ObjectiveThis study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg^-1， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg^-1）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBPβ in gastric mucosa. ResultsCompared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （P<0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.

OBJECTIVE To investigate the improving effect and mechanism of Wenyang huayu formula on cerebral ischemia-reperfusion injury in rats based on nuclear factor-erythroid 2-related factor 2 （Nrf2）/glutathione peroxidase 4 （GPX4） signaling pathway and mitochondrial ferroptosis pathway. METHODS SD rats were randomly divided into sham operation group， model group，Nimodipine tablet group （10.8 mg/kg ）， and Wenyang huayu formula group （28 g/kg）， with 24 rats in each group. Except for the sham operation group， rats in other groups were all subjected to middle cerebral artery occlusion model by Longa thread occlusion method. After successful modeling， rats in each administration group were intragastrically gavaged with corresponding liquid for 7 days or 14 days， while rats in sham operation group and model group were given equal volume of normal saline once a day. At 7 and 14 days after administration， neurological deficit scores of rats were calculated； the ultrastructure of neuronal mitochondria in ischemic brain tissue of rats was observed；the contents of malondialdehyde （MDA）， glutathione （GSH） and Fe 2+ ， as well as the protein and mRNA expression levels of Nrf2， solute carrier family 7 member 11 （SLC7A11） and GPX4 in ischemic brain tissue of rats were detected. RESULTS At 7 and 14 days after administration， compared with the sham operation group， the neuronal mitochondria in ischemic brain tissue of rats in the model group showed typical changes of ferroptosis， and the injury continued to worsen over time； the neurological deficit scores， the contents of MDA and Fe 2+ were significantly increased （ P ＜0.05），while the content of GSH and the protein and mRNA expression levels of Nrf2， SLC7A11 and GPX4 were significantly decreased （ P ＜0.05）. Compared with the model group， the morphology of neuronal mitochondria in ischemic brain tissue of rats in Nimodipine tablet group and Wenyang huayu formula group was gradually improved over time， and the above quantitative indicators were significantly reversed （ P ＜0.05）；moreover， the improvement effect of most indicators in Wenyang huayu formula group was significantly better than that in Nimodipine tablet group （ P ＜0.05）. CONCLUSIONS Wenyang huayu formula can improve cerebral ischemia-reperfusion injury in rats， and its mechanism may be related to activating Nrf2/GPX4 signaling pathway and inhibiting mitochondrial ferroptosis.

By analyzing the current application of multi-modal data in the diagnosis of gastric "inflammation-cancer" transformation， this study explored the feasibility and strategies for constructing a disease-syndrome integrated diagnosis and treatment system. Based on traditional Chinese medicine （TCM） phenomics， we proposed utilizing multi-modal data from literature research， cross-sectional studies， and cohort follow-ups， combined with artificial intelligence technology， to establish a multi-dimensional diagnostic and treatment index system. This approach aims to uncover the complex pathogenesis and transformation patterns of gastric "inflammation-cancer" progression. Additionally， by dynamically collecting TCM four-diagnostic information and modern medical diagnostic information through a long-term follow-up system， we developed three major modules including information extraction， multi-modal phenotypic modeling， and information output， to make it enable real-world clinical data-driven long-term follow-up and treatment of chronic atrophic gastritis. This system can provide technical support for clinical diagnosis， treatment evaluation， and research， while also offering insights and methods for intelligent TCM diagnosis.

BACKGROUND:U937 cells can be used as a cell model for studying the biological characteristics,signaling pathways,and therapeutic targets of acute myeloid leukemia.Although it has been reported that long non-coding RNA KIAA0125 is highly expressed in acute myeloid leukemia,its biological function in U937 cells remains unclear,and its mechanism of action in the occurrence and development of acute myeloid leukemia needs to be further clarified. OBJECTIVE:To investigate the expression level of long non-coding RNA KIAA0125 in peripheral blood of patients with acute myeloid leukemia and its effect on the proliferation and apoptosis of U937 cells. METHODS:RNA-sequencing was used to analyze the bone marrow monocyte samples from acute myeloid leukemia patients,and the differentially expressed gene long non-coding RNA KIAA0125 was screened.The expression of long non-coding RNA KIAA0125 in peripheral blood of patients with acute myeloid leukemia was detected by qRT-PCR.The relationship between long non-coding RNA KIAA0125 mRNA expression and prognosis in bone marrow cells of 173 acute myeloid leukemia patients and 70 healthy people was statistically analyzed by GEPIA database.Subsequently,recombinant lentivirus technology and CRISPR/Cas9-SAM technology were used to construct U937 cell lines with knockdown/overexpression of long non-coding RNA KIAA0125.qRT-PCR was used to detect the knockdown/overexpression efficiency of long non-coding RNA KIAA0125.Next,CCK-8 assay,flow cytometry,and western blot assay were used to detect the effects of knockdown/overexpression of long non-coding RNA KIAA0125 on the proliferation and apoptosis of U937 cells.Finally,western blot assay was used to detect the effect of knockdown/overexpressed long non-coding RNA KIAA0125 on Wnt/β-catenin signaling pathway-related proteins. RESULTS AND CONCLUSION:(1)The results of qRT-PCR showed that long non-coding RNA KIAA0125 was highly expressed in peripheral blood of acute myeloid leukemia patients.The results of GEPIA database showed that long non-coding RNA KIAA0125 was highly expressed in bone marrow cells of acute myeloid leukemia patients,and the high expression group had worse overall survival.(2)The knockdown efficiency of long non-coding RNA KIAA0125 in knockdown group was 70%,and the U937 cells that stably down-regulated long non-coding RNA KIAA0125 expression were successfully constructed.The expression of long non-coding RNA KIAA0125 in overexpression group was four times that of vector group,and stable U937 cells were successfully constructed.(3)Knockdown of long non-coding RNA KIAA0125 inhibited the proliferation of U937 cells and promoted their apoptosis.Overexpression of long non-coding RNA KIAA0125 promoted the proliferation of U937 cells but had no significant effect on the apoptosis of U937 cells.(4)Knockdown of long non-coding RNA KIAA0125 inhibited the activity of Wnt/β-catenin signaling pathway,while overexpression of long non-coding RNA KIAA0125 activated Wnt/β-catenin signaling pathway.These results confirm that long non-coding RNA KIAA0125 is highly expressed in acute myeloid leukemia peripheral blood.Long non-coding RNA KIAA0125 may affect the proliferation and apoptosis of U937 cells by regulating the Wnt/β-catenin signaling pathway,and may be a potential prognostic marker for acute myeloid leukemia.

During orthodontic treatment, clinical monitoring of patients is a crucial factor in determining treatment success. It aids in timely problem detection and resolution, ensuring adherence to the intended treatment plan. In recent years, digital technology has increasingly permeated orthodontic clinical diagnosis and treatment, facilitating clinical decision-making, treatment planning, and follow-up monitoring. This review summarizes recent advancements in digital technology for monitoring orthodontic tooth movement, related complications, and appliance-wearing compliance. It aims to provide insights for researchers and clinicians to enhance the application of digital technology in orthodontics, improve treatment outcomes, and optimize patient experience. The digitization of diagnostic data and the visualization of dental models make chair-side follow-up monitoring more convenient, accurate, and efficient. At the same time, the emergence of remote monitoring technology allows orthodontists to promptly identify oral health issues in patients and take corresponding measures. Furthermore, the multimodal data fusion method offers valuable insights into the monitoring of the root-alveolar relationship. Artificial intelligence technology has made initial strides in automating the identification of orthodontic tooth movement, associated complications, and patient compliance evaluation. Sensors are effective tools for monitoring patient adherence and providing data-driven support for clinical decision-making. The application of digital technology in orthodontic monitoring holds great promise. However, challenges like technical bottlenecks, ethical considerations, and patient acceptance remain.

To introduce the general thinking, guidelines, work objectives and elaboration process of the general technical requirements adopted by volume Ⅳ of the Chinese Pharmacopoeia 2025 Edition, and to summarize and figure out the main characteristics on dosage forms, physico-chemical testing, microbial and biological testing, reference standards and guidelines The newly revised general chapters of pharmacopoeia give full play to the normative and guiding role of the Chinese Pharmacopoeia standard, track the frontier dynamics of international drug regulatory science and the elaboration of monographs, expand the application of state-of-the-art technologies, and steadily promote the harmonization and unification with the ICH guidelines； further enhance the overall capacity of TCM quality control, actively implement the 3 R principles on animal experiments, and practice the concept of environmental-friendly； replace and/or reduce the use of toxic and hazardous reagents, strengthen the requirements of drug safety control This paper aims to provide a full-view perspective for the comprehensive, correct understanding and accurate implementation of general technical requirements included in the Chinese Pharmacopoeia 2025 Edition.

BACKGROUND:Ferroptosis is a mode of programmed cell death distinct from apoptosis,necrosis,and other novel cellular deaths,which occurs mainly due to accumulated lipid peroxidation.Ferroptosis has been shown to be involved in the pathological process following subarachnoid hemorrhage.Baicalein,serving as an adept sequestered of iron,evinces its prowess by quelling lipid peroxidative cascades.Nonetheless,the enigma lingers as to whether baicalein possesses the capacity to ameliorate neuronal ferroptosis,elicited in the wake of early brain injury after subarachnoid hemorrhage. OBJECTIVE:To investigate the effect and mechanism of baicalein on neuronal ferroptosis after subarachnoid hemorrhage. METHODS:Primary neuronal cells were extracted from C57BL/6L fetal mice at 16-17 days of gestation.Hemoglobin was used to stimulate primary neuronal cells to simulate an in vitro subarachnoid hemorrhage model.The viability of primary neuronal cells treated with baicalein at concentrations of 5,15,25,50,and 100 μmol/L for 24 hours was detected by CCK-8 assay to determine the optimal concentration of baicalein.Primary neuronal cells were divided into control group,hemoglobin group,and hemoglobin+baicalein group.The levels of reactive oxygen species and malondialdehyde in cells were detected by kits.The mRNA expressions of ferroptosis-related markers PTGS2,SLC7A11,and glutathione peroxidase 4 were detected by RT-PCR.The primary neuronal cells were further divided into control group,SLC7A11 inhibitor Erastin group,hemoglobin group,hemoglobin+baicalein group,and hemoglobin+baicalein+Erastin group.The expression of the ferroptosis related markers SLC7A11 and glutathione peroxidase 4 was detected by western blot assay. RESULTS AND CONCLUSION:(1)Baicalein(25 μmol/L)was selected as the following experimental concentration.(2)Compared with the hemoglobin group,the level of malondialdehyde and the level of reactive oxygen species were significantly decreased(P<0.05)in the hemoglobin+baicalein group.(3)Compared with the hemoglobin group,the mRNA expression of PTGS2 significantly decreased,and the mRNA expression of SLC7A11 and glutathione peroxidase 4 significantly increased(P<0.000 1)in the hemoglobin+baicalein group.(4)SLC7A11 inhibitor Erastin could reverse the baicalin-improved ferroptosis effect to a certain extent(P<0.05).(5)The results showed that baicalein could alleviate the ferroptosis of neuronal cells after subarachnoid hemorrhage through the SLC7A11/GPX4 pathway.

BackgroundAttention deficit hyperactivity disorder （ADHD） is a neurodevelopmental disorder characterized by age-inappropriate inattention， excessive activities incongruous with setting， and emotional impulsivity. Subthreshold ADHD （sADHD） is clinically defined as the presence of ADHD symptoms that do not meet the full diagnostic criteria for ADHD. Children with sADHD exhibit deficits in executive function， demonstrate more conduct， learning， and anxiety-related problems compared to typically developing children， and show even poorer working memory performance than children diagnosed with ADHD. Currently， there is limited epidemiological research on sADHD in China， with few studies simultaneously investigating the prevalence of both ADHD and sADHD in children. ObjectiveTo investigate the prevalence of ADHD and sADHD among children aged 6–13 years in Chongqing， analyzing their distribution characteristics within this population， with the aim of providing references for developing preventive measures against both ADHD and sADHD. MethodsFrom October to November 2023， a total of 3 398 students in grades 1–6 from six primary schools in Jiangbei District， Chongqing were selected using a stratified cluster random sampling method. The occurrence of ADHD and sADHD was evaluated by using the short version （18-item version） of the Swanson， Nolan， and Pelham IV rating scales （SNAP-IV） and the Chinese vision of Schedule for Affective Disorder and Schizophrenia for School-aged Children-Present and Lifetime Version （K-SADS-PL）. ResultsThe ADHD detection rate among children in Chongqing was 1.90% （95% CI： 0.014–0.024）. Boys showed a significantly higher ADHD detection rate than girls （χ²=7.733， P=0.005）. No statistically significant differences were found in ADHD detection rates across different grades or age groups （χ²=7.347， 12.362， P>0.05）. The sADHD detection rate was 6.32% （95% CI： 0.054–0.072）. Similarly， boys exhibited significantly higher sADHD detection rates than girls （χ²=21.005， P<0.01）. Significant differences emerged across different grades （χ²=20.559， P=0.001）， while no statistically significant difference was observed in age groups （χ²=12.070， P=0.060）. ConclusionThe ADHD detection rates were comparable across all grade levels and age groups from 6–13 years old. Second-grade children demonstrated notably higher sADHD rates compared to other grades， while boys demonstrated higher prevalence rates than girls for both ADHD and sADHD. ［Funded by Science and Health Joint Medical Research Project in Jiangbei District， Chongqing City in the Second Half of 2023 （number， 2023JBKWLH022）］

Objective: To investigate the effects of occlusal alterations on masseter muscle atrophy after the applica⁃tion of excessive orthodontic tension , and the role and mechanism of prophylactic nitrate supplementation in the pre⁃vention and treatment of masseter muscle atrophy. Methods: Eight⁃week⁃old male SD rats were selected. An ortho⁃dontic appliance was placed in the oral cavity of the rats to obtain a rat model of occlusal alterations , and the mas⁃seter muscles were taken at various times after excessive orthodontic force application for relevant tests. Masseter muscle weighing , HE staining , Western blot and immunohistochemistry assays were used to detect the atrophic state of the masseter muscle. Meanwhile , immunofluorescence staining was used to detect the hypoxic status of the mas⁃[ cluster of differentiation 31 (CD31) , vascular endothelial growth factor (VEGF)] . After 28 days of prophylactic nitrate supplementation and application of orthodontic tension , the status of masseter muscle atrophy , tissue hypoxi⁃ growth factor receptor (EGFR) , protein kinase B (AKT ) , extracellular signal⁃regulated kinases 1/2 (ERK1/2) to detect masseter muscle apoptosis. Results : The molar displacement caused by overload traction could lead to masseter muscle atrophy , accompanied by hypoxia in the masseter tissue and decreased expression of angiogenesis⁃related proteins. Preventive nitrate supplementation could prevent masseter muscle atrophy , alleviate tissue hypoxi⁃a , and promote angiogenesis. The anti⁃apoptotic effects of the EGFR⁃AKT/ERK1/2 signaling pathway contributed to the preventive effects of nitrate on masseter muscle atrophy. Conclusion Occlusal alterations brought about by excessive orthodontic tension exertion in rats may lead to masseter muscle atrophy , and prophylactic nitrate supple⁃mentation may resist hypoxia and atrophy of masseter muscle tissues by promoting angiogenesis through the anti⁃ap⁃optotic effects of the EGFR⁃AKT/ERK1/2 pathway.

Objective : To explore the impacts and fundamental mechanisms of the PU. 1 inhibitor DB2313 on the immune function in MRL/lpr mice. Methods: A total of thirty MRL/lpr lupus mice were randomly distributed into three separate groups : the model control group , the PU. 1 inhibitor DB2313 treatment group ( administered at a dose of 17 mg/kg) , and the positive drug control Telitacicept (TACI_Ig) group (administered at a dose of 7. 5 mg/ kg) . Furthermore , a group of ten BALB/c mice were assigned as the normal group. The DB2313 administration group was treated with intraperitoneal injections of the drug on three occasions per week , while the TACI_Ig group received subcutaneous injections every second day; both treatment protocols were maintained for a duration of five weeks. Both the control group and the model group were administered intraperitoneal injections of a volume of saline that was equivalent across groups. After the drug was given , mice were sacrificed by dislocation after orbital vein blood collection. The thymus and spleen were aseptically excised , individually weighed , and subsequently utilized to compute the thymus index and spleen index. The relative distribution of T lymphocyte subsets within the spleen was ascertained through flow cytometry. Serum concentrations of anti_nuclear antibodies ( ANA) and antidouble_stranded DNA antibodies were quantified using an enzyme_linked immunosorbent assay (ELISA) . The levels of inflammatory factors interleukin_6 (IL_6) , tumor necrosis factor_α (TNF_α) , interferon_γ(IFN_γ) were meas ured by CBA method. Hematoxylin and eosin ( HE) staining was employed to examine pathological alterations in the spleen. The expression of PU. 1 and IL_9 in spleen tissue was detected using immunohistochemistry. Additionally , the expression level of PU. 1 protein in the spleen tissue was ascertained through Western blot analysis. Results: The administration of DB2313 significantly ameliorated spleen lesions in MRL/lpr mice and decreased the levels of anti_ds_DNA , ANA , TNF_α , IL_6 , and IFN_γ . It also reduced the proportion of total T cells , TFH cells , Th17 cells , and Th9 cells in the mouse spleen , while increasing the proportion of Treg cells. Furthermore , it lowered the level of PU. 1 protein in the spleen. Immunohistochemistry results demonstrated that DB2313 treatment significantly diminished the expression of PU. 1 and IL_9 in spleen tissue. Conclusion The PU. 1 inhibitor DB2313 can improve spleen lesions in MRL/lpr mice and slow the progression of the disease , and its mechanism is related to the regulation of immune cell functions.