Diabetic cardiomyopathy （DCM） is a common chronic complication of diabetes， categorized as consumptive thirst in traditional Chinese medicine （TCM）， and it subsequently gives rise to chest impediment. DCM is characterized by a complex pathogenesis and exhibits long-term progression with poor prognosis in clinical practice. Astragali Radix， as a medicinal material with edible value， possesses diverse active components including saponins， polysaccharides， and flavonoids. It has the effects of tonifying Qi， elevating Yang， promoting fluid production， nourishing blood， expressing toxin， and expelling pus. Modern pharmacological studies have confirmed that Astragali Radix and its active components exert therapeutic effects in various aspects such as inhibition of inflammation， alleviation of stress injury， regulation of programmed cell death， modulation of glucose and lipid metabolism， inhibition of myocardial fibrosis， and regulation of gut microbiota and metabolites， treating DCM in a multi-component， multi-target， and multi-pathway manner. The compatibility of Astragali Radix exerts both synergistic and antagonistic effects. The compound preparations and extracts of Astragali Radix are widely used in clinical practice， and the development of novel nano and gel materials and extracellular vesicles helps to improve the oral bioavailability， providing more possibilities for the clinical application of Astragali Radix in DCM， though its potential for clinical translation requires ongoing exploration. This review summarizes the TCM theoretical basis of Astragali Radix in the treatment of DCM， and integrates modern pharmacological research results to delve into the effects and mechanisms of the herb combinations， compound preparations， extracts， and new composite materials of Astragali Radix in the treatment of DCM， aiming to provide a reference for in-depth research and new drug development of Astragali Radix for DCM.

Guided by the theories of yin-yang and collateral disease， this paper identifies the dysregulation of yang qi ascent and descent as the core pathomechanism of hypertension. Based on clinical experience， a treatment approach centered on the method of raising yang and promoting descent was proposed. Clinically， three major syndrome types were identified. Firstly， deficiency of zong qi （ancestral qi） with blood stasis， obstruction of phlegm-turbidity and blood stasis， and hyperactivity of liver yang. Corresponding empirical formulation， Yizong Huoxue Decoction （益宗活血汤） was applied to tonify zong qi， invigorate blood， and raise yang. Secondly， Lizong Huoxue Decoction （理宗活血汤） was used to resolve phlegm， promote yang qi circulation， and regulate qi and blood. Thirdly， Qinggan Tongluo Decoction （清肝通络饮） was used to clear the liver， dredge collaterals， and subdue hyperactive yang. For special types such as non-dipper hypertension， time-specific syndrome differentiation and treatment can be applied based on a thorough understanding of the underlying pathomechanism， aiming to provide new insights into clinical diagnosis and treatment of hypertension.

Objective:To assess the diagnostic performance of a panel of autoantibodies against multiple tumor-associated antigens (BRCA2, P53, ANXA11, PARP1, TRIM21, ATAD2, NY-ESO-1 and CAGE) in the detection of breast cancer.Methods:This was a retrospective case-control study. A total of 545 patients diagnosed with breast cancer (BC) by pathological examination, and eligible for enrolment at Jiangsu Cancer Hospital from January 2022 to December 2023 were selected as the patient group. In the same period, 200 patients with benign breast disease (BD) and 200 healthy individuals (HC) were included. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum levels of tumor-associated autoantibodies in each group. The tumor markers including carcinoembryonic antigen (CEA), glycoconjugate antigen 125 (CA125) and glycoconjugate antigen 153 (CA153) were detected using electrochemiluminescence. Univariate and multivariate logistic regression analyses were used to screen the factors associated with breast cancer. The receiver operating characteristic (ROC) curve was applied to evaluate diagnostic value.Results:The levels of seven autoantibodies against BRCA2, P53, ANXA11, PARP1, ATAD2, NY-ESO-1 and CAGE were significantly higher in the BC group compared to HC group (all P<0.05). Additionally, the levels of six autoantibodies against BRCA2, P53, PARP1, ATAD2, NY-ESO-1 and CAGE were significantly higher in the BC group than those in BD group (all P<0.05). The levels of PARP1 and ATAD2 in the BD group were higher than those in HC group ( P<0.05). Logistic multivariate analysis revealed that BRCA2 ( OR=1.099, 95% CI 0.824-1.107), P53 ( OR=1.534, 95% CI 0.813-2.898), NY-ESO-1( OR=1.159, 95% CI 0.789-1.712) and CA153 ( OR=1.029, 95% CI 0.778-1.495) were potential indicators for breast cancer (all P<0.05). The ROC curves indicated that the AUCs for breast cancer using BRCA2, P53, NY-ESO-1, and CA153 were 0.602 (95% CI 0.549-0.635), 0.688 (95% CI 0.642-0.734), 0.729 (95% CI 0.677-0.781), 0.714 (95% CI 0.663-0.764), respectively. The sensitivities were 0.405, 0.588, 0.683 and 0.653, while the specificities were 0.770, 0.825, 0.851 and 0.790, respectively. The AUC of the combined detection including BRCA2, P53, NY-ESO-1, and CA153 for breast cancer was 0.857 (95% CI 0.832-0.883), with a sensitivity of 0.719 and a specificity of 0.835. Conclusions:The levels of tumor-associated autoantibodies to BRCA2, P53 and NY-ESO-1 were significantly elevated in breast cancer patients, and the combination of the three autoantibodies and CA153 has high diagnostic value for breast cancer.

Objective:To assess the diagnostic performance of a panel of autoantibodies against multiple tumor-associated antigens (BRCA2, P53, ANXA11, PARP1, TRIM21, ATAD2, NY-ESO-1 and CAGE) in the detection of breast cancer.Methods:This was a retrospective case-control study. A total of 545 patients diagnosed with breast cancer (BC) by pathological examination, and eligible for enrolment at Jiangsu Cancer Hospital from January 2022 to December 2023 were selected as the patient group. In the same period, 200 patients with benign breast disease (BD) and 200 healthy individuals (HC) were included. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum levels of tumor-associated autoantibodies in each group. The tumor markers including carcinoembryonic antigen (CEA), glycoconjugate antigen 125 (CA125) and glycoconjugate antigen 153 (CA153) were detected using electrochemiluminescence. Univariate and multivariate logistic regression analyses were used to screen the factors associated with breast cancer. The receiver operating characteristic (ROC) curve was applied to evaluate diagnostic value.Results:The levels of seven autoantibodies against BRCA2, P53, ANXA11, PARP1, ATAD2, NY-ESO-1 and CAGE were significantly higher in the BC group compared to HC group (all P<0.05). Additionally, the levels of six autoantibodies against BRCA2, P53, PARP1, ATAD2, NY-ESO-1 and CAGE were significantly higher in the BC group than those in BD group (all P<0.05). The levels of PARP1 and ATAD2 in the BD group were higher than those in HC group ( P<0.05). Logistic multivariate analysis revealed that BRCA2 ( OR=1.099, 95% CI 0.824-1.107), P53 ( OR=1.534, 95% CI 0.813-2.898), NY-ESO-1( OR=1.159, 95% CI 0.789-1.712) and CA153 ( OR=1.029, 95% CI 0.778-1.495) were potential indicators for breast cancer (all P<0.05). The ROC curves indicated that the AUCs for breast cancer using BRCA2, P53, NY-ESO-1, and CA153 were 0.602 (95% CI 0.549-0.635), 0.688 (95% CI 0.642-0.734), 0.729 (95% CI 0.677-0.781), 0.714 (95% CI 0.663-0.764), respectively. The sensitivities were 0.405, 0.588, 0.683 and 0.653, while the specificities were 0.770, 0.825, 0.851 and 0.790, respectively. The AUC of the combined detection including BRCA2, P53, NY-ESO-1, and CA153 for breast cancer was 0.857 (95% CI 0.832-0.883), with a sensitivity of 0.719 and a specificity of 0.835. Conclusions:The levels of tumor-associated autoantibodies to BRCA2, P53 and NY-ESO-1 were significantly elevated in breast cancer patients, and the combination of the three autoantibodies and CA153 has high diagnostic value for breast cancer.

Myocardial fibrosis （MF） is a prevalent pathological process in a spectrum of cardiac conditions， including myocardial infarction， hypertensive heart disease， and dilated cardiomyopathy. It is marked by an overabundance of extracellular matrix deposition， diminished myocardial compliance， and impaired cardiac function， which can lead to arrhythmias and sudden cardiac death. The current therapeutic approach primarily aims to suppress the progression of fibrosis， yet the therapeutic outcomes are poor. The pathogenesis of MF involves multiple signaling pathways， including the transforming growth factor-beta （TGF-β）/Smads signaling pathway， nuclear factor-kappa B （NF-κB） signaling pathway， phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， and mitogen-activated protein kinase （MAPK） signaling pathway. Traditional Chinese medicine （TCM） boasts a rich history in the treatment of cardiovascular diseases， offering distinctive benefits such as minimal side effects and high safety， and it has demonstrated promising therapeutic effects in the treatment of MF. In recent years， research has turned its attention to the application of TCM in modulating the signaling pathways associated with MF. It has been demonstrated that TCM can modulate the MF-related signaling pathways to exert anti-inflammatory effects， regulate cellular autophagy， cell proliferation， and apoptosis， reduce myocardial oxidative stress and damage， and inhibit the activation of fibroblasts and collagen synthesis， thereby exhibiting the potential to mitigate or even reverse the progression of MF. Experimental research and clinical observations indicate that TCM formulas such as Yixin Futing decoction， Luhong prescription， Zhilong Huoxue Tongyu capsules， and Kangjian Yixin prescription can effectively ameliorate MF and enhance cardiac function through the multi-component regulation of multiple cellular pathways. Specific TCM constituents， including isoliquiritigenin and astragaloside， have been shown to inhibit the expression of TGF-β₁， thereby disrupting the Smad signaling pathway. Compounds like glycyrrhizic acid and allicin can suppress the NF-κB signaling pathway and curtail collagen synthesis in myocardial cells， and forsythoside can activate the PI3K/Akt signaling pathway， contributing to its anti-fibrotic effects.

Objective:To investigate the expression level of serum microRNA-122-5p (miR-122-5p) in elderly patients with chronic atrophic gastritis (CAG) and its correlation with inflammatory factors and disease severity.Methods:A total of 120 CAG patients admitted to our hospital from Dec. 2019 to Dec. 2021 were selected as as the experimental group. According to the gastric mucosa pathological score, the patients were grouped into 58 cases with normal condition and 62 cases with severe condition. Another 105 patients with chronic non-atrophic gastritis during the same period were included as the control group. The expression level of serum miR-122-5p was detected by qRT-PCR, the level of serum hs-CRP was detected by immunoturbidimetry, the levels of serum TNF-α and IL-6 were detected by enzyme-linked immunosorbent assay (ELISA), and the correlation of serum miR-122-5p expression level with hs-CRP, IL-6, TNF-α and disease severity in CAG patients was analyzed by Pearson method. Logistic regression was used to analyze the risk factors of affecting CAG.Results:There were no significant differences in gender, age, or the proportion of patients with smoking history between the CAG group and the control group ( P>0.05). The proportions of drinking and Hp positive patients in the CAG group were 52.50% and 62.50%, which were significantly higher than those in the control group (25.71%, 43.80%) ( P<0.05) ; The serum levels of miR-122-5p, hs-CRP, IL-6, and TNF-α in the CAG group were (2.31±0.42), (24.89±4.56) mg/L, (39.26±7.68) ng/mL, and (85.42±9.65) pg/ml, respectively, which were significantly higher than the control group [ (1.05±0.12), (16.54±3.85) mg/L, (22.39±5.21) ng/ml, (862.34±7.46) pg/ml] ( P<0.05) ; Serum hs-CRP, IL-6, TNF-αlevels, miR-122-5p expression levels, Hp positive infection rate and pathological score in patients with severe CAG disease were (28.14±3.21) mg/L, (44.55±5.73) ng/ml, (93.42±8.81) pg/ml, 2.74±0.30, 72.58%, (4.30±1.20) points, respectively, which were significantly higher than those of patients with normal disease [ (21.42±3.67) mg/L, (33.61±5.54) ng/ml, (76.87±7.59) pg/mL, 1.85±0.36, 51.72%, (1.60±0.30) points] ( P<0.05) ; correlation analysis showed that serum miR-122-5p expression level in CAG patients was positively correlated with hs-CRP, IL-6, TNF-α and disease severity ( r=0.475, 0.453, 0.505, 0.563, P<0.001). Multivariate logistic analysis showed that Hp positive infection ( OR=2.527, 95% CI=1.125-5.678), miR-122-5p ( OR=2.323, 95% CI=1.341-4.025) were independent risk factors for CAG ( P<0.05) . Conclusion:The expression level of serum miR-122-5p in elderly patients with CAG is increased, which is related to serum inflammatory factors, disease severity and Hp infection, and may be a marker for the diagnosis of CAG.

Objective:To investigate the association between ureaplasma urealyticum (UU) colonization in the respiratory tract and bronchopulmonary dysplasia (BPD) in extremely preterm or extremely low birth weight infants.Methods:This was a retrospective study involving preterm infants with gestational age <28 weeks or birth weight <1 000 g who was hospitalized in the Neonatal Intensive Care Unit (NICU) of Chengdu Women's and Children's Central Hospital from June 2019 to March 2022. Respiratory tract secretion was collected for UU DNA detection within 24 h after admission. All the participants were divided into the UU-positive or negative groups based on the detection results. Clinical characteristics of the two groups were analyzed using Mann-Whitney U, t-, or Chi-square tests (Fisher exact test). Results:A total of 82 infants were enrolled, including 31 cases (37.8%) in the UU-positive group and 51 patients (62.2%) in the negative group. Among the 30 cases treated with azithromycin in the positive group, 27 (90.0%, 27/30) turned negative after two courses of treatment. The rates of premature rupture of membranes [51.6% (16/31) vs 17.6% (9/51), χ2=10.50] and prenatal antibiotic exposure [71.0% (22/31) vs 47.1% (24/51), χ2=4.47] in the UU-positive group were both higher than those in the UU-negative group (both P<0.05). Multivariate logistic regression analysis showed that premature rupture of membranes ( OR=5.893, 95% CI: 2.016-17.228) and gestational age ( OR=0.663, 95% CI: 0.441-0.999) were independent risk factors for UU colonization (both P<0.05). UU-positive group had a longer duration of oxygen use [ M ( P25- P75), 1 756 h (1 385-2 088 h) vs 1 357 h (1 128-1 656 h), Z=2.98], a longer length of hospital stay [81 d (70-105 d) vs 68 d (59-84 d), Z=3.05], and higher hospitalization costs [(201 574±70 326) yuan vs (161 288±53 412) yuan, t=－2.74] compared to the UU negative group (all P<0.05). The incidence of BPD [74.2% (23/31) vs 47.1% (24/51), χ2=5.80] and retinopathy of prematurity [93.4% (29/31) vs 74.5% (38/51), χ2=4.68] in the UU positive group was higher than those in the UU-negative group (both P<0.05). No significant correlation was found between UU colonization and the severity of BPD ( P>0.05). Conclusion:UU colonization may increase the incidence of BPD, but there was no clear correlation with the severity of BPD.

Objective To explore the role of long noncoding RNA ( lncRNA) CTD-2012K14. 6 in the development of gestational diabetes mellitus (GDM) related macrosomia. Methods The quantitative real-time PCR ( qRT-PCR) was performed to measure the expression of CTD-2012K14.6 in placentas of women with or without GDM, and the quantity of CTD-2012K14. 6 expression and its association with fetal weights were analyzed; Bioinformatic analysis was performed to predict the downstream molecules. CTD-2012K14. 6 over-expressing lentiviral and siRNA was constructed in human trophoblastic cell line HTR-8/SVneo cells, qRT-PCR and Western blot (WB) were used to invest its effect in modulating the expression of downstream molecules. Results The expression of CTD-2012K14.6 in GDM placentas was significantly higher than that in normal controls (1.70 ± 0.63 vs 1.00 ± 0.56,t=3.68,P＜0.01), and positively correlated with fetal weight (r=0.8501, P＜0.01); on-line analysis showed that CTD-2012K14.6 was located at chr16:67,549,214-67,563,958, which was located in the intron of CCCTC-binding factor( CTCF); Up-regulating CTD-2012K14.6 could significantly reduce the expression of CTCF mRNA and protein, and increase the expression of insulin-like growth factor-Ⅱ( IGF-Ⅱ) mRNA and protein, while down-regulating CTD-2012K14.6 could significantly increase the expression of CTCF mRNA and protein, and reduce the expression of IGF-ⅡmRNA and protein. Conclusion The CTD-2012K14. 6 may play an important role in the pathogenesis of GDM related macrosomia by upregulating the expression of CTCF and IGF-Ⅱ.

Objective: To investigate the detection of thyroid nodules and related risk factors in nuclear power workers, and to provide scientific evidence for thyroid protection of nuclear power workers. Methods: In December 2018, select 295 workers of a nuclear power production enterprise and 238 administrative staff of it, and select 250 staff members of a thermal power generation enterprise 70 kilometers away from the nuclear power station to conduct thyroid ultrasound examination and questionnaire survey for single factor. Analysis and further multivariate logistic regression analysis were used to study the risk factors of thyroid nodules in the population. Results: Women and smoking history were independent risk factors for the increased incidence of thyroid nodules in the study population; three shifts work pattern was an independent risk factor for the increased prevalence of thyroid nodules in nuclear power workers (P<0.05) , and other factors such as the history of nuclear exposure had no significant correlation with thyroid nodules (P>0.05) . Conclusion Nuclear exposure has little effect on the prevalence of thyroid nodules in nuclear power workers.

Objective: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on the polarization and infiltration of M2 macrophages and the invasion and metastasis of tumor cells in ovarian cancer microenvironment. Methods: A co-culture system consisting of ovarian cancer cells (A2780 and SKOV3) and THP-1 derived macrophages was established in vitro. The M-CSF levels in culture medium and M-CSF mRNA levels in cancer cells and macrophages were detected by ELISA and qRT-PCR, respectively. The proportion of CD68+CD163+ M2 macrophages (polarization cells) was determined by flow cytometry. The invasive and metastatic ability of A2780 and SKOV3 cells after co-culturing with M2 macrophages were analyzed using Transwell assay. The expression levels of M-CSF, CD68+, CD163+ and E-cad in paraffin sections of 52 patients with ovarian cancer and 18 patients with benign ovarian tumor were detected by the immunohistochemistry staining, and their correlations and the relationship between M-CSF and clinicopathological features of ovarian cancer patients were analyzed. Results: The M-CSF levels in culture medium of the co-culture group (A2780 and SKOV3 cells co-cultured with M2 macrophages) were significantly higher than that of A2780 and SKOV3 cells alone (t=14.315 and 12.338, P＜0.01). Fluorescence quantitative PCR results showed that the increased M-CSF originated from the secretion of co-cultured ovarian cancer cells (t=29.915 and 36.826, P＜0.01). The proportions of CD68+CD163+ M2 macrophages in the A2780 cells co-cultured with M2 macrophages group and SKOV3 cells co-cultured with M2 macrophages group were (6.14±0.50)% and (7.32±0.67)%, respectively, which were significantly higher than that in the M2 macrophages alone group ([1.82±0.34]%, t=12.289 and 12.711, P＜0.01). Transwell assay showed that the co-culture environment enhanced the invasion of A2780 and SKOV3 cells (24.00±4.81 vs 75.20±6.42, t=11.058; 18.40±2.31 vs 61.60±9.66, t=7.537, P＜0.01). The expression levels of M-CSF in ovarian cancer tissues were positively correlated with the number of CD68+ cells and CD163+ cells (r=0.690 and 0.596, P＜0.01), and negatively with the expression levels of E-cad (r=-0.566, P＜0.01). Moreover, the expression levels of M-CSF and the number of CD68+ cells and CD163+ cells in ovarian cancer tissues were significantly higher than that in benign ovarian tumor tissues, however, the expression levels of E-cad were on the contrary. The expression levels of M-CSF in ovarian cancer tissues were significantly correlated with tumor stage, differentiation and lymphatic node metastasis (χ2=6.240, 6.612 and 4.544, respectively, P＜0.05). Conclusion The increased expression of M-CSF in ovarian cancer microenvironment may induce the polarization and infiltration of CD68+CD163+ M2 macrophages, and then promote the invasion and metastasis of ovarian cancer cells.