Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

This study investigated a novel coronary knobby scoring balloon through finite element analysis (FEA) and in vitro anti-slippage testing, evaluating its dilation process under various vascular conditions and comparing it with other balloons. The FEA results indicated that in the cases of healthy artery and diseased artery with different stenosis rates, the stress on the vessels caused by the knobby scoring balloon was significantly smaller than that of the scoring balloon, and was close to that of the plain balloon. In vitro anti-slippage testing showed that the slippage distance of a plain balloon was 0.11±0.06 mm, and there was no slippage for knobby scoring balloon under nominal pressure. Knobby scoring balloon can effectively expand calcified lesion while providing anti-slippage function, and has a lower risk of vascular injury.
Finite Element Analysis ; Humans ; Angioplasty, Balloon, Coronary/instrumentation* ; Equipment Design ; Biomechanical Phenomena ; Coronary Vessels

The precise and rapid monitoring of multiple organ dysfunction is crucial in drug discovery. Traditional methods, such as pathological analysis, are often time-consuming and inefficient. Here, we developed a multiplexed near-infrared window two (NIR-II) fluorescent bioimaging method that allows for real-time, rapid, and quantitative assessment of multiple organ dysfunctions. Given that existing probes did not fully meet requirements, we synthesized a range of NIR-II hemicyanine dyes (HDs) with varying absorption and emission wavelengths. By modifying these dyes, we achieved high spatial and temporal resolution imaging of the liver, kidneys, stomach, and intestines. This method was further applied to investigate disorders induced by cisplatin, a drug known to cause gastric emptying issues along with liver and kidney injuries. By monitoring the metabolic rate of the dyes in these organs, we accurately quantified multi-organ dysfunction, which was also confirmed by gold-standard pathological analysis. Additionally, we evaluated the effects of five aristolochic acids (AAs) on multiple organ dysfunction. For the first time, we identified that AA-I and AA-II could cause gastric emptying disorders, which was further validated through transcriptomics analysis. Our study introduces a novel approach for the simultaneous monitoring of multi-organ dysfunction, which may significantly enhance the evaluation of drug side effects.

Computational analysis can accurately detect drug-gene interactions (DGIs) cost-effectively. However, transductive learning models are the hotspot to reveal the promising performance for unknown DGIs (both drugs and genes are present in the training model), without special attention to the unseen DGIs (both drugs and genes are absent in the training model). In view of this, this study, for the first time, proposed an inductive learning-based model for the precise identification of unseen DGIs. In our study, by integrating disease nodes to avoid data sparsity, a multi-relational drug-disease-gene (DDG) graph was constructed to achieve effective fusion of data on DDG intro-relationships and inter-actions. Following the extraction of graph features by utilizing graph embedding algorithms, our next step was the retrieval of the attributes of individual gene and drug nodes. In this way, a hybrid feature characterization was represented by integrating graph features and node attributes. Machine learning (ML) models were built, enabling the fulfillment of transductive predictions of unknown DGIs. To realize inductive learning, this study generated an innovative idea of transforming known node vectors derived from the DDG graph into representations of unseen nodes using node similarities as weights, enabling inductive predictions for the unseen DGIs. Consequently, the final model was superior to existing models, with significant improvement in predicting both external unknown and unseen DGIs. The practical feasibility of our model was further confirmed through case study and molecular docking. In summary, this study establishes an efficient data-driven approach through the proposed modeling, suggesting its value as a promising tool for accelerating drug discovery and repurposing.

ObjectiveTo investigate the therapeutic effect and mechanism of coptisine on chronic atrophic gastritis （CAG） in rats based on the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway. MethodA CAG rat model was induced by multiple factors， including sodium salicylate， N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， and irregular feeding. The successfully modeled rats were randomly divided into the model group， folic acid group， and high- and low-dose coptisine groups. The high- and low-dose coptisine groups were given coptisine （50， 10 mg·kg^-1， respectively）， and the folic acid group was given folic acid at 2 mg·kg^-1 for 60 days. The pathological changes were detected by hematoxylin-eosin （HE） staining. The ultrastructure of gastric mucosal cells was observed by electron microscopy. Serum pepsinogen Ⅰ （PGⅠ）， pepsinogen Ⅱ （PGⅡ）， and PGⅠ/PGⅡ ratio （PGR） were detected by immunoturbidimetry. Serum gastrin-17 （G-17） level was detected by radioimmunoassay. The content of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in serum of rats was detected by enzyme-linked immunosorbent assay （ELSIA）. Western blot analysis was used to detect the expression levels of TGF-β₁， PI3K， phosphorylated-Akt （p-Akt）， mTOR， and phosphatase and tensin homolog deleted on chromosome 10 （PTEN） in gastric mucosa. The mRNA levels of TGF-β₁， PI3K， Akt， mTOR， PTEN， microtubule-associated protein light chain 3Ⅱ （LC3Ⅱ）， and Beclin-1 were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultCompared with the normal group， the model group showed atrophy and reduced number of intrinsic glands in the gastric mucosal tissues， as well as inflammatory cell infiltration. The ultrastructure of gastric mucosal cells in the model group displayed nuclear condensation， reduced and swollen mitochondria， and abnormal structure. The serum levels of G-17， PGⅠ， PGR， and the protein and mRNA levels of PTEN in gastric tissues were significantly lower in the model group （P<0.01）， while serum levels of IL-6， IL-1β， TNF-α， and the protein and mRNA levels of TGF-β₁， PI3K， Akt， and mTOR in gastric tissues were significantly higher （P<0.01）. Compared with the model group， various drug intervention groups showed different degrees of improvement in pathological damage and gastric mucosal cell ultrastructure， significantly increased serum levels of G-17， PGⅠ， and PGR （P<0.05，P<0.01）， and significantly decreased levels of IL-6， IL-1β， and TNF-α （P<0.05，P<0.01）. The high-dose coptisine group significantly downregulated the protein and mRNA levels of TGF-β₁， PI3K， Akt， and mTOR （P<0.05，P<0.01）. ConclusionBerberine has a therapeutic effect on CAG in rats， possibly exerting a protective effect on gastric mucosa by inhibiting inflammation and blocking the PI3K/Akt/mTOR signaling pathway.

177Lu-prostate specific membrane antigen(PSMA)radio-ligand therapy has been approved abroad for advanced prostate cancer and has been in several clinical trials in China.Based on domestic clinical practice and experimental data and referred to international experience and viewpoints,the expert group forms a consensus on the clinical application of 177Lu-PSMA radio-ligand therapy in prostate cancer to guide clinical practice.

Compared to the general population, there is a higher prevalence of epilepsy in individuals with cerebral palsy (CP). Epilepsy serves as an indicator of CP severity and has a significant impact on the early survival and future quality of life of children with CP. Therefore, it is crucial to investigate the shared mechanisms underlying CP and epilepsy. This study aims to summarize the comorbidity of CP and epilepsy from genetic factors, risk factors, and pathophysiological mechanisms, in order to provide a reference for further research.

Objective To establish a nomogram prediction model of hyperuricemia(HUA)onset risk in overweight and obese children and adolescents in order to provide reference for the prevention and treatment of HUA in this population.Methods The clinical data of 1 410 overweight and obese children and adolescents aged 6-17 years old visiting in this hospital from September 2021 to August 2022 were retrospectively analyzed.A total of 987 overweight and obese children and adolescents were randomly extracted according to a ratio of 7:3 to establish the model,and the remaining 423 cases were validated internally.Referring to the definition of high uric acid in"Zhu-futang Practical Pediatrics",the subjects were divided into high uric acid group and non-high uric acid group.The logis-tic regression analysis was used to analyze the influencing factors of HUA in overweight and obese children and adoles-cents.The nomogram model was constructed by using the R language.The area under the receiver operating character-istic(ROC)curve(AUC),decision analysis curve(DIC),clinical impact curve(CIC)and C-index were used to evalu-ate the predictive ability of the model,and the Bootstrap repeated sampling method(taking samples for 1000 times)was used for internal validation of the model.Results The results of multivariate analysis showed that the age(OR=2.324,95％CI:1.155-4.672,P=0.018),gender(OR=0.456,95％CI:0.256-0.810,P=0.007),triglycerides(OR=3.775,95％CI:2.321-6.138,P＜0.001),blood calcium(OR=26.986,95％CI:3.186-228.589,P=0.003)and blood creatinine(OR=1.047,95％CI:1.026-1.070,P＜0.001)were the influen-cing factors of HUA in overweight and obese children and adolescents.AUC of the ROC curve of the model was 0.840,the sensitivity was 0.786,the specificity was 0.762,the Youden index was 0.548,and the C-index was 0.840.The risk probability of DC A was 0.1-0.8,the net benefit rate of both models was＞0,AUC of ROC curve in the internal verification was 0.871.Conclusion The constructed nomogram in this study has a good predictive efficiency for the onset risk of HUA in overweight and obese children and adolescents,and may provide reference for the early diagnosis and treatment of this population.

Objective To apply ultrasound to monitor cardiac function changes after anthracycline exposure in children with acute leukemia,in order to obtain the indicators of early changes in their cardiac function.Methods Children with acute leukemia from 2018 March to December 2020 in the Children's Hospital of Kunming Medical University were enrolled according to the inclusion and exclusion criteria,their routine cardiac ultrasound and tissue Doppler condition were recorded,and the changes in systolic function were evaluated by Tei index including TeiS,TeiRL,TeiM and TeiT.Results The mean values of LVEF in the normal and the experimental group were both above 60%.FS,SV,and EDV were all in the normal range.While common indicant,the index of TDI or Tei was not statistically significant(P>0.05).The levels of TeiM,TeiRL and TieT in the groups that received a total dose of 200 mg/m2 anthracyclines and 250 mg/m2 were significantly different from that before treatment(P<0.05).Conclusion Tei index can be utilized as a sensitive indicator for early changes in left and right heart function after children with acute leukemia are exposed to anthracyclines.