 ST types were detected, the dominant type was ST11; ST types were in good consistency with serotypes; The detection rates of resistant genes referred to aminoglycosides, fluoroquinolones, β-lactams, sulfonamides and tetracyclines are more than 48%, and the first two reached 100%. The prediction of drug resistance genes was consistent with the results of antimicrobial resistance phenotype. A total of 122 virulence genes were predicted, 74 of which existing among all isolates.Conclusion:Salmonella in meat from the wholesale markets of Beijing has a high proportion of multiple drug resistance, a complex drug resistance spectrum, a variety of serotypes and ST types, and a high carrying rate of drug resistance gene and virulence gene; drug resistance phenotype and genotype are relatively consistent.

Objective:To analyze the phenotypic and genomic characteristics of Salmonella isolates recovered from meat products in Beijing wholesale markets. Methods:A total of 336 Salmonella strains from meat products collected from wholesale markets in Beijing were tested for antimicrobial resistance to 25 antimicrobial compounds by micro-broth dilution method; whole genome data were sequenced, followed by the serotype and ST type prediction by Seqsero2 and SISTR software, and the drug resistance genes and virulence factors were also predicted with CARD and VFDB databases of Abricate software; Salmonella serotyping assay kit and serum agglutination method were used for serotype confirmation of some isolates with different genome prediction results. Results:The resistance rates to Nalidixic acid and Ampicillin were 62.5% (210/336) and 55.1% (185/336), respectively, and all isolates were susceptible to Tigecyclin, Cefoxitin and Carbapenem antimicrobial compounds; 207 isolates (61.6%, 207/336) were multi-drug resistant, some could even be resistant to ten categories of drugs at the same time, and the most common antimicrobial resistance spectrum was NAL-AMP-SAM. A total of 24 serotypes were detected with predominant serotypes of Enteritidis (34.5%, 116/336), Derby (17.3%, 58/336) and Indiana (10.4%, 35/336). A total of 27 ST types were detected, the dominant type was ST11; ST types were in good consistency with serotypes; The detection rates of resistant genes referred to aminoglycosides, fluoroquinolones, β-lactams, sulfonamides and tetracyclines are more than 48%, and the first two reached 100%. The prediction of drug resistance genes was consistent with the results of antimicrobial resistance phenotype. A total of 122 virulence genes were predicted, 74 of which existing among all isolates.Conclusion:Salmonella in meat from the wholesale markets of Beijing has a high proportion of multiple drug resistance, a complex drug resistance spectrum, a variety of serotypes and ST types, and a high carrying rate of drug resistance gene and virulence gene; drug resistance phenotype and genotype are relatively consistent.

Objective:To observe the effect of sodium fluoride (NaF) on the expression of phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signal and apoptosis in human osteosarcoma Saos-2 cells.Methods:Saos-2 cells were divided into 0 (control), 5, 10, 20 and 40 mg/L fluoride groups ( n= 3) according to the dose of NaF. The cells were collected after 24 and 48 h of culture in vitro. Western blotting was used to detect the expressions of PI3K/Akt signal and Forkhead transcription factor (FoxO) 1, and the apoptosis level of Saos-2 cells was detected by flow cytometry. Results:There were no significants differences in the expressions of PI3K and Akt in Saos-2 cells at 24 and 48 h ( P > 0.05). At 24 h, the expressions of phosphorylated PI3K (p-PI3K) in 5, 10, 20 and 40 mg/L fluoride groups (0.40 ± 0.06, 0.45 ± 0.02, 0.37 ± 0.06, 0.32 ± 0.06) were higher than that in the control group (0.28 ± 0.04, P < 0.05); at 48 h, the expressions of p-PI3K in 5 and 10 mg/L fluoride groups (0.46 ± 0.06, 0.58 ± 0.03) were higher than that in the control group (0.29 ± 0.04, P < 0.05), and that in the 40 mg/L fluoride group (0.21 ± 0.03) was lower than that in the control group ( P < 0.05). At 24 h, the expressions of phosphorylated Akt (p-Akt) in 5, 10 and 20 mg/L fluoride groups (0.27 ± 0.01, 0.30 ± 0.03, 0.27 ± 0.03) were higher than that in the control group (0.20 ± 0.02, P < 0.05); at 48 h, the expressions of p-Akt in 5 and 10 mg/L fluoride groups (0.42 ± 0.04, 0.60 ± 0.02) were higher than that in the control group (0.27 ± 0.01, P < 0.05), and that in the 40 mg/L fluoride group (0.18 ± 0.02) was lower than that in the control group ( P < 0.05). The expressions of FoxO1 in 10, 20 and 40 mg/L fluoride groups at 24 h (0.38 ± 0.07, 0.41 ± 0.06, 0.47 ± 0.08) were higher than that in the control group (0.34 ± 0.04, P < 0.05). At 48 h, the expressions of FoxO1 in 5, 10, 20 and 40 mg/L fluoride groups (0.36 ± 0.08, 0.37 ± 0.10, 0.54 ± 0.04, 0.73 ± 0.04) were higher than that in the control group (0.28 ± 0.04, P < 0.05). At 24 and 48 h, the apoptosis rates of control group and 5, 10, 20 and 40 mg/L fluoride groups were (2.867 ± 0.583)%, (3.647 ± 0.035)%, (3.773 ± 0.095)%, (5.440 ± 0.325)%, (7.203 ± 0.476)%; (3.707 ± 0.286)%, (4.023 ± 0.241)%, (4.970 ± 0.368)%, (12.473 ± 0.949)%, (19.387 ± 1.892)%, respectively. The apoptosis level of 40 mg/L fluoride group was higher than that of control group at 24 h ( P < 0.05), and that of 20 and 40 mg/L fluoride groups were higher than that of control group at 48 h ( P < 0.05). Conclusion:Fluoride can directly activate the PI3K/Akt signaling pathway in osteoblasts, and then has anti-apoptotic effect.

OBJECTIVE: To investigate the mechanism by which epigallocatechin gallate (EGCG) induces gene demethylation and promotes the apoptosis of acute myeloid leukemia KG-1 and THP-1 cell lines. METHODS: KG-1 and THP-1 cells treated with 25, 50, 75, 100 or 150 μg/mL EGCG for 48 h were examined for gene methylation using MSP and for cell proliferation using MTT assay. The changes in cell cycle and apoptosis of the two cell lines after treatment with EGCG for 48 h were detected using flow cytometry. The mRNA and protein expressions of DNMT1, CHD5, p19, p53 and p21 in the cells were detected using RT-quantitative PCR and Western blot. RESULTS: EGCG dose-dependently reversed hypermethylation of gene and reduced the cell viability in both KG-1 and THP-1 cells ( < 0.05). EGCG treatment caused obvious cell cycle arrest in G1 phase, significantly increased cell apoptosis, downregulated the expression of DNMT1 and upregulated the expressions of CHD5, p19, p53 and p21 in KG-1 and THP-1 cells ( < 0.05). CONCLUSIONS EGCG reduces hypermethylation of gene in KG-1 and THP-1 cells by downregulating DNMT1 to restore its expression, which results in upregulated expressions of p19, p53 and p21 and induces cell apoptosis.