1.Research progress of digital health intervention platforms for perinatal depression
SONG Zhen ; ZHANG Jiayi ; WU Dadong ; GONG Ni
Journal of Preventive Medicine 2025;37(9):907-912
Perinatal depression (PND) is a critical public health issue affecting maternal and offspring health. Digital health intervention platforms, leveraging advantages in accessibility, privacy, and cost-effectiveness, demonstrate good application in PND prevention and treatment. This review systematically searched literature and policy documents published between January 2018 and March 2025 in CNKI, PubMed, Web of Science and World Health Organization. It summarized the development trajectory of digital health intervention platforms and their current applications and effectiveness in PND prevention and treatment. Existing evidence was evaluated across dimensions of efficacy, systematicity, and practicality, identifying major challenges faced by these platforms. Studies indicate that while PND digital health intervention platforms have achieved preliminary success in alleviating PND symptoms, widespread issues persist, including incomplete service closed-loop systems, low user adherence, and insufficient sustainability. Future efforts should focus on optimizing intervention content and interactive design, advancing intelligent assessment and tiered intervention strategies, strengthening continuous monitoring and crisis response mechanisms, and constructing a multidisciplinary collaborative support system. These steps are essential for achieving efficient, intelligent, and sustainable development of digital health intervention platforms for PND.
2.Effect of PFKFB3 on inflammatory activation of polymorphonuclear myeloid-derived suppressor cell in acute myocardial infarction
Zongying YU ; Yanjun WU ; Dadong LIU
Chinese Critical Care Medicine 2024;36(1):44-49
Objective:To investigate the correlation between 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3) and the inflammatory activation of polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) in acute myocardial infarction (AMI), and to evaluate the effect of intervention targeting PFKFB3 on the inflammatory activation of PMN-MDSC during AMI.Methods:① Clinical trial section: a observational study was conducted. The patients with acute coronary syndrome (ACS) admitted to Zhenjiang Fourth People's Hospital were enrolled, and they were divided into AMI group and non-AMI group according to clinical diagnosis. The peripheral venous blood of the two groups was collected to detect the proportion of PMN-MDSC, and the expression of PFKFB3 gene in mononuclear cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR). ② Basic experiment section: a total of 30 male C57 mice (aged 6-8 weeks) were divided into normal control group ( n = 5), Sham group ( n = 5), AMI model group ( n = 10) and PFKFB3 inhibitor PKF-15 intervention group ( n = 10) according to random number table method. The AMI model of mice was reproduced by left anterior descending coronary artery (LADCA) ligation, and the mice in the Sham group did not attach the artery after thoracotomy. The PKF-15 intervention group was intraperitoneally injected with PKF-15 (20 μg/g) at the same time of LADCA ligation. Normal control mice did not receive any treatment. Peripheral venous blood and myocardial tissue of mice were collected 24 hours after modeling. Both the circulating PMN-MDSC ratio and the infiltration of PMN-MDSC in myocardial tissue were detected. After staining with hematoxylin-eosin (HE), the degree of inflammatory damage in mouse myocardial tissue was observed under light microscopy. PMN-MDSC were isolated from mice with flow cytometry, and the gene expressions of PFKFB3 and inflammatory factors were measured by RT-qPCR. Results:① Clinical trial section: the circulating PMN-MDSC ratio of patients in the AMI group ( n = 25) was significantly higher than that in the non-AMI group [ n = 20; (8.53±0.96)% vs. (1.13±0.39)%, P < 0.01], and PFKFB3 gene expression in the peripheral blood mononuclear cells was also increased (2 -ΔΔCt: 1.18±0.19 vs. 0.96±0.16, P < 0.01). Pearson correlation analysis showed that circulating PMN-MDSC ratio was positively correlated with PFKFB3 gene expression in mononuclear cells in AMI patients ( r = 0.608, P = 0.001). ② Basic experimental section: the circulating PMN-MDSC ratio and the infiltration of PMN-MDSC in myocardial tissue of AMI mice were significantly higher than those in the normal control group and Sham group. PFK-15 intervention could reduce the ratio of PMN-MDSC in the peripheral blood and myocardial tissue of AMI mice [(26.33±5.27)% vs. (75.12±5.02)% in peripheral blood, (20.87±2.97)% vs. (35.28±4.36)% in myocardial tissue, both P < 0.01]. Under light microscopy, the myocardial cells in the AMI modal group were disordered and a large number of inflammatory cells infiltrated. PFK-15 intervention could maintain a normal arrangement of cardiomyocytes and reduce the infiltration of inflammatory cells. The gene expression levels of PFKFB3 in the peripheral blood and myocardial tissue as well as the inflammatory factors in the myocardial tissue of AMI mice were significantly higher than those in the normal control group and Sham group. PKF-15 intervention could effectively reduce the gene expression levels of PFKFB3 in the peripheral blood and myocardial tissue as well as the inflammatory factors in the myocardial tissue of AMI mice [PFKFB3 mRNA (2 -ΔΔCt): 1.01±0.09 vs. 1.40±0.12 in peripheral blood, 0.95±0.09 vs. 1.47±0.10 in myocardial tissue; myocardial tissue tumor necrosis factor-α (TNF-α) mRNA (2 -ΔΔCt) was 14.55±3.99 vs. 29.66±3.90, interleukin-1β (IL-1β) mRNA (2 -ΔΔCt) was 8.72±1.35 vs. 18.53±2.43, IL-6 mRNA (2 -ΔΔCt) was 11.87±2.97 vs. 19.82±4.32, all P < 0.01]. Conclusions:The activation of PFKFB3 is closely related to the inflammatory activation of PMN-MDSC during AMI. Inhibition of PFKFB3 activity can inhibit the inflammatory activation of PMN-MDSC and reduce myocardial inflammatory injury.
3.The value of combined sampling at multiple sites of gastric mucosa for Helicobacter pylori culture
Jiaochang WANG ; Dadong HUANG ; Xianzuo XU ; Min LIN ; Qiuxiang LIU ; Ningmin YANG ; Fei MENG ; Jiansheng WU
Chinese Journal of Digestive Endoscopy 2017;34(3):200-202
Objective To evaluate combined sampling at multiple sites of gastric mucosa for Helicobacter pylori (HP) culture.Methods A total of 258 patients with upper gastrointestinal symptoms received 13C-urea breath test between August 2014 and May 2015.During endoscopy,gastric mucosa biopsy samples from the lesser curvature of the antrum (A),the greater curvature of the antrum (B),gastric angle (C) and the body of the stomach (D) were collected to isolate HP strains.The positive rates of HP based on combined sampling and single site sampling were compared with a Nemenyi test.Results Consistency between 13C-urea breath test and HP culture was 82.56%.There was significant difference between the single site sampling and two-site sampling in the positive rate of HP,except for the body of the stomach (P<0.05).There was significant difference in the positive rate of HP between the single site sampling and three-site sampling (P < 0.05).There was no significant difference between any two-site sampling in the lesser curvature of the antrum and the body of the stomach,gastric angle and the body of the stomach,the greater curvature of the antrum and the body of the stomach,and any three-site sampling (P>0.05).Conclusion The combined sampling of the lesser curvature of the antrum and the body of the stomach have the highest cost-effectiveness in HP culture compared with the single site sampling and three-site sampling.
4.Effect of ultraviolet B irradiation on the expression of plasma membrane calcium ATPase 3 in human lens epithelial cells
Qiuxin, WU ; Dadong, GUO ; Hongsheng, BI ; Daoguang, WANG
Chinese Journal of Experimental Ophthalmology 2014;32(6):485-491
Background Plasma membrane calcium ATPase 3 (PMCA3) participates in the regulation of Ca2+ level in lens epithelial cells (LECs),which may be associated with the pathogenesis of cataract.It has been proved that ultraviolet B (UVB) is one of causing-factors of cataract.However,the effect of UVB on the expression of PMCA3 in LECs is unclear.Objective This study was to investigate the effects of UVB irradiation on the expression of PMCA3 in human LECs B-3.Methods HLE B-3 cells were cultured and passaged.The cells were exposed to 0,5,10 and 20 mJ · s/cm2 UVB for 0,20,40,80 s,respectively and further cultured for 24,48 and 72 hours.MTT assay was used to detect the cell proliferation rate.JC-1 staining was used to detect the changes of mitochondrial membrane potential (△ψm) in the cells.The intracellular reactive oxygen species (ROS) level was detected by DCFH-DA staining,and cell apoptosis was evaluated using annexin V-FITC/PI staining.In addition,the intracellular calcium ion (Ca2+) concentration in the cells was assayed with Fluo-3/AM staining.The expression levels of PMCA3 mRNA and PMCA protein in the HLE B-3 cells were detected by real-time PCR and Western blot,respectively.Results The survival rates of the cells were significantly reduced with the increase of irradiated intensity of UVB and the lapse of time (Fgroup =72.411,P =0.000 ; Ftime =36.588,P =0.000),and the survival rates of the cells in the 10 mJ · s/cm2 and 20 mJ · s/cm2 UVB for 24 hours were (75.3 ± 2.2) % and (48.7 ±4.5) %,respectively,which were significantly lower than those in the 0 mJ · s/cm2 UVB group ([100.0±0.0] %) (P=0.001,0.000).The survival rates of the cells in the 5,10,20 mJ · s/cm2 UVB for 48 hours were (84.9± 1.2) %,(69.3±17.4)% and (32.8±4.5)%,showing significant declines in comparison with the 0 mJ · s/cm2 UVB group ([100.0±0.0] %) (P =0.047,0.000,0.000).In 72 hours following 5,10,20 mJ · s/cm2 UVB irradiation,the survival rates of the cells were (55.1 ± 3.0) %,(42.1 ± 1.9) % and (26.1 ±4.7) %,respectively,with significant differences in comparison with the 0 mJ · s/cm2 UVB group ([100.0 ± 0.0] %) (P =0.000,0.000,0.000).JC-1staining exhibited the intracellular red fluorescence in the normal cells group.However,in the 5 mJ · s/cm2 UVB group,weak green fluorescence was seen,and the green fluorescence was enhanced in the 10 mJ · s/cm2 and 20 mJ · s/cm2 UVB groups.After irradiated by 5,10 and 20 mJ · s/cm2 UVB,the ROS levels in the cells increased from 0.4% to 35.8%,51.9% and 76.7%,respectively.The apoptosis and necrosis rate of the cells was 2.0% in the 0 mJ · s/cm2 UVB and 4.2%,7.6%,15.1% in the 5,10,20 mJ · s/cm2 UVB groups,respectively.The Ca2+ level raised by (1.2±0.1) and (1.3±0.1) folds in the 10 and 20 mJ · s/cm2 UVB groups more than that in the 0 mJ · s/cm2 group (P =0.039,0.004).The expression levels of PMCA3 mRNA in the cells were significantly reduced (P=0.001,0.004,0.000),and the expression levels of the PMCA protein were declined in the 5,10 and 20 mJ · s/cm2 UVB groups compared with the 0 mJ · s/cm2 UVB group (P=0.000,0.000,0.001).Conclusions UVB irradiation causes cataract probably through downregulating the expression of PMCA3 in human LECs and inducing apoptosis of LECs in a dose-and time-dependent manner.
5.The design and construction of medical multimedia teaching resource library
Yu WU ; Dadong XUE ; Yunsheng LIU ; Chanjuan LI ; Weimin LI
Chinese Journal of Medical Education Research 2011;10(5):628-629
Building a medical multimedia teaching resource library is beneficial to distance medical education and the efficiency of multimedia resource usage. Its construction depends on not only modern information technology and the network, but also a comprehensive design from the angle of resource integration.


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