ObjectiveThis paper aims to investigate and evaluate the staged efficacy and safety of the representative empirical prescription of the “Zhu Ke Jiao” theory， Qijia Rougan prescription， combined with entecavir in the treatment of hepatic fibrosis in chronic hepatitis B. MethodsA multicenter randomized controlled clinical study was conducted， and 101 patients diagnosed with chronic hepatitis B-related hepatic fibrosis （CHB-HF） who met the diagnosis and inclusion criteria were randomly assigned to an observation group （Qijia Rougan prescription + entecavir） and a control group （entecavir）. The treatment duration was 24 weeks. Liver stiffness measurement （LSM）， fibrosis-4 index （FIB-4）， portal vein diameter， hepatitis B serology， biochemical indicators， hepatic fibrosis markers in serum ［hyaluronic acid （HA）， laminin （LN）， procollagen Ⅲ peptide （PⅢP）， and type Ⅳ collagen （Ⅳ-C）］， and traditional Chinese medicine syndrome scores were used as efficacy evaluation indicators. Efficacy assessments and explorations of different staged subgroups of Qijia Rougan prescription were conducted according to LSM values based on the Metavir pathological staging standard. ResultsA total of 98 cases were included for statistical analysis， with 49 cases in the observation group and 49 in the control group. The general data of the patients in both groups were comparable. Compared with the same group before treatment， the observation group showed a significant reduction in LSM and FIB-4 （P<0.01）， as well as notable improvements in LN， Ⅳ-C， and various TCM syndrome scores （P<0.05， P<0.01）. When compared to the control group after treatment， the observation group demonstrated significant improvements in LSM， FIB-4， and various TCM syndrome score indicators （P<0.05， P<0.01）， indicating that the observation group performed better than the control group. Subgroup analysis of the regression of hepatic fibrosis stages showed that compared to the same group before treatment， the observation group had better improvement in regression of stages F2 and F3 （P<0.05）. When compared to the control group after treatment， the observation group exhibited superior improvement in regression of stage F3 （P<0.05）. No adverse events occurred in either group during the treatment period. ConclusionCompared with entecavir alone， the combination of Qijia Rougan prescription and entecavir significantly improves the degree of hepatic fibrosis and clinical TCM symptoms in patients. The optimal intervention period is primarily during stage F3， which is a potential “interception” point of the “Zhu Ke Jiao” theory.

OBJECTIVE: Although dietary preferences influence chronic diseases, few studies have linked dietary preferences to mortality risk, particularly in large cohorts. To investigate the relationship between dietary preferences and mortality risk (all-cause, cancer, and cardiovascular disease [CVD]) in a large adult cohort. METHODS: A cohort of 1,160,312 adults (mean age 62.48 ± 9.55) from the Shenzhen Healthcare Big Data Cohort (SHBDC) was analyzed. Hazard ratios ( HRs) for mortality were estimated using the Cox proportional hazards model. RESULTS: The study identified 12,308 all-cause deaths, of which 3,865 (31.4%) were cancer-related and 3,576 (29.1%) were attributed to CVD. Compared with a mixed diet of meat and vegetables, a mainly meat-based diet (hazard ratio [ HR] = 1.13; 95% confidence interval [ CI]: 1.02, 1.27) associated with a higher risk of all-cause mortality, while mainly vegetarian ( HR = 0.87; 95% CI: 0.78, 0.97) was linked to a reduced risk. Furthermore, there was a stronger correlation between mortality risk and dietary preference in the > 65 age range. CONCLUSION A meat-based diet was associated with an increased risk of all-cause mortality, whereas a mainly vegetarian diet was linked to a reduced risk.
Humans ; China/epidemiology* ; Middle Aged ; Male ; Female ; Prospective Studies ; Aged ; Cardiovascular Diseases/mortality* ; Diet/statistics & numerical data* ; Neoplasms/mortality* ; Adult ; Cause of Death ; Food Preferences ; Proportional Hazards Models ; Mortality ; Cohort Studies

The pathogenesis of cardiovascular diseases (CVD) is complex, and dynamic imbalances in protein acylation modification are significantly associated with the development of CVD. In recent years, most studies on exercise-regulated protein acylation modifications to improve cardiovascular function have focused on acetylation and lactylation. Protein acylation modifications are usually affected by exercise intensity. High-intensity exercise directly affects oxidative stress and cellular energy supply, such as changes in ATP and NAD⁺ levels; moderate-intensity exercise is often accompanied by improvements in aerobic metabolism, such as fatty acid β-oxidation and TCA cycle, which modulate mitochondrial biogenesis. The above processes may affect the acylation status of relevant regulatory enzymes and functional proteins, thereby altering their function and activity and triggering signaling cascades to adapt to exercise’s metabolic demands and stresses. Exercise regulates the levels of acylation modifications of H3K9, H3K14, H3K18, and H3K23, which are involved in regulating the transcriptional expression of genes involved in oxidative stress, glycolysis, inflammation, and hypertrophic response by altering chromatin structure and function. Exercise can regulate the acylation modification of non-histone-specific sites in the cardiovascular system involved in mitochondrial function, glycolipid metabolism, fibrosis, protein synthesis, and other biological processes, and participates in the regulation of protein activity and function by altering the stability, localization, and interaction of proteins, and ultimately works together to achieve the improvement of cardiovascular phenotypes and biological functions. Exercise affects acyl donor concentration, acyltransferase, and deacetylase expression and activity by influencing acyl donor concentration, acyltransferase, and deacetylase. Exercise regulates the abundance of acyl donors such as acetyl coenzyme A, propionyl coenzyme A, butyryl coenzyme A, succinyl coenzyme A, and lactoyl coenzyme A by promoting glucose and lipid metabolism and improving intestinal bacterial flora, which in turn affects protein acylation modification, accelerates oxidative decarboxylation of pyruvic acid in the body, and activates the energy-sensing molecule, adenosine monophosphate-activated protein kinase (AMPK), to improve cardiovascular function. Exercise may affect protein acylation modifications in the cardiovascular system by regulating the activity and expression of adenoviral E1A binding protein of 300 kDa (p300)/cyclic adenosine monophosphate response element-binding protein (CBP), general control nonderepressible 5-related N-acetyltransferases (GNAT), and alanyl-transfer t-RNA synthetase (AARS), which in turn improves cardiovascular function. The relationship between exercise and cardiovascular deacetylases has attracted much attention, with SIRT1 and SIRT3 of the silence information regulator (SIRT) family of proteins being the most studied. Exercise may exert transient or long-term stable cardiovascular protective benefits by promoting the enzymatic activity and expression of SIRT1, SIRT3, and HDAC2, inhibiting the enzymatic activity and expression of HDAC4, and mediating the deacylation of metabolic regulation-related enzymes, cytokines, and molecules of signaling pathways. This review introduces the role of protein acylation modification on CVD and the effect of exercise-mediated protein acylation modification on CVD. Based on the existing studies, it analyzes the possible mechanisms of exercise-regulated protein acylation modification to improve CVD from the perspectives of acylation modification donors, acyltransferases, and deacetylases. Deciphering the regulation of cardiovascular protein acylation and modification by exercise and exploring the essential clues to improve cardiovascular disease can enrich the theoretical basis for exercise to promote cardiovascular health. However, it is also significant for developing new cardiovascular disease prevention and treatment targets.

Objective To explore the predictive value of fat attenuation index(FAI)and fibrous plaque index(FPI)for the prognosis of patients with acute coronary syndrome(ACS).Methods A retrospective cohort study was conducted on 334 ACS patients undergoing percutaneous coronary intervention(PCI)in the First Affiliated Hospital of Army Military Medical University and Yongchuan Hospital of Chongqing Medical University from March 2021 to July 2023.All patients received coronary computed tomography angiography(CCTA)to measure FAI and FPI.According to the occurrence of major adverse cardiovascular events(MACE)with 1 year of follow-up,they were divided into MACE group(n=108)and non-MACE group(n=226).The baseline data,CCTA data and results of laboratory tests were collected and compared between the 2 groups.Multivariate logistic regression analysis was used to analyze the relationship of FAI and FPI with the prognosis of ACS patients,and ROC curve was drawn to evaluate its predictive efficiency.Results Among the 334 ACS patients,108(32.34%)experienced MACE.When compared with the non-MACE group,the MACE group exhibited significantly larger proportions of diabetes(72.22%vs 31.86%)and left main coronary artery disease(18.52%vs 7.08%),but lower success rate of operation(79.63%vs 93.81%,P<0.05).Radiologic results showed that the proportion of severe stenosis(20.37%vs 10.62%),FAI(-80.12±6.41 HU vs-72.34±7.09 HU)and FPI(0.58±0.41 vs 0.26±0.12)were obviously increased in the MACE group than the non-MACE group(P<0.05).Laboratory tests indicated that there were statistical differences between the 2 groups in high-density lipoprotein-cholesterol(HDL-C,1.20±0.15 vs 1.09±0.16 mmol/L),miR-126(0.91±0.12 vs 0.96±0.15)and SST2(38.45±5.67 vs 34.30±4.89 ng/mL,P<0.05).Multivariate Logistic regression analysis revealed that FAI(OR=1.200,95%CI:1.136～1.268),FPI(OR=63.157,95%CI:14.126～282.374),moderate stenosis(OR=1.332,95%CI:1.024～1.859),severe stenosis(OR=1.480,95%CI:1.074～2.039),miR-126(OR=0.007,95%CI:0.001～0.077),and sST2(OR=1.192,95%CI:1.113～1.277)were independent predictors of MACE(P<0.05).ROC curve analysis displayed that stenosis degree(AUC=0.622,95%CI:0.561～0.683,P=0.001),FAI(AUC=0.790,95%CI:0.741～0.839,P=0.001)and FPI(AUC=0.700,95%CI:0.638～0.761,P=0.001),miR-126(AUC=0.646,95%CI:0.584～0.707,P=0.001),sST2(AUC=0.700,95%CI:0.638～0.761,P=0.001)had certain predictive values for ACS prognosis.Conclusion Coronary FAI and FPI can be used as independent prognostic indicators of ACS patients,and their numerical changes are closely related to plaque stability and inflammatory state.

Investigating the correlation between micronucleus formation and male infertility has the potential to improve clinical diagnosis and deepen our understanding of pathological progression. Our study enrolled 2252 male patients whose semen was analyzed from March 2023 to July 2023. Their clinical data, including semen parameters and age, were also collected. Genetic analysis was used to determine whether the sex chromosome involved in male infertility was abnormal (including the increase, deletion, and translocation of the X and Y chromosomes), and subsequent semen analysis was conducted for clinical grouping purposes. The participants were categorized into five groups: normozoospermia, asthenozoospermia, oligozoospermia, oligoasthenozoospermia, and azoospermia. Patients were randomly selected for further study; 41 patients with normozoospermia were included in the control group and 117 patients with non-normozoospermia were included in the study group according to the proportions of all enrolled patients. Cytokinesis-block micronucleus (CBMN) screening was conducted through peripheral blood. Statistical analysis was used to determine the differences in micronuclei (MNi) among the groups and the relationships between MNi and clinical data. There was a significant increase in MNi in infertile men, including those with azoospermia, compared with normozoospermic patients, but there was no significant difference between the genetic and nongenetic groups in azoospermic men. The presence of MNi was associated with sperm concentration, progressive sperm motility, immotile spermatozoa, malformed spermatozoa, total sperm count, and total sperm motility. This study underscores the potential utility of MNi as a diagnostic tool and highlights the need for further research to elucidate the underlying mechanisms of male infertility.
Humans ; Male ; Infertility, Male/genetics* ; Adult ; Micronucleus Tests ; Semen Analysis ; Oligospermia/genetics* ; Azoospermia/genetics* ; Chromosome Aberrations ; Sperm Count ; Micronuclei, Chromosome-Defective ; Middle Aged

[This corrects the article DOI: 10.11909/j.issn.1671-5411.2017.08.005.].

OBJECTIVE: To assess the efficacy of Qingda Granule (QDG) in ameliorating hypertension-induced cardiac damage and investigate the underlying mechanisms involved. METHODS: Twenty spontaneously hypertensive rats (SHRs) were used to develope a hypertension-induced cardiac damage model. Another 10 Wistar Kyoto (WKY) rats were used as normotension group. Rats were administrated intragastrically QDG [0.9 g/(kg•d)] or an equivalent volume of pure water for 8 weeks. Blood pressure, histopathological changes, cardiac function, levels of oxidative stress and inflammatory response markers were measured. Furthermore, to gain insights into the potential mechanisms underlying the protective effects of QDG against hypertension-induced cardiac injury, a network pharmacology study was conducted. Predicted results were validated by Western blot, radioimmunoassay immunohistochemistry and quantitative polymerase chain reaction, respectively. RESULTS: The administration of QDG resulted in a significant decrease in blood pressure levels in SHRs (P<0.01). Histological examinations, including hematoxylin-eosin staining and Masson trichrome staining revealed that QDG effectively attenuated hypertension-induced cardiac damage. Furthermore, echocardiography demonstrated that QDG improved hypertension-associated cardiac dysfunction. Enzyme-linked immunosorbent assay and colorimetric method indicated that QDG significantly reduced oxidative stress and inflammatory response levels in both myocardial tissue and serum (P<0.01). CONCLUSIONS Both network pharmacology and experimental investigations confirmed that QDG exerted its beneficial effects in decreasing hypertension-induced cardiac damage by regulating the angiotensin converting enzyme (ACE)/angiotensin II (Ang II)/Ang II receptor type 1 axis and ACE/Ang II/Ang II receptor type 2 axis.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Hypertension/pathology* ; Renin-Angiotensin System/drug effects* ; Rats, Inbred SHR ; Oxidative Stress/drug effects* ; Male ; Rats, Inbred WKY ; Blood Pressure/drug effects* ; Myocardium/pathology* ; Rats ; Inflammation/pathology*

This consensus will introduce the characteristics of fillers used in the surgical cavities of domestic nasal surgery patients based on relevant literature and expert opinions. It will also provide recommendations for the selection of cavity fillers for different nasal diseases, with chronic sinusitis as a representative example.
Humans ; Nasal Cavity/surgery* ; Nasal Surgical Procedures ; China ; Consensus ; Sinusitis/surgery* ; Dermal Fillers

Ovarian tumor (OT) is the most lethal form of gynecologic malignancy, with minimal improvements in patient outcomes over the past several decades. Metastasis is the leading cause of ovarian cancer-related deaths, yet the underlying mechanisms remain poorly understood. Psychological stress is known to activate the glucocorticoid receptor (NR3C1), a factor associated with poor prognosis in OT patients. However, the precise mechanisms linking NR3C1 signaling and metastasis have yet to be fully elucidated. In this study, we demonstrate that chronic restraint stress accelerates epithelial-mesenchymal transition (EMT) and metastasis in OT through an NR3C1-dependent mechanism involving nuclear protein 1 (NUPR1). Mechanistically, NR3C1 directly regulates the transcription of NUPR1, which in turn increases the expression of snail family transcriptional repressor 2 (SNAI2), a key driver of EMT. Clinically, elevated NR3C1 positively correlates with NUPR1 expression in OT patients, and both are positively associated with poorer prognosis. Overall, our study identified the NR3C1/NUPR1 axis as a critical regulatory pathway in psychological stress-induced OT metastasis, suggesting a potential therapeutic target for intervention in OT metastasis.

With the extended survival period of breast cancer patients and the increasing health demands, the concomitant diseases of breast cancer have gradually attracted the attention of both doctors and patients, and it is imperative to conduct comprehensive management of these diseases, in which the general practitioners, as the more comprehensive and complex medical talents, have not yet played their due roles. In this article, we report two cases of comprehensive management of concomitant diseases of breast cancer through collaboration of general practitioners and specialists (integrated general and specialist care). The role and function of general practitioners in this process were deeply analyzed, and the establishment of a consultation-liaison general practice model to further promote the role of integrated general and specialist care in integrated oncology care was advocated.