Objective To explore the levels and clinical significance of serum myeloid-related protein 8/14(MRP8/14)and galectin(Gal)-13 in patients with acute exacerbation of chronic obstructive pulmonary dis-ease(AECOPD).Methods A total of 103 AECOPD patients who were admitted to the hospital from Febru-ary 2021 to February 2024 were collected as AECOPD group,and were divided into mild group(n=37),mod-erate group(n=45),severe group(n=21)according to the degree of disease,and the patients also were di-vided into good prognosis group(n=66)and poor prognosis group(n=37)according to prognosis of 28 d of admission to the hospital.During the same period,a total of 70 patients with stable chronic obstructive pulmo-nary disease(SCOPD)were selected as SCOPD group,and 70 healthy individuals who underwent the physical examination were selected as control group.Serum MRP8/14 and Gal-13 levels were measured by enzyme-linked immunosorbent assay,and lung function was examined by lung function detection instrument.Pearson product moment correlation or Spearman rank correlation was used to analyze correlation between serum MRP8/14,Gal-13 and degree of disease,lung function indexes in the AECOPD patients.Multivariate Logistic regression was used to analyze the factors influencing poor prognosis in the AECOPD patients.Receiver oper-ating characteristic curve was used to assess predictive value of serum MRP8/14 and Gal-13 for poor prognosis in the AECOPD patients.Results Compared with the control group,serum MRP8/14 and Gal-13 levels were increased in the AECOPD group and the SCOPD group(P＜0.05),and serum MRP8/14 and Gal-13 levels in the AECOPD group were higher than those in the SCOPD group(P＜0.05).Compared with the control group,first second forced expiratory volume(FEV1),percentage of FEV1 to expected value(FEV1％),forced vital capacity(FVC),percentage of FVC to expected value(FVC％)and FEV1/FVC were decreased in the AECOPD group and the SCOPD group(P＜0.05),and FEV1,FEV1％,FVC,FVC％,and FEV1/FVC in the AECOPD group were lower than those in the SCOPD group(P＜0.05).Serum MRP8/14 and Gal-13 levels in the AECOPD patients were positively correlated with degree of disease(P＜0.05),and negatively correlated with FEV1,FEV1％,FVC,FVC％,FEV1/FVC(P＜0.05).Age,MRP8/14 and Gal-13 were risk factors for poor prognosis in the AECOPD patients(OR=1.390,1.586,1.471,P＜0.05),and FEV1/FVC was a protec-tive factor for poor prognosis in the AECOPD patients(OR=0.752,P＜0.05).The area under the curve of serum MRP8/14,Gal-13 and the combination of the two for predicting poor prognosis in AECOPD patients were 0.850,0.846 and 0.931,respectively.The predictive value of the combination of the two was greater than that of single indicator,respectively(Z=1.866,1.881,P＜0.05).Conclusion The expression of serum MRP8/14 and Gal-13 are up-regulated in AECOPD patients,which are closely correlate with degree of disease and lung func-tion.Early combined detection of two indicators could predict the prognosis in AECOPD patients.

Objective To study the effect of Liuwei Dihuangwan on autophagy level and its mechanism in SAMP8 mice and Aβ-stimulated BV2 cell model,and to explore the molecular mechanism of tonifying the kidney and filling up the essence to prevent and control Alzheimer's disease(AD)through interfering with autophagy.Methods Ten 7-month-old male anti-aging mice(SAMR1)were taken as the normal group,and 40 7-month-old male rapid aging mice(SAMP8)were randomly control and model groups,equal volumes of saline were administered by gavage twice a day for 4 weeks,and the levels of Aβ expression in the hippocampus of the mice in each group were detected by immunofluorescence;The expression levels of FcγRⅡB,c-Src and SHP-1 in the hippocampus of each group were detected by Western blot;BV2 cells were cultured and Fcγ receptor Ⅱ-b(FcγRⅡB)overexpression vectors were constructed;the AD state cell model was established by treating the BV2 cells with 5 μmol·L-1 Aβ1-42,and the Liuwei Dihuangwan drug-containing serum was prepared.The cells were divided into NC group,Aβ1-42 group,blank serum group,drug-containing serum group,Vector group,FcγRⅡB OE group,and drug-containing serum+FcγRⅡB OE group;immunofluorescence was used to detect the expression level of Aβ protein in the cells of each group;Western blot was used to detect the expression level of p62,LC3 Ⅱ/Ⅰ,FcγRⅡB,SHP-1,and c-Src in cells of each group.Results Compared with the normal group,the hippocampal Aβ,FcγRⅡB,SHP-1,and c-Src expression levels in the model group of mice were significantly higher(P<0.01),and compared with the model group,the expression levels of Aβ,FcγRⅡB,SHP-1,and c-Src in the low-,medium-,and high-dose groups of Liuwei Dihuangwan were significantly lower(P<0.01),it also showed a significant dose dependent relationship.Compared with NC group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in Aβ1-42 group were significantly increased(P<0.01),and LC3Ⅱ/Ⅰ was significantly decreased(P<0.01);Compared with Aβ1-42 group and blank serum group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in drug-containing serum group were significantly decreased(P<0.01),and LC3Ⅱ/Ⅰ was significantly increased(P<0.01);Compared with NC group and Vector group,the expression of Aβ in FcγRⅡB OE group was increased,the protein expressions of p62,FcγRⅡB,SHP-1 and c-Src were significantly increased(P<0.01),and LC3Ⅱ/Ⅰ was significantly decreased(P<0.01);Compared with the drug-containing serum group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in the drug-containing serum+FcγRⅡB OE group were significantly increased(P<0.01),and the protein expression levels of LC3Ⅱ/Ⅰ were significantly decreased(P<0.01).Conclusion Liuwei Dihuangwan improved AD by inhibiting microglia FcγRⅡB/c-Src pathway and increasing autophagy level.

Objective To study the effect of Liuwei Dihuangwan on autophagy level and its mechanism in SAMP8 mice and Aβ-stimulated BV2 cell model,and to explore the molecular mechanism of tonifying the kidney and filling up the essence to prevent and control Alzheimer's disease(AD)through interfering with autophagy.Methods Ten 7-month-old male anti-aging mice(SAMR1)were taken as the normal group,and 40 7-month-old male rapid aging mice(SAMP8)were randomly control and model groups,equal volumes of saline were administered by gavage twice a day for 4 weeks,and the levels of Aβ expression in the hippocampus of the mice in each group were detected by immunofluorescence;The expression levels of FcγRⅡB,c-Src and SHP-1 in the hippocampus of each group were detected by Western blot;BV2 cells were cultured and Fcγ receptor Ⅱ-b(FcγRⅡB)overexpression vectors were constructed;the AD state cell model was established by treating the BV2 cells with 5 μmol·L-1 Aβ1-42,and the Liuwei Dihuangwan drug-containing serum was prepared.The cells were divided into NC group,Aβ1-42 group,blank serum group,drug-containing serum group,Vector group,FcγRⅡB OE group,and drug-containing serum+FcγRⅡB OE group;immunofluorescence was used to detect the expression level of Aβ protein in the cells of each group;Western blot was used to detect the expression level of p62,LC3 Ⅱ/Ⅰ,FcγRⅡB,SHP-1,and c-Src in cells of each group.Results Compared with the normal group,the hippocampal Aβ,FcγRⅡB,SHP-1,and c-Src expression levels in the model group of mice were significantly higher(P<0.01),and compared with the model group,the expression levels of Aβ,FcγRⅡB,SHP-1,and c-Src in the low-,medium-,and high-dose groups of Liuwei Dihuangwan were significantly lower(P<0.01),it also showed a significant dose dependent relationship.Compared with NC group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in Aβ1-42 group were significantly increased(P<0.01),and LC3Ⅱ/Ⅰ was significantly decreased(P<0.01);Compared with Aβ1-42 group and blank serum group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in drug-containing serum group were significantly decreased(P<0.01),and LC3Ⅱ/Ⅰ was significantly increased(P<0.01);Compared with NC group and Vector group,the expression of Aβ in FcγRⅡB OE group was increased,the protein expressions of p62,FcγRⅡB,SHP-1 and c-Src were significantly increased(P<0.01),and LC3Ⅱ/Ⅰ was significantly decreased(P<0.01);Compared with the drug-containing serum group,the protein expressions of Aβ,p62,FcγRⅡB,SHP-1 and c-Src in the drug-containing serum+FcγRⅡB OE group were significantly increased(P<0.01),and the protein expression levels of LC3Ⅱ/Ⅰ were significantly decreased(P<0.01).Conclusion Liuwei Dihuangwan improved AD by inhibiting microglia FcγRⅡB/c-Src pathway and increasing autophagy level.

Objective:To evaluate the status of, differences in, and factors influencing quality of life (QoL) in patients with chronic graft-versus-host disease (GVHD).Methods:From September 2021 to February 2023, a cross-sectional study of 140 patients with chronic GVHD was conducted at our center. Symptom burden was assessed by the Lee Symptomatology Scale (LSS), and QoL was assessed by the Medical Outcome Study 36-Item Short-Form Health Survey (SF-36) (version 1) and five-level EuroQoL five-dimensional questionnaire (EQ-5D-5L).Results:Data from 140 respondents, including 32 (22.9%) with mild chronic GVHD, 87 (62.1%) with moderate chronic GVHD, and 21 (15.0%) with severe chronic GVHD, were analyzed. Of the respondents, 61.4% were male, and the median transplantation age was 34 (15-68) years. The primary diagnoses were acute myeloid leukemia (50.0%), acute lymphoblastic leukemia (20.0%), and myelodysplastic syndrome (15.0%). The common chronic GVHD-affected organs included the skin in 74 patients (52.9%), the eyes in 57 patients (40.7%), and the liver in 50 patients (35.7%). Among the whole cohort, the eye (20.48±23.75), psychological (16.13±17.00), and oral (13.66±20.55) scores were highest in the LSS group. The physiological function (36.07±11.13), social function (36.10±10.68), and role-emotional functioning (38.36±11.88) scores were lowest in the SF-36 group. The EQ-5D index was 0.764. The total LSS scores for mild, moderate, and severe chronic GVHD were 6.51±6.15, 10.07±5.61, and 20.90±10.09, respectively. The SF-36 physical component scores (PCSs) were 43.12±6.38, 40.73±7.14, and 36.97±6.97, respectively, and the mental component scores (MCSs) were 43.00±8.47, 38.90±9.52, and 28.96±9.63, respectively. The EQ-5D values were 0.810±0.124, 0.762±0.179, and 0.702±0.198, respectively. The multivariate analysis showed that the overall symptom burden ( β=-0.517), oral symptom burden ( β=-0.456), National Institute of Health (NIH) criteria for the eyes ( β=-0.376), and nutrition-related symptom burden ( β=-0.211) were significantly negatively correlated with the PCS. The NIH score ( β=-0.260) was negatively correlated with the MCS score. Oral symptom burden ( β=-0.400), joint/fascia NIH criteria ( β=-0.332), number of involved systems ( β=-0.253), overall NIH criteria ( β=-0.205), and number of immunosuppressants taken ( β=-0.171) were significantly negatively correlated with the EQ-5D score (all P<0.05). Medium to strong correlations were found between the EQ-5D score and the SF-36 score (| r|=0.384-0.571, P<0.001). Conclusions:The QoL of patients with chronic GVHD is impaired, and the more severe the disease, the poorer the QoL. Overall symptom burden, severity of eyes, and oral symptom burden were the most important factors affecting QoL.

Objective:To investigate the association between cytokines and ocular chronic graft-versus-host disease (cGVHD) and identify specific biomarkers for ocular cGVHD to enhance clinical diagnosis, treatment, and evaluation.Methods:A mouse model of cGVHD was established to explore the correlation between cGVHD and serum cytokines. Based on the findings from the animal experiments and literature review, a panel of 16 cytokine combinations was identified. Enzyme-linked immunosorbent assay (ELISA) was used to compare the cytokine concentrations in the serum and tear samples from patients who underwent allogeneic hematopoietic stem cell transplantation from June 2017 to March 2022 at the Medical Center of Hematology, Xinqiao Hospital, Army Medical University.Results:① Compared with the control group, mice with cGVHD exhibited elevated serum IL-1β, IL-6, IL-8, IL-17, IFN-γ, CX3CL1, CXCL11, CXCL13, CCL11, and CCL19 concentrations (all P<0.05). ② Analysis of the cytokine profiles of the serum and tear samples revealed that compared with patients without ocular cGVHD, those with ocular cGVHD exhibited increased serum IL-8 [ P=0.032, area under the curve (AUC) =0.678]; decreased serum IL-10 ( P=0.030, AUC=0.701) ; elevated IL-8, IFN-γ, CXCL9, and CCL17 in tear samples; and lower IL-10 and CCL19 in tear samples (all P<0.05, all AUC>0.7). Moreover, cytokines in tear samples showed correlations with ocular surface parameters related to ocular cGVHD. Conclusions:Tear fluid demonstrates greater specificity and sensitivity as a biomarker for diagnosing ocular cGVHD than serum biomarkers. Among the identified cytokines in tear samples, IL-8, IL-10, IFN-γ, CXCL9, CCL17, and CCL19 serve as diagnostic biomarkers for ocular cGVHD post-transplantation, offering practical reference value for diagnosis.

Objective:To explore the effects of Liuwei Dihuang Wan on the behaviors and Toll-like receptor 4/nuclear factor kappa-B(TLR4/NF-κB) signal transduction pathway of amyloid β-precursor protein/presenilin-1(APP/PS1) double transgenic mice.Methods:Forty 3-month-old female APP/PS1 mice were randomly divided into model group, low-dose group(0.59 g/kg), medium-dose group(1.18 g/kg), high-dose group(2.36 g/kg)of Liuwei Dihuang Wan(gavaged according to grouped doses), and ibuprofen group(0.04 g/kg, gavage) using a random number table method, with 8 mice in each group.Eight 3-month-old wild-type female C57BL/6 mice with matched body weight were used as the control group.The mice in control group and model group were given an equal volume of 0.9% sodium chloride solution by gavage.The gavage administration was twice a day for a continuous period of 3 months.Morris water maze test was used to detect the learning and memory abilities of mice. ELISA was used to detect the serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β) and immunohistochemistry was used to detect the levels of amyloid β-protein (Aβ), glial fibrillary acidic protein(GFAP) and NF-κB in hippocampal tissue.Western blot was used to detect the expression levels of TLR4, myeloid differentiation primary response gene 88(MyD88), and phosphorylated NF-κB(p-NF-κB) proteins in hippocampal tissue.The SPSS 20.0 software was used for data analysis. Multiple group comparisons were conducted by repeated measure ANOVA or one-way ANOVA.Results:The results of repeated measure ANOVA showed that as for the escape latency of the 6 groups of mice, the interaction effect between time and group was significant ( Finteraction=117.219, P<0.001). The escape latencies of mice in the 6 groups on the 5th day were all lower than those on the 1st day (all P<0.05). The escape latencies of mice in the ibuprofen group and the medium-dose and high-dose groups of Liuwei Dihuang Wan were lower than that in the model group from 1st day to 5th day(all P<0.05). On the 3rd to 5th day, the escape latencies of mice in the medium-dose and high-dose groups of Liuwei Dihuang Wan were lower than those in the low-dose group of Liuwei Dihuang Wan (all P<0.05). There were statistically significant differences in the percentage of residence time in the platform quadrant and the numbers of crossing platform among the 6 groups of mice ( F=5.451, 4.824, both P<0.05). The percentage of residence time in the platform quadrant (50.77±5.49)%, (54.39±5.71)%, (51.98±6.12)%), and the numbers of crossing platform((5.9±1.1) times, (6.0±1.3) times, (5.1±0.8) times) in the high-dose and medium-dose groups of Liuwei Dihuang Wan and the ibuprofen group were all higher than those in the model group ((27.32±3.22)%, (2.2±1.0) times )(all P<0.05). The immunohistochemical results showed that there were statistically significant differences in the integrated optical density values of Aβ, GFAP and NF-κB in the hippocampal tissues of 6 groups of mice ( F=57.52, 45.37, 79.10, all P<0.05). The integrated optical density values of Aβ, GFAP and NF-κB in the high-dose and medium-dose groups of Liuwei Dihuang Wan and the ibuprofen group were all lower than those in the model group (all P<0.05). And the integrated optical density values of Aβ, GFAP, and NF-κB in the high-dose and medium-dose groups of Liuwei Dihuang Wan were all lower than those in the low-dose group of Liuwei Dihuang Wan (all P<0.05). There were statistically significant differences in the levels of serum TNF-α and IL-1β detected by ELISA ( F=3.996, 6.395, both P<0.05) and the proteins levels of TLR4, MyD88, and p-NF-κB in hippocampal tissue detected by Western blot among the 6 groups( F=15.710, 3.522, 4.119, all P<0.05). The serum TNF-α and IL-1β levels in the high-dose and medium-dose groups of Liuwei Dihuang Wan and ibuprofen group were all lower than those in the model group (all P<0.05). The serum TNF-α ((18.90±2.33) ng/L, (21.56±2.49) ng/L) and IL-1β ((5.88±0.80) ng/L, (6.75±0.83) ng/L) levels in the high-dose and medium-dose groups of Liuwei Dihuang Wan were lower than those in the low-dose group ((30.77±2.89) ng/L, (9.11±1.27) ng/L) (all P<0.05). The protein expression levels of TLR4, MyD88, and p-NF-κB in the hippocampus of the high-dose and medium-dose groups of Liuwei Dihuang Wan and ibuprofen group were lower than those of the model group (all P<0.05). The protein expression levels of TLR4 ((0.254±0.091), (0.318±0.122)), MyD88 ((0.229±0.077), (0.386±0.119)), and p-NF-κB ((0.412±0.188), (0.358±0.119)) in the hippocampus of the high-dose and medium-dose groups of Liuwei Dihuang Wan were lower than those of the low-dose group ((0.617±0.172), (0.672±0.166), (0.799±0.227)) (all P<0.05). Conclusion:Liuwei Dihuang Wan can significantly alleviate learning and memory impairment in Alzheimer's disease model mice, possibly by inhibiting TLR4/NF-κB signal pathway, reducing TNF-α and IL-1β expression, thereby alleviate central immune inflammatory response and exert anti Alzheimer's disease effects.

Background and objective Lung cancer is a leading cause of cancer-related deaths.Non-small cell lung cancer(NSCLC)is the most common pathological subtype,with adenocarcinoma being the predominant type.FAT atypical cadherin 1(FAT1)is a receptor-like protein with a high frequency of mutations in lung adenocarcinoma.The protein encoded by FAT1 plays a crucial role in processes such as cell adhesion,proliferation,and differentiation.This study aims to investigate the expression of FAT1 in lung adenocarcinoma and its relationship with immune infiltration.Methods Gene expression levels and relevant clinical information of 513 lung adenocarcinoma samples and 397 adjacent lung samples were obtained through The Cancer Genome Atlas(TCGA)and Genotype-Tissue Expression(GTEx)data.The mRNA expression levels of the FAT1 gene in lung adenocarcinoma tissues were analyzed,along with its association with the prognosis of lung adenocarcinoma patients.Pathway enrichment analysis was conducted to explore the signaling pathways regulated by the FAT1 gene.Immu-noblotting was used to detect the differential expression of FAT1 in lung epithelial cells and various lung cancer cell lines,while immunohistochemistry was employed to assess FAT1 expression in lung cancer and adjacent tissues.Results FAT1 gene muta-tions were identified in 14%of lung adenocarcinoma patients.TCGA database data revealed significantly higher FAT1 mRNA expression in lung adenocarcinoma tissues compared to adjacent lung tissues.Kaplan-Meier analysis indicated lower survival rates in lung adenocarcinoma patients with higher FAT gene expression.Pathway enrichment analysis suggested the involve-ment of FAT1 in tumor development pathways,and its expression was closely associated with immune cell infiltration.Immu-nohistochemical validation demonstrated significantly higher expression of FAT1 in cancer tissues compared to adjacent lung tissues.Conclusion FAT1 mRNA is highly expressed in lung adenocarcinoma tissues,and elevated FAT1 mRNA expression is associated with poor prognosis in lung adenocarcinoma patients.FAT1 may serve as a potential biomarker for lung cancer.

BACKGROUND: Imatinib mesylate (IM) resistance is an emerging problem for chronic myeloid leukemia (CML). Previous studies found that connexin 43 (Cx43) deficiency in the hematopoietic microenvironment (HM) protects minimal residual disease (MRD), but the mechanism remains unknown. METHODS: Immunohistochemistry assays were employed to compare the expression of Cx43 and hypoxia-inducible factor 1α (HIF-1α) in bone marrow (BM) biopsies of CML patients and healthy donors. A coculture system of K562 cells and several Cx43-modified bone marrow stromal cells (BMSCs) was established under IM treatment. Proliferation, cell cycle, apoptosis, and other indicators of K562 cells in different groups were detected to investigate the function and possible mechanism of Cx43. We assessed the Ca 2+ -related pathway by Western blotting. Tumor-bearing models were also established to validate the causal role of Cx43 in reversing IM resistance. RESULTS: Low levels of Cx43 in BMs were observed in CML patients, and Cx43 expression was negatively correlated with HIF-1α. We also observed that K562 cells cocultured with BMSCs transfected with adenovirus-short hairpin RNA of Cx43 (BMSCs-shCx43) had a lower apoptosis rate and that their cell cycle was blocked in G0/G1 phase, while the result was the opposite in the Cx43-overexpression setting. Cx43 mediates gap junction intercellular communication (GJIC) through direct contact, and Ca 2+ is the key factor mediating the downstream apoptotic pathway. In animal experiments, mice bearing K562, and BMSCs-Cx43 had the smallest tumor volume and spleen, which was consistent with the in vitro experiments. CONCLUSIONS Cx43 deficiency exists in CML patients, promoting the generation of MRD and inducing drug resistance. Enhancing Cx43 expression and GJIC function in the HM may be a novel strategy to reverse drug resistance and promote IM efficacy.
Animals ; Humans ; Mice ; Apoptosis ; Bone Marrow Cells ; Cell Communication ; Connexin 43/genetics* ; Gap Junctions/metabolism* ; Imatinib Mesylate/therapeutic use* ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology* ; Mesenchymal Stem Cells/metabolism* ; Tumor Microenvironment ; Calcium/metabolism*

Objective:To study the trend of menarche age in Han and Mongolian women born from 1951 to 2005 in Mongolian region.Methods:A cross-sectional cluster sampling survey method was adopted, From 2003 to 2019, a retrospective survey was carried out in three banners/counties in Tongliao region on the female population of Han and Mongols nationalities aged 16 to 46 and conducted under standardized survey procedures and quality control standards. The basic data of menarche age of women born between 1951 and 2005 were obtained. The changes and rules were analyzed by taking 1 year, 5 years and 10 years as nodes.Results:Totally 46 and conducted under standardized survey procedures and quality control standards 928 pepole (24 450 Han and 22 478 Mongolian) were recruited, the survey response rate was 96.09% (46 928/48 836). In one-year-period analysis, the menarche age gradually decreased from 1951 to 2005. The mean menarche age of Han and Mongolian women changed from (16.22±0.52) years and (15.86±1.24) years in 1951 to (12.37±1.15) years and (12.33±0.98) years in 2005, respectively. The mean menarche age of Han and Mongolian women decreased 3.85 years and 3.54 years. The trend of the mean menarche age's change showed a significant negative correlation with the years (all P<0.000 1). In five-year-period analysis, the mean menarche age of Han and Mongolian women changed from (15.54±1.45) years and (15.53±1.48) years from 1951 to 1955 to (12.41±0.97) years and (12.47±0.96) years from 2001 to 2005, the mean menarche age decreased 3.13 years (3.41 months ahead of schedule every 5 years on average) and 3.06 years (3.34 months ahead of schedule every 5 years on average) in Han and Mongolian women respectively. In ten-year-period analysis, the mean menarche age of Han and Mongolian women changed from (15.79±0.95) years and (15.53±1.33) years from 1951 to 1960 to (12.41±0.97) years and (12.47±0.96) years from 2001 to 2005, the mean menarche age decreased 3.38 years (6.76 months ahead of schedule every 10 years on average) and 3.06 years (6.12 months ahead of schedule every 10 years on average) in Han and Mongolian women respectively. During the 15 years from 1951 to 1965, 1966 to 1970, 1971 to 1990, and 1991 to 2000, they were concentrated at the ages of 15-16, 14-15, 13-14, and 12-13, respectively. The proportion of women at 11 years, 12 years and 13 years menarche age were 26.79% (457/1 706), 73.27% (1 250/1 706), and 92.85% (1 584/1 706) during 2001—2005 in Han women, while the proportion were 23.25% (653/2 809), 62.01% (1 742/2 809), and 90.14% (2 532/2 809) in Mongolian women. Conclusion:The menarche age decreased in Han and Mongolian women from 1951 to 2005, and the ethnic groups tended to be the same. It is recommended to start adolescent education at the age of 8-9 years and pay attention to the changing pattern of early onset of menarche.

Objective:To study the trend of menarche age in Han and Mongolian women born from 1951 to 2005 in Mongolian region.Methods:A cross-sectional cluster sampling survey method was adopted, From 2003 to 2019, a retrospective survey was carried out in three banners/counties in Tongliao region on the female population of Han and Mongols nationalities aged 16 to 46 and conducted under standardized survey procedures and quality control standards. The basic data of menarche age of women born between 1951 and 2005 were obtained. The changes and rules were analyzed by taking 1 year, 5 years and 10 years as nodes.Results:Totally 46 and conducted under standardized survey procedures and quality control standards 928 pepole (24 450 Han and 22 478 Mongolian) were recruited, the survey response rate was 96.09% (46 928/48 836). In one-year-period analysis, the menarche age gradually decreased from 1951 to 2005. The mean menarche age of Han and Mongolian women changed from (16.22±0.52) years and (15.86±1.24) years in 1951 to (12.37±1.15) years and (12.33±0.98) years in 2005, respectively. The mean menarche age of Han and Mongolian women decreased 3.85 years and 3.54 years. The trend of the mean menarche age's change showed a significant negative correlation with the years (all P<0.000 1). In five-year-period analysis, the mean menarche age of Han and Mongolian women changed from (15.54±1.45) years and (15.53±1.48) years from 1951 to 1955 to (12.41±0.97) years and (12.47±0.96) years from 2001 to 2005, the mean menarche age decreased 3.13 years (3.41 months ahead of schedule every 5 years on average) and 3.06 years (3.34 months ahead of schedule every 5 years on average) in Han and Mongolian women respectively. In ten-year-period analysis, the mean menarche age of Han and Mongolian women changed from (15.79±0.95) years and (15.53±1.33) years from 1951 to 1960 to (12.41±0.97) years and (12.47±0.96) years from 2001 to 2005, the mean menarche age decreased 3.38 years (6.76 months ahead of schedule every 10 years on average) and 3.06 years (6.12 months ahead of schedule every 10 years on average) in Han and Mongolian women respectively. During the 15 years from 1951 to 1965, 1966 to 1970, 1971 to 1990, and 1991 to 2000, they were concentrated at the ages of 15-16, 14-15, 13-14, and 12-13, respectively. The proportion of women at 11 years, 12 years and 13 years menarche age were 26.79% (457/1 706), 73.27% (1 250/1 706), and 92.85% (1 584/1 706) during 2001—2005 in Han women, while the proportion were 23.25% (653/2 809), 62.01% (1 742/2 809), and 90.14% (2 532/2 809) in Mongolian women. Conclusion:The menarche age decreased in Han and Mongolian women from 1951 to 2005, and the ethnic groups tended to be the same. It is recommended to start adolescent education at the age of 8-9 years and pay attention to the changing pattern of early onset of menarche.