Chronic atrophic gastritis （CAG） is a digestive system disease characterized by the reduction and atrophy of the intrinsic glands of the gastric mucosa. This disease is closely related to risk factors such as Helicobacter pylori （Hp） infection，long-term unhealthy eating habits and lifestyle. As CAG is a key link in the development of gastric cancer，effectively preventing its deterioration is of great significance for the prevention of gastric cancer. At present，Western medicine mainly uses symptomatic treatments such as eradicating Hp，protecting gastric mucosa， and promoting gastrointestinal motility. However， long-term use is prone to drug resistance and cannot reverse limitations such as gland atrophy， making it urgent to explore new intervention strategies. In recent years，with the deepening of CAG mechanism research，the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway，as one of the classic signaling pathways，plays a significant role in the occurrence and development of CAG，while its systematic summary is still blank. Based on the regulatory advantages of "multi-target，multi-pathway，and low toxicity"，traditional Chinese medicine can improve the pathological process of CAG by intervening in key nodes of the PI3K/Akt pathway. In this paper，the research progress of traditional Chinese medicine regulating PI3K/Akt pathway to improve CAG was systematically reviewed for the first time. The expression of PI3K/Akt signaling pathway in CAG was discussed，including the regulation of inflammation and oxidative stress，cell proliferation and apoptosis，and autophagy. The traditional Chinese medicine flavonoids，alkaloids，terpenoids and other compounds that regulate this pathway were summarized. The traditional Chinese medicine compounds mainly include classic famous prescriptions such as Xiaochaihu Tang，Banxia Xiexin Tang，Morodan concentrated pills，Elian granules and other traditional Chinese patent medicines，as well as empirical prescriptions such as modified Leweiyin formula，and Qiling prescription. This study aims to give full play to the advantages of traditional Chinese medicine and lay a solid foundation for the wide application and further development of CAG treatment，and provide new ideas for clinical research and drug research on CAG.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Objective To construct a comprehensive cost management index system for public hospitals.Methods Literature review,policy analysis,and the Delphi expert consultation method were used to establish the index system.Data from a tertiary grade A public hospital in Beijing from 2019 to 2024 were analyzed.Results The response rate for both rounds of expert consultation was 100％,indicating high expert engagement.The average authority level of the experts was 0.905.x2 tests of Kendall's W coefficient for the importance,operability,and sensitivity of the indicators yielded P＜0.001.A comprehensive cost management system comprising 5 dimensions and 13 indicators was established.Conclusion The constructed comprehensive cost management index system for public hospitals is scientifically sound and highly reliable.It enables effective cost control,risk warning,and continuous improvement,laying a solid foundation for the comprehensive advancement of cost management efforts.

Objective To study the mechanism of Kangxian Ruangan Granules in improving mouse liver fibrosis by regulating TGF-β1/Smad signaling pathway.Methods Eight out of 50 SPF grade male C57BL/6J mice were randomly selected as the normal group,and the remaining mice were intraperitoneally injected with 20%CCl4 olive oil solution(2 mL/kg,3 times a week for 4 weeks)to establish the liver fibrosis model.The successfully modeled mice were randomly divided into model group,silibinin group,and Kangxian Ruangan Granules low-,medium-and high-dosage groups using a random number table method,with 8 mice in each group.Each group of Kangxian Ruangan Granules was orally administered at dosages of 1.95,3.90 and 7.80 g/kg;the silibinin group was orally administered at a dosage of 100 mg/kg,while the normal group and model group were given equal volume of physiological saline by gavage,once a day for 8 weeks.The body mass and liver mass of mice were weighed and the liver index was calculated,the contents of serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),hydroxyproline(HYP),hyaluronic acid(HA),type Ⅲ procollagen(PC-Ⅲ),type Ⅳ collagen(ColⅣ)and laminin(LN)were detected by ELISA;liver tissue morphology was observed using HE,Masson and sirius red staining;immunohistochemistry,RT-qPCR and Western blot were used to detect the expressions of type Ⅰ collagen(ColⅠ),α-smooth muscle actin(α-SMA)and TGF-β1/Smad signaling pathway related factors in liver tissue.Results Compared with the normal group,the body mass of the model group mice decreased(P<0.01),while the liver mass and liver index increased(P<0.01);the contents of ALT,AST,HYP,HA,LN,PC-Ⅲ and ColⅣ were increased(P<0.01);the structure of liver lobules was disordered,with diffuse steatosis of liver cells,disordered arrangement of hepatic cords,infiltration of inflammatory cells,and significant fibrosis in the central and portal vein areas of liver lobules;the mRNA expressions of TGF-β1,Smad2 and Smad3 in liver tissue increased(P<0.05,P<0.01),and the protein expressions of ColⅠ,α-SMA,TGF-β1,Smad2,Smad3,p-Smad2 and p-Smad3 increased(P<0.05,P<0.01).Compared with the model group,the body mass of mice in silibinin group and each dosage of Kangxian Ruangan Granules increased(P<0.01),while the liver mass and liver index decreased(P<0.01);the contents of ALT,AST,HYP,HA,LN,PC-Ⅲ and ColⅣ in serum decreased(P<0.01);the hepatic steatosis in mice was reduced,the necrotic area was narrowed,the infiltration of inflammatory cells was reduced,the arrangement of hepatic cords tended to be regular,collagen deposition was reduced,and the structure of liver lobules was partially restored;the mRNA expressions of TGF-β1,Smad2 and Smad3 in liver tissue of silibinin group and Kangxian Ruangan Granules medium-dosage group decreased(P<0.05,P<0.01),while the protein expression of ColⅠ,α-SMA,TGF-β1,Smad2,Smad3,p-Smad2 and p-Smad3 decreased(P<0.05,P<0.01).Conclusion Kangxian Ruangan Granules can reduce the expressions of fibrosis related proteins,inhibit the deposition of extracellular matrix and improve liver fibrosis by inhibiting TGF-β1/Smad signaling pathway.

OBJECTIVE To explore the expression levels of microribonucleic acid-21(miR-21)and helper T cell(Th)1/Th2 cytokines in peripheral blood of the asthma children complicated with respiratory tract infections of vi-ruses and analyze the significance.METHODS A total of 90 asthma children with respiratory tract infections of vi-ruses(the infection group)and 43 asthma children without respiratory tract infections of viruses(the no infection group)who were treated in the 904th Hospital of the Joint Logistics Support Force of The People's Liberation Ar-my of China were enrolled in the study,and the clinical data were collected from the enrolled patients.The distri-bution of viruses from the children of the infection group was analyzed.The levels of peripheral blood miR-21,Th1 cytokines[interferon-γ(IFN-γ),interleukin(IL)-2]and Th2 cytokines[IL-4,IL-5]were compared between the two groups.The children of the infection group were divided into the mild group,the moderate group and the severe group according to the severity of disease.The levels of the above indexes were compared among the chil-dren with the various degree of illness condition.The association of the illness condition with miR-21,IFN-γ,IL-2,IL-4 and IL-5 was analyzed.RESULTS Respiratory syncytial virus was dominant among the respiratory tract vi-ruses in the infection group,accounting for 32.22％.The levels of IFN-γ and IL-2 of the infection group were low-er than those of the no infection group(P＜0.05),the levels of miR-21,IL-4 and IL-5 of the infection group were higher than those of the no infection group(P＜0.05).The levels of IFN-γ and IL-2 of the severe group were lower than those of the mild group and the moderate group(P＜0.05),while the levels of miR-21,IL-4 and IL-5 of the severe group were higher than those of the mild group and the moderate group(P＜0.05);the levels of IFN-γ and IL-2 of the moderate group were lower than those of the mild group(P＜0.05),and the levels of miR-21,IL-4 andIL-5 of the moderate group were higher than those of the mild group(P＜0.05).Spearman correlation analysis showed that the illness condition of the children was positively correlated with miR-21,IL-4 and IL-5(P＜0.05),which was negatively correlated with IFN-γ and IL-2(P＜0.05).CONCLUSIONS The respiratory tract infections of viruses may aggravate the abnormal rise of peripheral blood miR-21 and the imbalance of Th1/Th2.The above indexes are closely associated with the illness condition of the children.

Non-alcoholic fatty liver disease （NAFLD） is a chronic liver disease closely related to metabolism， which is mainly characterized by abnormal lipid deposition in hepatocytes. In recent years， with the increasing prevalence of obesity and metabolic syndrome， NAFLD has become one of the most common chronic diseases in the world. The pathogenesis of NAFLD is complex and varied， involving the cross-regulation of multiple signaling pathways such as glucose-lipid metabolism， oxidative stress， and inflammation. The TLR4 signaling pathway plays a key role in the development and progression of NAFLD， and abnormal activation of this pathway accelerates the deterioration of NAFLD by promoting the release of pro-inflammatory cytokines， inducing oxidative stress， and exacerbating insulin resistance. Studies have shown that traditional Chinese medicine （TCM） can regulate the TLR4 signaling pathway to alleviate the symptoms and pathological features of NAFLD. The present review summarizes the experimental research progress in the TCM regulation of the TLR4 signaling pathway in treating NAFLD in the past 5 years， covering a wide range of TCM active ingredients （such as polysaccharides， terpenoids， alkaloids， flavonoids） and compound prescriptions. The active ingredients and compound prescriptions of TCM can effectively ameliorate lipid metabolism disorders， reduce insulin resistance， regulate intestinal flora， and inhibit inflammation and oxidative stress by regulating the TLR4 signaling pathway via multiple targets and pathways， thus slowing down the progression of NAFLD. Through in-depth analysis of the pathological mechanisms of NAFLD and exploration of the potential of TLR4 signaling pathway as a therapeutic target， we can provide theoretical support for the application of TCM in the treatment of NAFLD， as well as new perspectives and directions for future clinical research and new drug development， thereby promoting the innovation and development of therapeutic strategies for NAFLD.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Background: Both sodium-glucose cotransporters (SGLTs) and Na+/H+ exchangers (NHEs) rely on a favorable Na-electrochemical gradient. Gastrin, through the cholecystokinin B receptor (CCKBR), can induce natriuresis and diuresis by inhibiting renal NHEs activity. The present study aims to unveil the role of renal CCKBR in diabetes through SGLT2-mediated glucose reabsorption. Methods: Renal tubule-specific Cckbr-knockout (CckbrCKO) mice and wild-type (WT) mice were utilized to investigate the effect of renal CCKBR on SGLT2 and systemic glucose homeostasis under normal diet, high-fat diet (HFD), and HFD with a subsequent injection of a low dose of streptozotocin. The regulation of SGLT2 expression by gastrin/CCKBR and the underlying mechanism was explored using human kidney (HK)-2 cells. Results: CCKBR was downregulated in kidneys of diabetic mice. Compared with WT mice, CckbrCKO mice exhibited a greater susceptibility to obesity and diabetes when subjected to HFD. In vitro experiments using HK-2 cells revealed an upregulation of glucose transporters after incubation with high glucose, a response that was significantly attenuated following gastrin intervention. The glucose uptake from the culture medium of cells was altered accordingly. Moreover, gastrin administration effectively mitigated hyperglycemia in WT diabetic mice by inhibition of SGLT2 mediated glucose reabsorption, but this effect was compromised in the absence of CCKBR, as seen in CckbrCKO mice. Mechanistically, gastrin/CCKBR substantially reduced SGLT2 expression in HK-2 cells exposed to high glucose, via modulating Erkuclear factor-kappa B (NF-κB) pathway. Conclusion Our study underscores the crucial role of renal gastrin/CCKBR in SGLT2 regulation and glucose reabsorption, and renal gastrin/CCKBR can be a promising therapeutic target for diabetes.

Objective:To investigate the association between serum levels of transforming growth factor beta-induced protein (TGFBI) and type X alpha1 collagen (COL10A1) in patients with early gastric cancer and the recurrence of cancer after endoscopic submucosal dissection (ESD).Methods:A prospective study was conducted involving 110 patients with early gastric cancer who underwent ESD at the Hanzhong Central Hospital from March 2020 to March 2023. This study used a cross-sectional study design, with patients followed up for 1 year post-ESD to assess recurrence. Patients were categorized into the recurrence group and the non-recurrence group. Upon admission, all patients underwent serum testing for TGFBI and COL10A1, and baseline data were collected. The dose-response relationship between serum levels of TGFBI and COL10A1 and the recurrence of cancer after ESD was analyzed.Results:After 1 year of follow-up, recurrence was observed in 17 out of 110 patients with early gastric cancer who underwent ESD, resulting in a recurrence rate of 15.45%. In the recurrent group, the longest diameter of the tumors [(2.37 ± 0.41) cm] was significantly longer than that in the non-recurrent group [(1.85 ± 0.34) cm]. Additionally, serum levels of TGFBI and COL10A1 in the recurrence group were (27.85 ± 6.27) μg/L and (7.03 ± 1.05) μg/L, respectively, which were significantly higher than those in the non-recurrence group [(19.28 ± 4.15) μg/L, (6.14 ± 0.77) μg/L]. The proportion of patients with clinical stages Ⅱa-b and submucosal infiltration depth was significantly greater in the recurrence group [52.94% (9/17), 70.59% (12/17)] than in the non-recurrence group [24.73% (23/93), 43.01% (40/93) in the non-recurrent group. All observed differences were statistically significant ( t = 5.61, 7.17, 4.12, χ2 = 4.26, 4.38, all P < 0.05). The results of the binary logistic regression analysis showed that the longest tumor diameter, high serum levels of TGFBI and COL10A1 expression were risk factors for recurrence after ESD in patients with early gastric cancer ( OR = 65.341, 1.401, 2.855, all P < 0.05). The results of the receiver operating characteristic curve analysis indicated that the areas under the curve for the predictive value of serum TGFBI and COL10A1, both individually and in combination, for recurrence after ESD were 0.869, 0.800, and 0.954, respectively. A linear dose-response relationship was identified between serum levels of TGFBI and COL10A1 and the risk of cancer recurrence after ESD in patients with early gastric cancer (all P < 0.05). Specifically, when serum TGFBI levels exceeded 22.29 μg/L and COL10A1 levels surpassed 6.95 μg/L, the risk of cancer recurrence increased with higher serum levels of both TGFBI and COL10A1. Conclusions:In patients with early gastric cancer, serum levels of TGFBI and COL10A1 are closely related to cancer recurrence after ESD. The higher the serum levels of TGFBI and COL10A1, the greater the risk of recurrence.