AIM: To investigate variation patterns of corneal biomechanical parameters and binocular symmetry among children of different genders aged 8-16 years.METHODS:A retrospective study was conducted, and children who underwent optometric examinations at the ophthalmology department of our hospital were enrolled between January 2022 and December 2024. Measurements included the flat keratometry(K1), steep keratometry(K2), and mean curvature(Km)of the anterior corneal surface, horizontal visible iris diameter(HVID), central corneal thickness(CCT), corneal endothelial cell density(CECD), average cell size(ACS), coefficient of variation(CV), and hexagonality(HEX). Corneal parameters and binocular differences were compared between genders and across age groups.RESULTS:A total of 621 children(1 242 eyes)were enrolled in this study, including 284 males(568 eyes), 337 females(674 eyes), 528 children aged 8-12 years(1 056 eyes), and 93 children aged 13-16 years(186 eyes). In children aged 8-16 years, the K1, K2, Km and CV of both eyes, as well as the interocular CCT differences in boys were significantly lower than those in girls(all P<0.05), while the HVID and HEX of both eyes, as well as the CCT of the left eye in boys were significantly higher than those in girls(all P<0.05). Children aged 8-12 years had significantly higher K1, Km, CECD and HEX in both eyes, and significantly lower ACS in both eyes than those aged 13-16 years(all P<0.05). K1, K2, Km, CECD and HEX in both eyes were negatively correlated with age(P<0.05); ACS in both eyes was positively correlated with age(P<0.001); K1 and Km of the right eye were positively correlated with the CECD of the right eye(P<0.05), and K1 and CCT of the left eye were positively correlated with the CECD of the left eye(P<0.05).CONCLUSION:Significant gender differences exist in corneal parameters among children aged 8 to 16 years, while binocular symmetry remained stable.

Since the founding of the People’s Republic of China, remarkable achievements have been gained in infectious disease prevention and control, and rich practical experiences have been accumulated. If these experiences are shared with developing countries, it will greatly contribute to global infectious disease control and global health security. Under the framework of Forum on China-Africa Cooperation, a series of China-Africa public health capacity training programs have been recently held in China, in order to help improve the capability of infectious disease control in African countries. This article summarized and refined good design concepts and practices from these programs, so as to provide insights into sustainable optimization of China-Africa public health capacity training and improvements of the training effectiveness.

Bone is a highly calcified and vascularized tissue. The vascular system plays a vital role in supporting bone growth and repair, such as the provision of nutrients, growth factors, and metabolic waste transfer. Moreover, the additional functions of the bone vasculature, such as the secretion of various factors and the regulation of bone-related signaling pathways, are essential for maintaining bone health. In the bone microenvironment, bone tissue cells play a critical role in regulating angiogenesis, including osteoblasts, bone marrow mesenchymal stem cells (BMSCs), and osteoclasts. Osteogenesis and bone angiogenesis are closely linked. The decrease in osteogenesis and bone angiogenesis caused by aging leads to osteoporosis. Long noncoding RNAs (lncRNAs) are involved in various physiological processes, including osteogenesis and angiogenesis. Recent studies have shown that lncRNAs could mediate the crosstalk between angiogenesis and osteogenesis. However, the mechanism by which lncRNAs regulate angiogenesis‒osteogenesis crosstalk remains unclear. In this review, we describe in detail the ways in which lncRNAs regulate the crosstalk between osteogenesis and angiogenesis to promote bone health, aiming to provide new directions for the study of the mechanism by which lncRNAs regulate bone metabolism.
RNA, Long Noncoding/physiology* ; Osteogenesis/physiology* ; Humans ; Neovascularization, Physiologic/genetics* ; Bone and Bones/metabolism* ; Animals ; Mesenchymal Stem Cells ; Signal Transduction ; Osteoblasts ; Osteoclasts ; Angiogenesis

Objective To explore the mechanism of Shengmai Decoction in improving heart failure by regulating mitochondrial apoptosis based on network pharmacology and experimental verification;To provide a basis for its clinical application.Methods The active components and targets of Shengmai Decoction were obtained through TCMSP and TCMID databases.Heart failure and mitochondrial apoptosis related targets were retrieved from GeneCards,OMIM,DrugBank,PharmGKB and TTD databases.A protein-protein interaction(PPI)network at the intersection of drugs and diseases was constructed using the STRING database,and a component-target network was constructed using Cytoscape 3.8.2 software.GO and KEGG pathway enrichment analysis was performed on intersecting targets using the DAVID database.Molecular docking was conducted to assess the binding affinity of key components to core target proteins.A rat model of heart failure was established,and the cardiac function of rats were detected by echocardiogram,ELISA was used to detect serum contents of BNP and NT-proBNP,mitochondrial ultrastructure was observed by transmission electron microscope,and Western blot was used to detect protein expressions of Bcl-2/Bax/Caspase-3 signaling pathway.Results A total of 66 active components and 146 targets of Shengmai Decoction were identified,and 22 intersecting targets with heart failure and mitochondrial apoptosis,including key proteins such as TNF,Bcl-2,Bax and Caspase-3.GO enrichment analysis revealed that the intersecting targets were closely associated with inflammation and cell signaling,while KEGG pathway analysis showed that the targets were primarily involved in the TNF signaling pathway,IL-17 signaling pathway,and mitochondrial function regulation.Molecular docking results indicated that Ginsenoside rh2,Beta-sitosterol and other components of Shengmai Decoction exhibited strong binding affinities with Bcl-2,Bax and Caspase-3.Animal experiments demonstrated that Shengmai Decoction significantly improved cardiac function(P<0.05,P<0.01),reduced serum BNP and NT-proBNP contents(P<0.01),alleviated mitochondrial damage,and inhibited mitochondrial apoptosis by upregulating Bcl-2 and downregulating Bax and Caspase-3 protein expression(P<0.01),thereby protecting cardiomyocytes.Conclusion Shengmai Decoction can target and regulate the Bcl-2/Bax/Caspase-3 signaling pathway,improving pathological processes associated with heart failure,which can provide a foundation for clinical optimization of Shengmai Decoction.

Objective:To explore the effects of IFN-γ on IL-8 secretion by human liver cancer cells and the impact on their malignant biological functions in vitro. Methods:HuH7 and Hep3B cells were treated with different concentrations of IFN-γ for 24 or 48 h. Changes in the cellular activity, IL-8 secretion, and the proportion of CD133 + liver cancer stem cells were evaluated using CCK8 kit and flow cytometry. Western blot was used to detect the effects of IFN-γ on the expression of several molecules such as phosphorylated protein kinase B (p-Akt), phosphorylated c-Jun N-terminal kinase (p-JNK), vimentin, and E-cadherin in the liver cancer cells. Effects of IFN-γ with or without IL-8 on the migration of liver cancer cells were detected by transwell assay. Additionally, effects of IFN-γ combined with IL-8 or IL-8 receptor inhibitor repertaxin on the differentiation of liver cancer stem cells were detected by flow cytometry. One-way analysis of variance and Tukey-Kramer test were used for statistical analysis. Results:HuH7 and Hep3B cells secreted significantly higher levels of IL-8 than normal hepatocytes LO2 ( P<0.01) and high expression level of IL-8 gene ( CXCL8) was closely correlated with the expression levels of vimentin gene ( VIMENTIN), CD133 gene ( PRCM1), PD-L1 gene ( CD274), PD-1 gene ( PDCD1), and CD163 gene ( CD163), as well as the poor prognosis of liver cancer patients ( P<0.01). IFN-γ (1-100 ng/ml) had no significant effect on the proliferative activity of HuH7 and Hep3B cells ( P>0.05), but could significantly inhibit IL-8 secretion, cell migration, CD133 + liver cancer stem cell differentiation and suspension tumor sphere formation through the Akt and JNK pathways ( P<0.01). IFN-γ combined with IL-8 could significantly reversed the inhibitory effects of IFN-γ on liver cancer cell migration, stem cell differentiation, and suspension tumor sphere formation ( P<0.01). IFN-γ in combination with repertaxin could synergistically inhibited the differentiation of CD133 + liver cancer stem cells ( P<0.01). Conclusion:IFN-γ inhibits the differentiation and migration of human liver cancer cells through the Akt/JNK-IL-8 signaling pathway, providing a new strategy for future clinical immunotherapy of liver cancer.

Different insect drugs have their own characteristics in terms of efficacy,including removing blood stasis and promoting blood circulation,dispelling phlegm and dispersing lumps,and nourishing the body.This article discussed the use of insect medicines in the treatment of chronic heart failure(CHF)based on the theory of"collateral deficiency and tonifying".Taking the TCM theory of"collateral deficiency and tonifying"as the entry point,this article categorized the pathogenesis of CHF into deficiency of qi and yang,deficiency of collaterals,phlegm retention and dampness stagnation,and accumulation of collaterals,and believes that the treatment should be based on resolving blood stasis and promoting collaterals,eliminating phlegm and promoting collaterals,dispersing lumps and promoting collaterals,and tonifying heart collaterals,thus achieving the effect of"collateral deficiency and tonifying".It also summarized the efficacy and modern pharmacological mechanisms of insect drugs,providing medication ideas for the treatment of CHF.

Objective To investigate the spatiotemporal expression pattern of metabotropic glutamate receptor 4(mGluR4)in the mouse cochlear basilar membrane and its dynamic changes during postnatal development until hair cell synaptic maturation.Methods Ten healthy 3-month-old C57BL/6L wild-type mice(5 males,5 females,25～35 g)were bred to obtain offspring.Cochlear samples from postnatal days 1～30(P1～P30)were analyzed.Frequency-specific auditory brainstem response(ABR)thresholds were measured at 45.2,32.0,22.6,16.0,11.3,8.0,5.6,and 4.0 kHz in P12,P14,P16,P21,and P30 mice.Immunofluorescence assay combined with confocal laser scanning microscopy was used to scan cochlear whole-mount preparations.Spatiotemporal co-localization profiling of mGluR4 and synaptic markers Ctbp2 and Snap25 was observed,and quantitative comparisons of fluorescent puncta density were performed.Results ABR testing revealed undifferentiated waveforms in all P12 mice,while 70%of P14 mice exhibited well-defined Wave I.In P14,P16,P21 and P30,mice undergoing ABR testing,50%failed to exhibit ABR waveforms when stimulated by 45.2 kHz tones,and 87.5%showed no response to 32.0 kHz stimuli.Auditory response thresholds for other frequencies progressively decreased with increasing postnatal age.Immunolocalization demonstrated stronger mGluR4 expression in inner hair cells(IHCs)versus outer hair cells(OHCs).Distinct mGluR4 puncta were observed at IHC presynaptic active zones(co-localized with Snap25)as early as P11,but showed minimal overlap with CtBP2-labeled ribbons.Quantitative analysis revealed significantly higher mGluR4 puncta density at P30 compared to P14 synapses(P<0.05).Conclusion Postnatal upregulation of mGluR4 at IHC synaptic regions correlates with functional maturation.These findings suggest mGluR4 may modulate vesicular exocytosis regulation and exert pharmacological inhibition on glutamate release,potentially influencing synaptic plasticity during auditory pathway refinement.

Objective To investigate the role and molecular mechanism of SOX4 in Helicobacter pylori(H.pylori)-mediated gastric mucosal epithelial dysplasia.Methods The expression of SOX4 in gastric tissues and cells was analyzed with reverse transcription-polymerase chain reaction(RT-PCR),Western blotting,and immunohistochemical staining.The effects of SOX4 on gastric epithelial cell proliferation and colony formation were determined with CCK-8 and colony formation assays.A PCR array was used to screen downstream target genes involved in H.pylori-induced dysplasia mediated by SOX4.The transcriptional regulation and binding sites of the target gene MLH3 by SOX4 were elucidated with luciferase reporter assay,promoter truncation assay,and chromatin immunoprecipitation(ChIP).Results SOX4 expression was significantly increased in H.pylori-infected gastric tissues(P<0.05).Overexpression of SOX4 markedly enhanced the proliferation and colony formation abilities of normal gastric epithelial cells(P<0.05).Elevated SOX4 led to the dysregulation of MLH3 and other DNA damage repair-related molecules after H.pylori infection in gastric epithelial cells(|logFC|>1,P<0.05).H.pylori promoted MLH3 expression in gastric epithelial cells through SOX4.SOX4 transcriptionally activated MLH3 expression by binding to the 5th site of the MLH3 promoter.The increased expression of SOX4 and MLH3 is associated with poor prognosis of gastric cancer patients.Conclusion SOX4 is closely associated with H.pylori-induced dysplasia in gastric epithelial cells.Upregulation of SOX4 promotes H.pylori-related dysplasia by transcriptionally activating MLH3,leading to the imbalance of proliferation and colony formation in gastric epithelial cells.

Objective:To investigate tetanus antibody levels and distribution characteristics in a healthy population of Henan Province.Methods:A cross-sectional survey was conducted in Henan Province from 2022 to 2023 to investigate the permanent population. Enzyme-linked immunosorbent assay (ELISA) was used to detect anti-tetanus toxoid IgG antibody (anti-TT), and the positive rate (≥0.01 IU/ml), protection rate (≥0.1 IU/ml) and concentration differences of tetanus antibodies in different populations were analyzed.Results:The age M ( Q1, Q3) of 5 494 participants was 14 (4, 40) years old, with a minimum age of 8 months and a maximum age of 81 years old. The male-to-female ratio was 1.00∶1.18. The total positive rate, protective rate and mean concentration (MC) [ M ( Q1, Q3)] of Anti-TT were 76.48%, 41.72% and 0.067 (0.010, 0.154) IU/ml, respectively. The positive rates of Anti-TT in individuals aged <3, 3-5, 6-9, and 10-14 were 95.32%, 96.05%, 97.81%, and 93.17%, respectively, but gradually decreased with age ( χ2trend=1 283.02, P<0.001). The antibody protection rate [82.13% (579/705)] and MC [ M ( Q1, Q3) of 0.160 (0.122, 0.259) IU/ml] in the population under 3 years old were relatively high, and both showed a decreasing trend with age (protection rate: χ2trend=1 889.49, P<0.001; MC: t=-54.22, P<0.001). There were significant differences in antibody levels among populations of different ages, regions, occupations, and immunization histories (all P<0.001). Within 13 years after the last dose of TTCV vaccination, the positive rate of Anti-TT was all greater than 90%, but the protection rate and MC continued to decrease with the prolongation of vaccination time (protection rate: χ2trend=160.58, P<0.001; MC: t=-14.93, P<0.001). After the last dose of vaccination, the protection rate and MC [ M ( Q1, Q3)] decreased to 30.43% and 0.055 (0.036, 0.115) IU/ml, respectively, for 10-13 years. The protection rates of Anti-TT for farmers, workers, people aged 60 and above, and women of childbearing age (20-45 years old) were 7.77%, 22.96%, 8.39%, and 12.72%, respectively. Conclusion:The level of tetanus antibodies in infants and young children in Henan Province is relatively high from 2022 to 2023, but it decreases with age and prolonged post-immunization time. There are significant differences in antibody levels among individuals of different ages, regions, occupations, and immunization histories. Occupational high-risk groups such as farmers and workers, elderly people, and women of childbearing age lack sufficient immunization protection.

Objective:To analyze the incidence, mortality, survival patterns, and distribution characteristics of modifiable risk factors for colorectal cancer in selected global regions.Methods:Secondary analysis was conducted using data from the GLOBOCAN database and previous literature. We described the number of cases and age-standardized rates (ASRs) of incidence and mortality for colorectal cancer in China, the United States, the United Kingdom, and globally in 2022 and 2020, with gender-stratified analysis. ASRs were calculated using Segi's world standard population. Temporal trends in 5-year net survival rates were compared across three periods (2000-2004, 2005-2009, 2010-2014) among countries. Regional distribution differences in colorectal cancer deaths attributable to modifiable risk factors by gender were assessed in China.Results:In 2022, global colorectal cancer incidence and mortality were estimated at 1.926 million new cases and 904 000 deaths. China accounted for 27% of both global incidence (517 000 cases) and mortality (240 000 deaths). China's age-standardized incidence rate (20.1 per 100 000) was lower than those of the United States (27.0 per 100 000) and the UK (30.9 per 100 000). However, China's mortality rate (8.6 per 100 000) exceeded that of the US (7.9 per 100 000) but was lower than the UK (11.8 per 100 000). Compared to 2020, China demonstrated significant mortality reductions in 2022: males declined from 14.8 to 10.9 per 100 000, females from 9.4 to 6.5 per 100 000. Five-year net survival rates in China improved across periods for colon cancer (51.4%, 55.6%, 57.6%) and rectal cancer (49.5%, 52.5%, 56.9%), yet remained consistently lower than US and UK rates. Modifiable risk factors contributed to 45.1% of male and 41.4% of female colorectal cancer deaths in China, with marked regional disparities.Conclusions:China exhibits higher colorectal cancer incidence and mortality than global averages, with survival gaps persisting compared to developed nations. Regionally tailored comprehensive prevention strategies are essential to reduce disease burden through risk factor modification and optimized clinical management.