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.

Objective:To develop a remote monitoring system for blood counting and temperature of banked blood in the transfusion department based on 2.4G wireless transmission technique with STM32 single-chip,so as to implement remotely dynamic monitoring for counting and temperature of banked blood in transfusion department.Methods:Based on 2.4G wireless transmission technique with STM32 single-chip,the NRF24L01 wireless transceiver was adopted in this design.STM32 single-chip was used as the processor,and QT50 infrared photoelectric sensor was used to sense the counting for stored blood,and LM35DT temperature sensor was used to collect temperature.The display screen adopted high-brightness digital tube of light emitting diode(LED)of Quanhai(QH)series,so as to achieve accurate data transmission and dynamic monitoring for temperature.Results:The measurement for multiple rooms indoors showed that the distance of wireless transmission can reach 45m without delay,and the counting for banked blood was accurate,and the range of controlling temperature was±0.24℃,which controlled precision was higher than that(±1℃)of national standard.It has ultra-high sensitivity for high and low alarm temperature,which buzzer will alarm when the temperature rises to 7℃or falls to 1℃,and the action time was less than 1s.Conclusion:The developed remote monitoring system for blood counting and temperature of banked blood in transfusion department is flexible in use,and it has stable performance,which can timely prevent the occurrence of blood damage,and greatly reduce the workload of transfusion department.It has a broad application prospect.

Objective:To establish a simple and efficient method for in vitro extraction,culture and identification of brain microvascular endothelial cells(BMECs)of rabbits.Method:The cerebral cortex of 3-week-old rabbits was cut up,sieved and digested with type II collagenase to obtain pure brain microvascular segments for primary culture and identification.Results:The cultured target cells grew in a typical"cobblestone-like"arrangement.Immunohistochemi-cal staining for von Willebrand factor(vWF)related antigen showed that the cytoplasm was presented as brownish red and the expression was positive.Conclusion:The physical sieving method combined with the chemical enzyme diges-tion method can simply and efficiently culture primary rabbit BMECs with strong activity and high purity.

Childhood obesity has become a global public health issue. The incidence rate of non-alcoholic fatty liver disease (NAFLD) in children has rapidly increased with the increase in obesity. Thus, NAFLD has become one of the most common causes of chronic liver disease in children. Currently, there are no officially approved drugs for the treatment of NAFLD in children. Lifestyle changes, including dietary and exercise interventions, are first-line treatment options for NAFLD in children in the absence of effective drugs. This article reviews the latest progress of these years in dietary and exercise interventions in the prevention and treatment of NAFLD in obese children.

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 effect of the antioxidant Tempol on the skin depigmentation of a vitiligo-like mouse model induced by the combination of the endogenous reactive oxygen species (ROS) producer AAPH and tyrosinase-related protein 2 (TRP2) -180 nonapeptide.Methods:A vitiligo-like skin depigmentation model was established by immunizing mice with injections of a TRP2-180 nonapeptide mixture into the foot pads twice and into the tails twice, with the injection interval being 1 week. After the first injection, 12 immune-induced mouse models of vitiligo were randomly divided into 4 groups (3 mice per group) : a model group, an AAPH group, a Tempol group, and a combined treatment group; additionally, 3 untreated mice injected with an ovalbumin (OVA) 257-264 peptide served as a sham control group. Mice in the AAPH group, the Tempol group, and the combined treatment group were subcutaneously injected with AAPH into the tails, intraperitoneally injected with Tempol, and received the above both treatments, respectively, while mice in the model group and the sham control group received phosphate-buffered saline injections into the tail and/or abdomen. Drug interventions were carried out 3 times per week for 3 consecutive weeks. Six weeks after the last immunization, mice were sacrificed. The area of depigmented macules on the tail was measured using a point-counting method, X-gal staining and double immunofluorescence staining were performed to assess the distribution and number of melanocytes, mast cells, and CD8 + T cells in depigmented macules on the tail. HaCaT cells were in vitro co-cultured with AAPH and/or Tempol, and a conventional culture group served as the control. Cellular ROS levels were measured by dichlorofluorescin diacetate labeling and flow cytometry; Western blot analysis was performed to determine the expression of matrix metalloproteinase 9 (MMP9) and stem cell factor (SCF) in cell lysates, and to detect soluble SCF levels in the culture supernatant. Comparisons among multiple groups were conducted using one-way analysis of variance, and multiple comparisons were performed using least significant difference- t test. Results:Depigmented macules were observed on the tails of mice in all groups except the sham control group. The area of depigmented macules was significantly larger in the AAPH group (7.27 ± 0.31 cm 2) than in the model group and combined treatment group (3.53 ± 0.21 cm 2, 4.07 ± 0.40 cm 2; t = 13.48, 11.56, respectively, both P < 0.001), while there was no significant difference between the Tempol group (3.30 ± 0.40 cm 2) and the model group ( P = 0.424). X-gal staining and double immunofluorescence staining showed that the number of melanocytes in the normal skin around the depigmented macules was significantly lower in the AAPH group and the combined treatment group than in the model group ( t = 6.31, 5.16, respectively, both P < 0.001), and no significant difference was observed between the AAPH group and the combined treatment group ( P = 0.516). The numbers of CD8 + T cells and mast cells were significantly higher in the AAPH group than in the model group and the combined treatment group (all P < 0.001). The numbers of the 3 types of cells mentioned above in the Tempol group did not differ from those in the model group (all P > 0.05). The ROS levels in HaCaT cells in the AAPH group were the highest, and significantly higher than those in the control group and the combined treatment group (both P < 0.001). Western blot analysis showed that the MMP9 level in the cell lysates and soluble SCF level in the culture supernatant were significantly higher in the AAPH group than in the control group and the combined treatment group (all P < 0.05) ; no significant difference was observed in the membrane-bound SCF level in cell lysates among the groups ( F = 0.06, P = 0.977) . Conclusion:The antioxidant Tempol could inhibit the formation of skin depigmented macules in vitiligo-like mouse models under AAPH-induced oxidative stress.