OBJECTIVE To compare the antihypertensive efficacy of sacubitril/valsartan versus benazepril in patients with perimenopausal hypertension， as well as their impacts on ventricular remodeling and inflammatory fibrosis. METHODS A total of 206 perimenopausal hypertensive patients in our hospital from January 1， 2023 to December 30， 2024 were retrospectively included.These patients were enrolled and divided into benazepril group （105 cases） and sacubitril/valsartan group （101 cases）. Benazepril group received Benazepril hydrochloride tablet， and sacubitril/valsartan group received Sacubitril valsartan sodium tablet. All patients were treated for 6 months. The blood pressure（systolic blood pressure and diastolic blood pressure） and blood pressure control status before and after treatment， echocardiographic indicators （left ventricular ejection fraction， left ventricular mass index， relative wall thickness， and early-diastolic peak transmitral flow velocity/early-diastolic peak velocity of the mitral annulus）， inflammatory fibrosis related indicators（high-sensitivity C-reactive protein，ratio of monocytes to lymphocytes，and ratio of neutrophils to lymphocytes）， as well as the occurrence of adverse reactions（hypotension，hyperkalemia，and angioedema） were observed in both groups before and after treatment. RESULTS The blood pressure control rate was significantly higher in the sacubitril/valsartan group than in benazepril group （ P ＜0.05）. After treatment， the blood pressure， echocardiographic indicators（except for left ventricular ejection fraction） ，and inflammatory fibrosis related indicators were significantly lower than those before treatment within the same group， and the sacubitril/valsartan group were significantly lower than the benazepril group （ P ＜0.05）. There were no statistically significant differences in the incidence of hypotension， hyperkalemia， angioedema， and overall adverse drug reactions between the two groups （ P ＞0.05）. CONCLUSIONS Compared with benazepril， sacubitril/valsartan provides superior blood-pressure control， reverses ventricular remodeling， attenuates inflammatory fibrosis in perimenopausal hypertensive patients， while maintaining a similar safety profile.

ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

ObjectiveTo explore the potential mechanism of Xianglian Huazhuo prescription （XLHZ） in treating chronic atrophic gastritis （CAG） by regulating cell cycle and inhibiting proliferation， using bioinformatics technology and animal experiments. MethodsDifferential expressed genes （DEGs） related to CAG were screened using GEO database and GEO2R tool. Weighted gene co-expression network analysis （WGCNA） was employed to search for hub genes of CAG. These hub genes were intersected with cell cycle proliferation based on GeneCards database. Eenrichment analysis of the intersecting genes was performed to obtain signaling pathways and biological processes related to CAG. Protein protein interaction （PPI） analysis of genes was conducted using the Protein Interaction Platform （STRING） database to search the super hub gene （hub 2.0）， and animal experiments were conducted for further validation. Fourteen of 70 male Wistar rats were randomly selected as the normal group， and the remaining 56 rats were prepared by the combined modeling method of "starvation disorder+N-methyl-N-nitro-N-nitrosoguanidine （MNNG） + sodium salicylate". The successfully modeled rats were randomly divided into the model group， XLHZ-H， XLHZ-M， and XLHZ-L groups （36， 18， 9 g·kg^-1， respectively）， and Morodan group （1.4 g·kg^-1）. Each group was given corresponding intervention for 60 days. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes of gastric mucosa in rats. The ultrastructure of gastric mucosal tissue cells was observed by transmission electron microscopy. The relative expression levels of TGF-β₁， Smad2 and Smad3 proteins， S/G₂/M phase marker geminin and proliferation marker MCM2 were detected by Western blot in gastric mucosal tissue， and Spearman correlation analysis was performed. ResultsA total of 15 hub 2.0 genes were identified， including TGF-β₁， suggesting the involvement of the TGF-β₁ signaling pathway in the CAG pathogenesis. Compared with the normal group， the expressions of TGF-β₁， Smad2， geminin and MCM2 proteins in the gastric mucosa tissue of the model group were increased （P<0.05）， and the expression of Smad3 protein was decreased （P<0.05）. Compared with the model group， the expressions of TGF-β₁ and geminin in the gastric mucosa were decreased in the drug groups （P<0.05）. The XLHZ-M group， XLHZ-H group and Morodan group had significantly decreased protein expression of Smad2 and MCM2 （P<0.05）. The protein expression of Smad3 was significantly increased in XLHZ-M， XLHZ-H， and Morodan groups （P<0.05）. Spearman correlation analysis showed that Smad3 was negatively correlated with other indicators， and positively correlated with other indicators （P<0.01）. ConclusionXLHZ may inhibit TGF-β₁/Smads signaling pathway， regulate cell cycle， and inhibit proliferation in the treatment of CAG.

ObjectiveThis paper aims to explore the risk factors for chronic atrophic gastritis （CAG） with turbidity toxin accumulation syndrome and establish a prediction model. MethodsClinical data of 180 patients with CAG who participated in the "clinical study of Xianglian Huazhuo Particles blocking CAG cancer transformation" of Hebei Sheng Zhong Yi Yuan from July 2021 to March 2022 were collected. After confounding factors were controlled by propensity score matching， patients were divided into a training set （namely dev） and a validation set （namely vad） in a seven to three ratio. The risk factors for CAG with turbidity toxin accumulation syndrome in the training set were investigated by using univariate Logistic regression analysis and least absolute shrinkage and selection operator （namely Lasso） regression algorithms. Subsequently， a model， named model 1se， was developed by using the training set data to predict the risk factors for CAG with turbidity toxin accumulation syndrome. The accuracy of the prediction model was assessed by using various methods， including the receiver operating characteristic （ROC） curve， Hosmer-Lemeshow test （H-L）， calibration plot， and decision curve analysis （DCA）. ResultsAge， body mass index （BMI）， family history of cancer， job and life satisfaction， yellow and greasy fur with slippery pulse， and heavy body sensation were independent risk factors of the model. The prediction model showed excellent predictive value for both the training and validation sets. ConclusionThe established prediction model for CAG with turbidity toxin accumulation syndrome has high discrimination and excellent calibration， which could provide an excellent clinical basis for disease diagnosis and individualized treatment of patients.

ObjectiveThis paper aims to explore the risk factors for chronic atrophic gastritis （CAG） with turbidity toxin accumulation syndrome and establish a prediction model. MethodsClinical data of 180 patients with CAG who participated in the "clinical study of Xianglian Huazhuo Particles blocking CAG cancer transformation" of Hebei Sheng Zhong Yi Yuan from July 2021 to March 2022 were collected. After confounding factors were controlled by propensity score matching， patients were divided into a training set （namely dev） and a validation set （namely vad） in a seven to three ratio. The risk factors for CAG with turbidity toxin accumulation syndrome in the training set were investigated by using univariate Logistic regression analysis and least absolute shrinkage and selection operator （namely Lasso） regression algorithms. Subsequently， a model， named model 1se， was developed by using the training set data to predict the risk factors for CAG with turbidity toxin accumulation syndrome. The accuracy of the prediction model was assessed by using various methods， including the receiver operating characteristic （ROC） curve， Hosmer-Lemeshow test （H-L）， calibration plot， and decision curve analysis （DCA）. ResultsAge， body mass index （BMI）， family history of cancer， job and life satisfaction， yellow and greasy fur with slippery pulse， and heavy body sensation were independent risk factors of the model. The prediction model showed excellent predictive value for both the training and validation sets. ConclusionThe established prediction model for CAG with turbidity toxin accumulation syndrome has high discrimination and excellent calibration， which could provide an excellent clinical basis for disease diagnosis and individualized treatment of patients.

ObjectiveTo investigate the mechanism of Huazhuo Jiedu prescription in treating ulcerative colitis （UC） by regulating mitophagy. MethodsThe genes related to mitophagy and UC were retrieved from GeneCards， and then the common genes of mitophagy and UC were analyzed by metascape to identify the genes related to mitophagy in UC. Animal experiments were carried out to decipher the mechanism by which Huazhuo Jiedu prescription treated UC by regulating mitophagy. Sixty C57BL/6 male mice were randomized into normal， model， high-， medium-， and low-dose （50， 25， 12.5 g·kg^-1， respectively） Huazhuo Jiedu prescription， and mesalazine （0.52 g·kg^-1·d^-1） groups， with 10 mice in each group. After successful modeling by the dextran sulfate sodium-free drinking method， the colonic mucosal damage was observed by hematoxylin-eosin staining， and the ultracellular structure of colon mucosa was observed by transmission electron microscopy. The expression levels of mitophagy-related proteins PTEN-induced putative kinase 1 （PINK1） and Parkin protein were determined by Western blot. The expression of prohibitin 2 （PHB2）， ubiquitin-specific protease 15 （USP15）， ubiquitin-specific protease 30 （USP30） in the colon tissue was detected by immunofluorescence （IF）. ResultsAll the drug intervention groups showed ameliorated pathological manifestations of the colonic mucosa and improved mitochondrial structures in UC mice. Compared with the normal group， the model group demonstrated up-regulated protein levels of PINK1 and Parkin （P<0.05）， enhanced average fluorescence intensity of PHB2 （P<0.05）， and weakened average fluorescence intensity of USP15 and USP30 （P<0.05）. Compared with the model group， the mesalazine group and the high- and medium-dose Huazhuo Jiedu prescription groups showcased down-regulated protein levels of PINK1 and Parkin （P<0.05）， decreased average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. The low-dose Huazhuo Jiedu prescription group showed down-regulated protein levels of PINK1 and Parkin （P<0.05）， weakened average fluorescence intensity of PHB2 （P<0.05）， and enhanced average fluorescence intensity of USP15 and USP30 （P<0.05）. ConclusionHuazhuo Jiedu prescription can attenuate the intestinal mucosal injury and improve the mitochondrial cell ultrastructure in UC mice by regulating the expression of PINK1-Parkin pathway and inhibiting excessive mitophagy.

BACKGROUND: The purpose of this study was to evaluate the safety and efficacy of subsequent radiotherapy (RT) following first-line treatment with durvalumab plus chemotherapy in patients with extensive-stage small cell lung cancer (ES-SCLC). METHODS: A total of 122 patients with ES-SCLC from three hospitals during July 2019 to December 2021 were retrospectively analyzed. Inverse probability of treatment weighting (IPTW) analysis was performed to address potential confounding factors. The primary focus of our evaluation was to assess the impact of RT on progression-free survival (PFS) and overall survival (OS). RESULTS: After IPTW analysis, 49 patients received durvalumab plus platinum-etoposide (EP) chemotherapy followed by RT (Durva + EP + RT) and 72 patients received immunochemotherapy (Durva + EP). The median OS was 17.2 months vs . 12.3 months (hazard ratio [HR]: 0.38, 95% confidence interval [CI]: 0.17-0.85, P = 0.020), and the median PFS was 8.9 months vs . 5.9 months (HR: 0.56, 95% CI: 0.32-0.97, P = 0.030) in Durva + EP + RT and Durva + EP groups, respectively. Thoracic radiation therapy (TRT) resulted in longer OS (17.2 months vs . 14.7 months) and PFS (9.1 months vs . 7.2 months) compared to RT directed to other metastatic sites. Among patients with oligo-metastasis, RT also showed significant benefits, with a median OS of 17.4 months vs . 13.7 months and median PFS of 9.8 months vs . 5.9 months compared to no RT. Continuous durvalumab treatment beyond progression (TBP) prolonged OS compared to patients without TBP, in both the Durva + EP + RT (NA vs . 15.8 months, HR: 0.48, 95% CI: 0.14-1.63, P = 0.238) and Durva + EP groups (12.3 months vs . 4.3 months, HR: 0.29, 95% CI: 0.10-0.81, P = 0.018). Grade 3 or 4 adverse events occurred in 13 (26.5%) and 13 (18.1%) patients, respectively, in the two groups; pneumonitis was mostly low-grade. CONCLUSION Addition of RT after first-line immunochemotherapy significantly improved survival outcomes with manageable toxicity in ES-SCLC.
Humans ; Small Cell Lung Carcinoma/therapy* ; Retrospective Studies ; Male ; Female ; Middle Aged ; Lung Neoplasms/therapy* ; Aged ; Antibodies, Monoclonal/therapeutic use* ; Adult ; Immunotherapy/methods* ; Aged, 80 and over

OBJECTIVE: To investigate effectiveness of the bridge combined fixation system (BCFS) for Bado typeⅠchronic Monteggia fractures (CMF) in children. METHODS: A clinical data of 8 children with Bado type ⅠCMF, who were treated with the BCFS between November 2023 and February 2025, was retrospectively analyzed. There were 6 boys and 2 girls, with a mean age of 7.0 years (range, 4-12 years). The time from injury to operation ranged from 29 to 370 days (median, 68.5 days). Preoperative elbow range of motion was (111.3±17.9)° in flexion, (13.1±13.9)° in extension, (71.9±14.6)° in pronation, and (75.6±13.5)° in supination. Fracture healing time and postoperative complications were observed, and clinical outcomes were evaluated using the Mayo elbow performance score. RESULTS: All incisions healed by primary intention without infection, non-healing of the incision, or iatrogenic nerve injury. All children were followed up 4-18 months (mean, 10.3 months). At last follow-up, the elbow range of motion significantly improved to (142.5±2.7)° in flexion, (2.5±2.7)° in extension, (87.5±2.7)° in pronation, and (88.8±2.3)° in supination ( P<0.05). According to the postoperative Mayo elbow performance score, all cases were rated as excellent. Radiographic review showed no radial head dislocation, nonunion at the ulnar osteotomy site, or elbow stiffness, and no breakage of the BCFS or screw loosening. The fracture healing time ranged from 3 to 6 months, with a median of 4 months. CONCLUSION The BCFS was confirmed to be effective in the treatment of pediatric Bado type Ⅰ CMF, with good restoration of elbow function and the advantage of avoiding secondary implant removal surgery.
Humans ; Child ; Monteggia's Fracture/surgery* ; Male ; Female ; Child, Preschool ; Range of Motion, Articular ; Retrospective Studies ; Fracture Fixation, Internal/instrumentation* ; Elbow Joint/physiopathology* ; Bone Plates ; Treatment Outcome ; Fracture Healing ; Bone Screws ; Elbow Injuries

In hypoxic-ischemic brain damage (HIBD), the programmed cell death known as ferroptosis is significantly activated. Microglial cells demonstrate a high level of sensitivity to iron accumulation. Understanding how to regulate the dual role of microglia and transforming the microglial ferroptosis to a moderate and controllable process has considerable implications for the targeted treatment in HIBD. This paper serves as an overview of microglia-mediated ferroptosis in HIBD as a disease model. We discuss various aspects centered around microglia, including pathophysiological mechanisms, polarization and functions of microglia, molecular mechanisms of ferroptosis, signaling pathways, and therapeutic strategies. The review aims to provide a reference for studies of ferroptosis in microglia.
Microglia/physiology* ; Ferroptosis/physiology* ; Humans ; Animals ; Hypoxia-Ischemia, Brain/pathology* ; Signal Transduction

Objective: To investigate the current status of refractive errors and insufficient hyperopia reserve in preschool children aged 3-6 years in Hefei and to analyze influencing factors, so as to provide a scientific basis for formulating targeted myopia prevention policies and comprehensive interventions. Methods: In May 2022, a stratified cluster random sampling method was used to select 897 preschool children from 8 kindergartens across four districts (Baohe, Yaohai, Shushan, and Economic and Technological Development Zone) in Hefei, and Children’s Visual Health related Behavior Assessment Scale was used to collect personal information and environmental factors. Pre and post cycloplegic refraction tests were conducted to assess insufficient hyperopic reserve and refractive development levels. Group comparisons were conducted using 2 test, t-test or analysis of variance. Multivariate regression analysis was performed to identify key factors influencing hyperopic reserve, axial length and spherical equivalent in preschool children. Results: The detection rates of refractive errors among preschool children were 6.8% for hyperopia, 1.6% for myopia, and 11.1% for astigmatism. Notably, the prevalence of myopia was significantly higher in boys (2.3%) than in girls (0.7%) ( χ 2=3.88, P <0.05). Additionally, 8.8% of the children exhibited insufficient hyperopic reserve. The results of multiple regression analysis showed that preschool children with high myopia in the father, high myopia in the mother, longer daily duration of near work, and longer daily electronic product use time had increased risks of axial growth ( β =0.12, 0.09, 0.15, 0.11), SE reduction ( β =-0.10, -0.07, -0.18, -0.13), and insufficient hyperopic reserve ( OR=1.87, 2.22, 1.40, 1.28) (P <0.05). While, preschool children with longer sleep time and daily outdoor activity duration had lower risks of axial growth ( β =-0.11, -0.10 ), SE reduction ( β =0.39, 0.51), and insufficient hyperopia reserve ( OR =0.54, 0.51) in preschool children ( P <0.05). Conclusions The rates of refractive errors and insufficient hyperopia reserve in preschool children in Hefei are relatively low, which are influenced by many factors. Parents, kindergartens and relevant departments should implement early vision monitoring and intervention for preschool children, and cultivate their scientific eye use habits.