ObjectiveTo investigate the effects of Huanglian Jiedutang （HLJDT） on cognitive function in mice with ischemic stroke （IS） and to elucidate whether its neuroprotective effects are mediated by inhibition of the nuclear factor-κB （NF-κB） signaling pathway and subsequent suppression of NF-κB-regulated neuronal apoptosis. MethodsAn IS model was established using middle cerebral artery occlusion （MCAO）. Sixty C57BL/6J mice were randomly assigned to five groups （n =12 per group）， i.e.， sham operation， model， HLJDT low-dose （3.9 g·kg^-1·d^-1）， HLJDT high-dose （7.8 g·kg^-1·d^-1）， and Ginkgo biloba extract （GBE， 31.2 mg·kg^-1·d^-1）. Post-operatively， neurological deficit scores （Longa score）， cerebral infarct volume assessed by 2，3，5-triphenyltetrazolium chloride （TTC） staining， and brain water content were evaluated. Learning and memory were assessed using new object recognition （NOR） and fear conditioning （FC） tests. Hippocampal pathology was examined via hematoxylin and eosin （HE） staining. Immunofluorescence detected expression of glial fibrillary acidic protein （GFAP， astrocyte marker）， cellular oncogene Fos （c-Fos， neuronal activation marker）， and glutamate decarboxylase 65 （GAD65）. Western blot measured nuclear factor-κB inhibitor protein α （IκBα）， phosphorylated IκBα （p-IκBα）， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65）， ionic calcium binding adapter molecule 1 （Iba-1）， tumor necrosis factor （TNF）-α， interleukin （IL）-1β， and apoptosis-related proteins， such as cleaved cysteinyl aspartate-specific protease 3 （Caspase-3）， B-cell lymphoma 2 （Bcl-2）， and Bcl-2-associated X protein （Bax）. Real-time quantitative PCR （Real-time PCR） was used to assess mRNA levels of Iba-1， TNF-α， IL-1β， NF-κB p65， cleaved Caspase-3， Bax， and Bcl-2. ResultsCompared with the sham group， the model group exhibited significantly increased neurological deficit scores， brain water content， and cerebral infarct volume （P<0.01）. Hippocampal CA1 neurons were disorganized， showing nuclear pyknosis and karyolysis. NOR exploration time and FC freezing time were significantly reduced （P<0.01）. GFAP and c-Fos expression were increased， while GAD65 expression was decreased （P<0.01）. Cleaved Caspase-3 and Bax were upregulated， Bcl-2 was downregulated， and the Bax/Bcl-2 ratio was elevated （P<0.01）. Expression levels of p-IκBα， p-NF-κB p65， IL-1β， TNF-α， and Iba-1 were significantly increased （P<0.01）. Compared with the model group， HLJDT high-dose， low-dose， and GBE groups showed significant improvements in all parameters （P<0.01）. Among them， the HLJDT high-dose group showed the most pronounced neuronal structural recovery and superior performance in NOR and FC tests （P<0.01）. In this group， GFAP and c-Fos decreased， GAD65 increased （P<0.01）， apoptosis-related protein expression was reversed， and NF-κB signaling and related inflammatory factor expression were suppressed （P<0.01）. ConclusionHLJDT ameliorates cognitive dysfunction in mice after IS， potentially by inhibiting the NF-κB signaling pathway， thereby reducing neuroinflammation and hippocampal neuronal apoptosis.

Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

OBJECTIVE To construct ensemble learning models for predicting high-use days of budesonide based on meteorological factors， thereby providing reference for hospital pharmacy management. METHODS Meteorological data for 2024 and outpatient budesonide usage data from the jurisdiction of Sanming Hospital of Integrated Traditional Chinese and Western Medicine were collected. High-use days were defined as the 75th percentile of outpatient budesonide usage， and a corresponding dataset was established. The prediction task was formulated as a classification problem， and three ensemble learning models were developed： Random Forest， Extreme Gradient Boosting （XGBoost）， and Histogram-based Gradient Boosting Classifier. Model performance was evaluated using accuracy， precision， recall， F1-score， and log-loss. Model interpretability was analyzed using Shapley Additive Explanations （SHAP）. RESULTS The Histogram-based Gradient Boosting Classifier achieved the best performance （accuracy＝0.75， F1-score＝0.48）， followed by XGBoost （accuracy＝0.74， F1-score＝0.43） and Random Forest （accuracy＝0.72， F1-score＝0.22）. SHAP results suggested that the prediction results of the last two models have the highest correction. CONCLUSIONS Ensemble learning models can effectively predict high-use days of budesonide， with the Histogram- based Gradient Boosting Classifier demonstrating the best predictive performance. Low temperature， high humidity， and low atmospheric pressure show significant positive impacts on the prediction of daily budesonide usage.

Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

Objective To investigate the relationship between serum autotaxin(ATX),energy balance re-lated protein(Adropin)and inflammatory factors and poor prognosis in patients with dilated cardiomyopathy(DCM).Methods A total of 105 DCM patients admitted to Qingdao Huangdao District Traditional Chinese Medicine Hospital from June 2017 to February 2020 were selected as the DCM group,and 100 healthy volun-teers who came to the hospital for physical examination during the same period were selected as the control group.The levels of serum ATX,Adropin and inflammatory factors[hypersensitive C-reactive protein(hs-CRP)and interleukin-6(IL-6)]in the two groups were detected,and the correlation between serum ATX,Adropin and inflammatory factors was analyzed by Pearson correlation analysis.Patients in DCM group were divided into good prognosis group and poor prognosis group according to the occurrence of endpoint events during follow-up.Logistic regression was used to analyze the risk factors of poor prognosis in DCM patients,and receiver operating characteristic(ROC)curve was used to analyze the predictive value of serum ATX and Adropinfor poor prognosis in DCM patients.Results The serum levels of ATX,hs-CRP and IL-6 in DCM group were higher than those in control group,and the level of Adropin was lower than that in control group,with statistical significance(P＜0.05).Pearson correlation analysis showed that serum ATX level was posi-tively correlated with hs-CRP and IL-6,and serum Adropin level was negatively correlated with hs-CRP and IL-6(P＜0.05).New York Heart Association(NYHA)functional classification m to Ⅳ and serum ATX lev-el in the poor prognosis group were higher than those in the good prognosis group,the heart failure duration and left ventricular end-diastolic diameter were higher than those in the good prognosis group,the left ventric-ular ejection fraction(LVEF)and serum Adropin levels were lower than those in the good prognosis group,the difference was statistically significant(P＜0.05).Logistic regression model analysis showed that NYHA functional classification Ⅲ to Ⅳ and high ATX were risk factors for poor prognosis in DCM patients,and high Adropin and high LVEF were protective factors for poor prognosis in DCM patients(P＜0.05).ROC curve a-nalysis showed that the area under the curve(AUC)of serum ATX and Adropin in predicting poor prognosis of DCM patients was 0.841 and 0.793,respectively,and the AUC of combined prediction of poor prognosis of DCM patients was greater than that of single prediction.Conclusion Serum ATX is abnormally elevated and serum Adropin is abnormally decreased in DCM patients,both of which are closely related to inflammatory factors.Detection of serum ATX and Adropin levels can provide reference for prognosis assessment of DCM patients.

Objective To investigate the effects of fentanyl citrate on pain in aged rats with hip fracture and its underlying mechanisms. Methods Thirty aged rats with hip fracture were divided into model group (n=10), fentanyl citrate group (n=10), and fentanyl citrate + Sar-SP group (n=10). Additionally, healthy rats from the same period were included as normal group (n=10).Rats in the fentanyl citrate group received intravenous tail injection of 10 μg/kg fentanyl citrate, while those in the fentanyl citrate + Sar-SP group underwent intrathecal injection of 10 μL Sar-SP for fentanyl citrate intervention. Rats in the normal and model groups received intravenous tail injection of an equal volume of saline. Pain threshold, weight-bearing capacity, temperature, and dorsoventral thickness of the hind paws were measured before treatment (0 h) and at 1, 6, 24, and 168 h post-treatment. Enzyme-linked immunosorbent assay (ELISA) was used to detect levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and glutamic acid (Glu) in the spinal cord tissue of rats. Immunohistochemical staining was employed to observe the positive expression rates of ionized calcium-binding adapter molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), and substance P (SP) in the spinal cord tissue. Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was conducted to detect the relative expression levels of SP and tachykinin receptor 1 (TACR1) mRNA in the hippocampus tissue of rats. Western blot analysis was performed to assess the relative expression levels of vimentin (VIM), nuclear receptor corepressor 1 (NOCR), ciliary neurotrophic factor receptor (CNTFR), and epidermal growth factor receptor (EGFR) proteins in the spinal cord tissue. Results Compared with the normal group, rats in the model group exhibited decreased pain threshold and weight-bearing capacity, increased hind paw temperature and dorsoventral thickness, as well as elevated levels of TNF-α, IL-6, IL-1β, and Glu, increased positive expression rates of Iba-1 and GFAP, heightened positive expression rate and relative mRNA expression levels of SP and TACR1, and augmented relative protein expression levels of VIM, NOCR, CNTFR, and EGFR in the spinal cord tissue at 0 h before treatment and at 1, 6, 24, and 168 h post-treatment (P < 0.05). Compared with the model group, rats in the fentanyl citrate group showed increased pain threshold and weight-bearing capacity, decreased hind paw temperature and dorsoventral thickness, as well as reduced levels of TNF-α, IL-6, IL-1β, and Glu, decreased positive expression rates of Iba-1 and GFAP, lowered positive expression rate and relative mRNA expression levels of SP and TACR1, and decreased relative protein expression levels of VIM, NOCR, CNTFR, and EGFR in the spinal cord tissue at 1, 6, 24, and 168 h post-treatment(P < 0.05). Compared with the fentanyl citrate group, rats in the fentanyl citrate+Sar-SP group demonstrated decreased pain threshold and weight-bearing capacity, increased hind paw temperature and dorsoventral thickness, elevated levels of TNF-α, IL-6, IL-1β, and Glu, increased positive expression rates of Iba-1 and GFAP, heightened positive expression rate and relative mRNA expression levels of SP and TACR1, and elevated relative protein expression levels of VIM, NOCR, CNTFR, and EGFR in the spinal cord tissue at 1, 6, 24, and 168 h post-treatment(P < 0.05). Conclusion The improvement in pain in aged rats with hip fracture by fentanyl citrate may be associated with the reduction of SP expression in the spinal cord that inhibits glial cell activation and exhibits anti-inflammatory effects.

Objective To investigate the application value of tenofovir alafenamide fumarate (TAF) in elderly patients with chronic hepatitis B (CHB) and its influence on bones and kidneys. Methods A total of 36 CHB patients, aged ≥60 years, who received TAF antiviral therapy in Qingdao Municipal Hospital, The Affiliated Hospital of Qingdao University, Qingdao Sixth People's Hospital, Chengyang People's Hospital, and Jimo People's Hospital from June 2021 to October 2022 were enrolled in this study, and all patients received TAF (25 mg/d) antiviral therapy. Related data were collected at baseline and weeks 24 and 48 of treatment, including virological indicators, biochemical parameters, urinary protein electrophoresis indices, transient elastography (FibroScan), and bone mineral density. Virological indicators included high-sensitivity HBV DNA quantification; biochemical parameters included total bilirubin, direct bilirubin (DBil), indirect bilirubin (IBil), alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, total bile acid (TBA), glucose, blood urea nitrogen, creatinine, estimated glomerular filtration rate, and cystatin C (Cys C); urinary protein electrophoresis indices included urinary β2 microglobulin (β2-MG), urinary retinol (URBP), and urinary α1 microspherin (α1-MG). The paired t -test was used for comparison of normally distributed continuous data before and after treatment, and the Wilcoxon signed-rank test was used for comparison of non-normally distributed continuous data before and after treatment; the chi-square test or the Fisher's exact test was used for comparison of categorical data. Results A total of 36 CHB patients completed 24 weeks of follow-up. The complete virological response rate after 24 weeks of treatment was higher than that at baseline [83.3% (30/36) vs 77.8% (28/36), χ 2 =0.36, P =0.55], and there were significant reductions in DBil ( t =-2.42, P =0.02) and Cys C ( t =-4.34, P < 0.001) from baseline to week 24. A total of 18 CHB patients completed 48 weeks of follow-up. The complete virological response rate after 48 weeks of treatment was higher than that at baseline (94.4% vs 77.8%, χ 2 =2.22, P =0.34), and there were significant increases in IBil ( t =2.43, P =0.03), TBA ( Z =-2.24, P =0.03), and bone mineral density T score of lumbar vertebra ( t =2.92, P = 0.01) and femoral neck ( t =2.42, P =0.03) and a significant reduction in liver stiffness measurement ( t =-2.31, P =0.03). There were no significant changes in β2-MG, URBP, and α1-MG after treatment (all P > 0.05). Conclusion TAF has a good antiviral effect in CHB patients aged ≥60 years and can help more CHB patients achieve complete virological response, without causing damage to the kidney, and it can also improve bone mineral density and liver fibrosis degree.

Objective::To build a reference fetal growth chart for the Chinese population based on fetal ultrasound measurements.Methods::This was a multicenter, population-based retrospective cohort study. Longitudinal ultrasound measurement data were collected from 24 hospitals in 18 provinces of China from 1 st September through 31 st October of 2019. The estimated fetal weight (EFW) was calculated based on head circumference, abdominal circumference, and femur length using Hadlock formula 3. Fetal growth curves were estimated using a two-level linear regression model with cubic splines. All participants were divided into two groups: the northern group ( n = 5829) and the southern group ( n = 3246) based on the geographical division of China and male fetus group ( n = 4775) and female fetus group ( n = 4300) based on fetal gender. The EFW was compared by fetal gender and geographical group. All statistical models were adjusted for maternal sociodemographic characteristics. Results::A total of 9075 participants with 31,700 ultrasound measurement records were included in this study. Male fetuses demonstrated significantly larger EFW compared to female ones starting at 16 weeks of gestation and extending to delivery (global test P < 0.01). The overall geographic difference in EFW was significant (global test P = 0.03), and week-specific comparisons showed that the northern group had a greater EFW starting at 15 weeks of gestation and extending to 29 weeks of gestation, although this difference did not extend to the time of delivery. The Z-score of EFW confirmed that our Chinese fetal growth charts differed from previously published standards. Conclusion::This study provides EFW and ultrasound biometric reference measurements for Chinese fetuses and reveals differences from other fetal growth charts. The chart is worth promoting in more regions of China but should be tested prudently before use.

Objective::To build a reference fetal growth chart for the Chinese population based on fetal ultrasound measurements.Methods::This was a multicenter, population-based retrospective cohort study. Longitudinal ultrasound measurement data were collected from 24 hospitals in 18 provinces of China from 1 st September through 31 st October of 2019. The estimated fetal weight (EFW) was calculated based on head circumference, abdominal circumference, and femur length using Hadlock formula 3. Fetal growth curves were estimated using a two-level linear regression model with cubic splines. All participants were divided into two groups: the northern group ( n = 5829) and the southern group ( n = 3246) based on the geographical division of China and male fetus group ( n = 4775) and female fetus group ( n = 4300) based on fetal gender. The EFW was compared by fetal gender and geographical group. All statistical models were adjusted for maternal sociodemographic characteristics. Results::A total of 9075 participants with 31,700 ultrasound measurement records were included in this study. Male fetuses demonstrated significantly larger EFW compared to female ones starting at 16 weeks of gestation and extending to delivery (global test P < 0.01). The overall geographic difference in EFW was significant (global test P = 0.03), and week-specific comparisons showed that the northern group had a greater EFW starting at 15 weeks of gestation and extending to 29 weeks of gestation, although this difference did not extend to the time of delivery. The Z-score of EFW confirmed that our Chinese fetal growth charts differed from previously published standards. Conclusion::This study provides EFW and ultrasound biometric reference measurements for Chinese fetuses and reveals differences from other fetal growth charts. The chart is worth promoting in more regions of China but should be tested prudently before use.

Objective:To investigate the cerebral blood flow autoregulation and cerebrovascular reactivity in patients with cerebral small vessel disease (SVD) and depression.Methods:Eighty patients who were treated in Dalian Municipal Central Hospital Affiliated with Dalian University of Technology from May 2020 to may 2021 were selected and divided into observation group and control group according to the existence of depression. Transcranial Doppler sonography combined with standing and lying position test, breath holding test and breath exchange test were used to observe the "w" wave slope, the "w" wave slope, the "w" wave velocity and the "w" wave velocity cerebral blood flow velocity difference, breath holding index, pulsation index (PI) change rate before and after breath holding, resistance index (RI) change rate before and after breath holding, mean velocity (Vm), PI, RI change rate before and after breath exchange. The correlation between depression score and blood flow index was analyzed.Results:There were 38 and 29 patients occurred "w" wave in the control group and observation group respectively, and the rate were 95.0% (38/40) and 72.5% (29/40) respectively ( χ2 = 7.44, P = 0.006). The slope of "w" descending branch of Vm and the slope of "w" ascending branch of Vm in the observation group were smaller than those of the control group respectively: (1.26 ± 0.23) cm/s vs. (2.45 ± 1.00) cm/s, (1.38 ± 0.71) cm/s vs. (2.56 ± 0.77) cm/s, the difference of which had statistical meanings ( P<0.05). The difference of cerebral blood flow velocity of Vm after different positions in the observation group was higher than that in the control group significantly: (7.20 ± 3.07) cm/s vs. (2.93 ± 1.46) cm/s ( P<0.05). The breath holding index PI change rate, RI change rate before and after breath holding test in the observation group were lower than those in the control group statistically: (0.88 ± 0.33)% vs. (1.49 ± 0.27)%, (14.42 ± 9.31)% vs. (21.51 ± 8.79)%, (11.07 ± 1.70)% vs. (15.31 ± 6.73)% ( P<0.05). The change rates of Vm, PI and RI in the observation group before and after ventilation were lower than those in the control group ( P<0.05). There was a negative correlation between depression score and "w" wave slope (Vm), breath holding index, Vm change rate before and after ventilation, and a positive correlation between depression score and cerebral blood flow velocity difference (Vm) in supine and upright position with statistical meanings ( P<0.05). Conclusions:Depression could lead to the decline of cerebral blood flow autoregulation and cerebrovascular reactivity in patients with SVD. And with the aggravation of depression, the decline of cerebral blood flow autoregulation and cerebrovascular reactivity in patients with SVD is more serious.