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 molecular mechanism by which the Bushen Kaixuan Tongluo prescription exerts a renal protective effect in mice with diabetic kidney disease （DKD） by regulating the cyclic adenosine monophosphate （cAMP） signaling pathway. MethodsThirty specific pathogen-free （SPF） male db/db mice were adaptively fed for three weeks. Mice with a random tail vein blood glucose level ≥ 11.1 mmol·L^-1 and urinary albumin-creatinine ratio （ACR） ≥ 30 mg·g^-1 were considered successfully modeled. The successfully modeled mice were randomly divided into five groups with six mice in each group： the model group， the low-， medium-， and high-dose Bushen Kaixuan Tongluo prescription groups （administered at doses of 7， 14， 28 g·kg^-1·d^-1 respectively）， and the positive drug irbesartan group （administered at a dose of 20 mg·kg^-1·d^-1）. Additionally， six db/m mice were selected as the blank group. Mice in each group were given intragastric administration of the Bushen Kaixuan Tongluo prescription at the corresponding concentrations， irbesartan， or an equal volume of pure water， and the intervention lasted for 12 weeks. During the experiment， the general conditions， body weight changes， and renal function indicators of the mice were dynamically monitored. After the intervention， a blood glucose meter was used to measure the fasting blood glucose （FBG） of the mice. An automatic biochemical analyzer was employed to detect the levels of serum creatinine （SCr）， blood urea nitrogen （BUN）， urinary microalbumin （uALB）， ACR， aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglycerides （TG）， leptin （LEP）， glycosylated serum protein （GSP）， and insulin （INS） in the mice. Renal tissues were collected for hematoxylin-eosin （HE） staining， periodic acid-Schiff （PAS） staining， and Masson's trichrome staining to observe the histopathological changes. Immunohistochemistry （IHC） was used to detect the expressions of protein kinase A （PKA） and cAMP response element-binding protein （CREB） in the mice. Western blot analysis was performed to determine the expression levels of PKA， phosphorylated protein kinase A （p-PKA）， CREB， phosphorylated cAMP response element-binding protein （p-CREB）， and B-cell lymphoma-2 （Bcl-2） proteins in the renal tissues of the mice. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression levels of PKA， CREB， and Bcl-2 in the renal tissues of the mice. ResultsCompared with the blank group， the mice in the model group showed listlessness， decreased activity， and a significant increase in body weight （P<0.01）. Biochemical indicators revealed that the levels of BUN， uALB， ACR， AST， ALT， TC， TG， FBG， LEP， GSP， and INS were significantly increased （P<0.01）， while SCr showed an increasing trend with no statistically significant difference. Compared with the model group， the mice in the Bushen Kaixuan Tongluo prescription intervention groups had improved general conditions and a decreasing trend in body weight. Biochemical indicators showed that the levels of BUN， uALB， ACR， TC， GSP， and INS were significantly decreased （P<0.05）， while SCr， AST， ALT， TG， and LEP showed a decreasing trend with no statistically significant difference. Renal histopathological analysis showed that the model group exhibited typical DKD pathological features such as thickening of the glomerular basement membrane， expansion of the mesangial matrix， and deposition of collagen fibers in the renal tubulointerstitium， and all treatment groups could alleviate the above pathological damages. The IHC results showed that compared with the blank group， the expression levels of p-PKA and p-CREB in the renal tissues of the model group were significantly decreased （P<0.01）. Compared with the model group， the expression level of p-PKA in the medium-dose Bushen Kaixuan Tongluo prescription group was significantly increased （P<0.01）， while the expression level of p-CREB showed an increasing trend with no statistically significant difference. Western blot results showed that compared with the blank group， the expression levels of p-PKA/PKA， p-CREB/CREB， and Bcl-2 in the model group were significantly decreased （P<0.05）. Compared with the model group， the expression levels of these proteins in the medium-dose Bushen Kaixuan Tongluo prescription group were significantly increased （P<0.01）. Real-time PCR results showed that compared with the blank group， the mRNA expressions of PKA， CREB， and Bcl-2 in the model group were significantly down-regulated （P<0.05）. Compared with the model group， the mRNA expressions of these genes in the medium-dose Bushen Kaixuan Tongluo prescription group were significantly up-regulated （P<0.05）. ConclusionThe Bushen Kaixuan Tongluo prescription can improve the liver and kidney functions of db/db mice， correct lipid metabolism disorders and glucose metabolism imbalance. Its renal protective effect is associated with up-regulating the cAMP signaling pathway to improve renal fibrosis and reduce the level of oxidative stress， thereby protecting renal function.

ObjectiveTo investigate the mechanisms by which Bushen Tongluo Jiangzhuo prescription improves renal fibrosis in rats with chronic kidney disease （CKD） through the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway. MethodsSeventy specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a control group （n=15） and a modeling group （n=55）. Rats in the modeling group were administered a 2.5% adenine suspension at a dose of 200 mg·kg^-1·d^-1 by gavage for 4 weeks to establish a CKD model. Successfully modeled rats were randomly divided into a model group， an irbesartan group （20.25 mg·kg^-1·d^-1）， and Bushen Tongluo Jiangzhuo prescription low-， medium-， and high-dose groups （5.82， 11.64， and 23.28 g·kg^-1·d^-1， respectively）， with 10 rats in each group. Each group was administered an equal volume of physiological saline， the corresponding concentration of irbesartan， or Bushen Tongluo Jiangzhuo prescription by gavage for 12 weeks. Body weight and renal function indices were dynamically monitored. Serum creatinine （SCr）， blood urea nitrogen （BUN）， urine albumin-to-creatinine ratio （ACR）， 24-hour urinary total protein （24 hUTP）， aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） levels were measured using an automatic biochemical analyzer. Renal histopathological changes were observed by hematoxylin-eosin （HE） and Masson staining. Immunohistochemistry （IHC） was used to detect the expression of PI3K， Akt， phosphorylated Akt （p-Akt）， and mTOR in renal tissues. Western blot was performed to assess the protein expression of PI3K， p-Akt， Akt， phosphorylated mTOR （p-mTOR）， and mTOR in renal tissues. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to determine the mRNA expression levels of PI3K， Akt， and mTOR in renal tissues. ResultsCompared with the model group， rats in the irbesartan group and the low-， medium-， and high-dose Bushen Tongluo Jiangzhuo prescription groups showed significantly decreased levels of SCr， BUN， ACR， 24 hUTP， IL-1β， IL-6， and TNF-α （P<0.01）. AST levels were significantly increased （P<0.01）， while no significant difference was observed in ALT levels. Histopathological examination revealed that， compared with the model group， renal tubular epithelial cell edema and necrosis and Bowman's capsule dilation were alleviated， inflammatory cell infiltration was reduced， and interstitial and glomerular fibrosis was markedly improved in all treatment groups， with the most pronounced effect observed in the high-dose Bushen Tongluo Jiangzhuo prescription group. Real-time PCR results showed that mRNA expression levels of PI3K， Akt， and mTOR were significantly downregulated in the high-dose group （P<0.01）. IHC results demonstrated that PI3K and p-Akt expression levels in renal tissues were significantly decreased in the high-dose group （P<0.01）. Western blot analysis further confirmed that the expression levels of PI3K， p-Akt/Akt， and p-mTOR/mTOR were significantly reduced in the high-dose group （P<0.01）. ConclusionBushen Tongluo Jiangzhuo prescription improves renal function indices in CKD rats， reduces collagen deposition in renal tissues， and decreases serum inflammatory factor levels. Its protective effect on renal function may be achieved by activating autophagy through downregulation of the PI3K/Akt/mTOR signaling pathway， thereby alleviating renal fibrosis.

ObjectiveTo develop and validate a nomogram for predicting the risk of concurrent cognitive impairment in older adults with heart disease. MethodsSelf-reported data from 2 673 respondents in the 2020 China Health and Retirement Longitudinal Study were analyzed. The participants were randomly divided into a training set (n = 1 871) and a validation set (n = 802). Heart disease status was determined using a self-report questionnaire. Logistic regression analysis was performed to identify predictors, and a nomogram for predicting the risk of concurrent cognitive impairment in older adults with heart disease was developed using R software. Bootstrap resampling was used for internal validation, and model performance was further evaluated in the randomly split validation set. The predictive performance of the model was assessed using the area under the receiver operating characteristic curve (AUC) and calibration curves.. ResultsA total of 2 673 older adults with heart disease were included, out of whom 315 participants in the training set had cognitive impairment. Lasso regression analysis identified age, education level, place of residence, instrumental activities of daily living and depression as predictors of concurrent cognitive impairment. A prediction model incorporating these five variables was constructed. The AUC were 0.827 (95%CI 0.804 to 0.850) in the training set and 0.847 (95%CI 0.812 to 0.882) in the validation set. The Hosmer-Lemeshow test yielded P = 0.154 and P = 0.716 in the training and validation sets, respectively. Calibration curves showed good agreement between predicted and observed probabilities. Decision curve analysis indicated that the model provided favorable net benefit and predictive performance. ConclusionThe nomogram may provide a useful reference for risk screening and early intervention for cognitive impairment in older adults with heart disease.

ObjectiveTo investigate the mechanism by which Xianglian Huazhuo prescription （XLHZ） ameliorates chronic atrophic gastritis （CAG） through regulating glycolysis via the microRNA-34b-5p （miR-34b-5p）/6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 1 （PFKFB1） signaling pathway. MethodsBioinformatic screening was performed to identify the target genes of miR-34b-5p. In the animal experiments， a mouse model of CAG was established through a combination of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， ranitidine， and irregular feeding. The mice were randomized into the following groups： normal， model， Morodan group （2 g·kg^-1）， and high-， medium-， and low-dose XLHZ groups（7.2，3.8，1.9 g·kg^-1）. In the cell experiments， GES-1 cells were treated with MNNG for the modeling of CAG and grouped as follows： GES-1， MNNG+GES-1， MNNG+GES-1+XLHZ（10%）， MNNG+GES-1+miR-34b-5p mimics， MNNG+GES-1+miR-34b-5p inhibitor， MNNG+GES-1+PFKFB1 inhibitor， and MNNG+GES-1+PFKFB1 mimics+XLHZ（10%）. The general conditions of mice were observed. Real-time PCR was adopted to measure the expression levels of miRNA-34b-5p and PFKFB1 mRNA in the gastric mucosa of mice in each group. Dual luciferase reporter gene was used to verify the targeting interaction between miR-34b-5p and PFKFB1 in GES-1 cells exposed to MNNG. The cell-counting kit-8 （CCK-8） was used to screen the drug-containing serum concentration. Real-time PCR was employed to verify the transfection efficiency. Fluorescent probes were used to detect the expression and nuclear translocation of hypoxia-inducible factor-1α （HIF-1α） in each group of cells. The protein levels of HIF-1α， hexokinase 2 （HK2）， PFKFB1， phosphofructokinase 1 （PFK1）， and lactate dehydrogenase （LDHA） in the gastric mucosa of mice were determined by Western blot. The levels of glucose consumption and lactate in the serum and cells were measured by biochemical methods. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the content of adenosine triphosphate （ATP） in the gastric mucosa tissue and cells. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited symptoms including mental fatigue， lethargy， sparse and dull fur， a tendency to curl up， sluggish responses， reduced food and water intake， and slow body weight gain. In addition， the model group showed decreased expression of miRNA-34b-5p （P<0.01）， increased mRNA level of PFKFB1 （P<0.01）， upregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.01）， and increased glucose consumption， lactate content， and ATP content （P<0.01）. Compared with the model group， the XLHZ group and Morodan group showed improved mental state， gradually improved fur， increased activity， food and water intake， and body weight. HE showed that each treatment group exhibited well arranged and increased gastric mucosal glands， reduced inflammatory cells， and recovered gastric pits. Transmission electron microscopy showed that the size of mitochondria in each treatment group returned to normal， with no obvious irregular shape， complete and clear cristae， and uniform matrix. Furthermore， each treatment group showed increased expression of miRNA-34b-5p （P<0.05）， reduced mRNA level of PFKFB1 （P<0.05）， downregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.05）， and decreased glucose consumption， lactic acid， and ATP （P<0.05）. The cell experiments showed that the expression and nuclear translocation of HIF-1α were reduced in all groups after treatment （P<0.05）. The cell transfection efficiency was satisfactory （P<0.05）. miR-34b-5p exhibited an effect comparable to that of XLHZ， effectively inhibiting glycolysis， whereas PFKFB1 promoted glycolysis and reversed the protective effect of XLHZ in CAG mice （P<0.05）. ConclusionXLHZ could regulate the miR-34b-5p/PFKFB1 axis to inhibit glycolysis， thereby ameliorating MNNG-induced gastric mucosal atrophy.

ObjectiveTo investigate the mechanism by which Xianglian Huazhuo prescription （XLHZ） ameliorates chronic atrophic gastritis （CAG） through regulating glycolysis via the microRNA-34b-5p （miR-34b-5p）/6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 1 （PFKFB1） signaling pathway. MethodsBioinformatic screening was performed to identify the target genes of miR-34b-5p. In the animal experiments， a mouse model of CAG was established through a combination of N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， ranitidine， and irregular feeding. The mice were randomized into the following groups： normal， model， Morodan group （2 g·kg^-1）， and high-， medium-， and low-dose XLHZ groups（7.2，3.8，1.9 g·kg^-1）. In the cell experiments， GES-1 cells were treated with MNNG for the modeling of CAG and grouped as follows： GES-1， MNNG+GES-1， MNNG+GES-1+XLHZ（10%）， MNNG+GES-1+miR-34b-5p mimics， MNNG+GES-1+miR-34b-5p inhibitor， MNNG+GES-1+PFKFB1 inhibitor， and MNNG+GES-1+PFKFB1 mimics+XLHZ（10%）. The general conditions of mice were observed. Real-time PCR was adopted to measure the expression levels of miRNA-34b-5p and PFKFB1 mRNA in the gastric mucosa of mice in each group. Dual luciferase reporter gene was used to verify the targeting interaction between miR-34b-5p and PFKFB1 in GES-1 cells exposed to MNNG. The cell-counting kit-8 （CCK-8） was used to screen the drug-containing serum concentration. Real-time PCR was employed to verify the transfection efficiency. Fluorescent probes were used to detect the expression and nuclear translocation of hypoxia-inducible factor-1α （HIF-1α） in each group of cells. The protein levels of HIF-1α， hexokinase 2 （HK2）， PFKFB1， phosphofructokinase 1 （PFK1）， and lactate dehydrogenase （LDHA） in the gastric mucosa of mice were determined by Western blot. The levels of glucose consumption and lactate in the serum and cells were measured by biochemical methods. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the content of adenosine triphosphate （ATP） in the gastric mucosa tissue and cells. ResultsThe animal experiments showed that compared with the normal group， the model group exhibited symptoms including mental fatigue， lethargy， sparse and dull fur， a tendency to curl up， sluggish responses， reduced food and water intake， and slow body weight gain. In addition， the model group showed decreased expression of miRNA-34b-5p （P<0.01）， increased mRNA level of PFKFB1 （P<0.01）， upregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.01）， and increased glucose consumption， lactate content， and ATP content （P<0.01）. Compared with the model group， the XLHZ group and Morodan group showed improved mental state， gradually improved fur， increased activity， food and water intake， and body weight. HE showed that each treatment group exhibited well arranged and increased gastric mucosal glands， reduced inflammatory cells， and recovered gastric pits. Transmission electron microscopy showed that the size of mitochondria in each treatment group returned to normal， with no obvious irregular shape， complete and clear cristae， and uniform matrix. Furthermore， each treatment group showed increased expression of miRNA-34b-5p （P<0.05）， reduced mRNA level of PFKFB1 （P<0.05）， downregulated protein levels of HIF-1α， HK2， PFKFB1， PFK1， and LDHA （P<0.05）， and decreased glucose consumption， lactic acid， and ATP （P<0.05）. The cell experiments showed that the expression and nuclear translocation of HIF-1α were reduced in all groups after treatment （P<0.05）. The cell transfection efficiency was satisfactory （P<0.05）. miR-34b-5p exhibited an effect comparable to that of XLHZ， effectively inhibiting glycolysis， whereas PFKFB1 promoted glycolysis and reversed the protective effect of XLHZ in CAG mice （P<0.05）. ConclusionXLHZ could regulate the miR-34b-5p/PFKFB1 axis to inhibit glycolysis， thereby ameliorating MNNG-induced gastric mucosal atrophy.

OBJECTIVE To investigate the current status of infection control departments setting,allocation of in-fection control professionals and their position competence in the secondary,tertiary traditional Chinese medi-cine institutions of Beijing.METHODS The questionnaire survey was conducted for all of the secondary and tertiary traditional Chinese medicine institutions in Beijing by Beijing Traditional Chinese Medicine Hospital Infection Man-agement Quality Control Center from Feb.17,2023 to Apr.11,2023.The content of the survey involved the in-formation of the hospitals,setting information of infection control departments and allocation of infection control professionals.RESULTS Totally 59 traditional Chines medicine medical institutions were involved in the survey,35(59.32％)were tertiary hospitals.The median of opened beds was 331(155,479)in the first quarter of 2023.The median of equipped infection control professionals was 4(3,5).The number of infection control professional e-quipped in 67.80％of the medical institutions conformed to requirements of"Notice regarding to further strength-en the management of infection control professionals allocation in medical institutions"released by The Joint Pre-vention and Control Mechanism of the State Council for the Response to the Novel Coronavirus Pneumonia Epi-demic in Aug.2021,with the ratio of infection control professionals to beds 1∶94.20.The principals in charge of the infection control department who had the qualifications for senior professional and technical position and en-gaged in infection control for more than 5 years accounted for 20.00％.Among the infection control professionals,nurses accounted for 49.17％,doctors 41.67％,other professionals 9.17％.CONCLUSIONS There is relatively adequate quantity of the infection control professional equipped in the secondary and tertia-ry medical institutions of Beijing,however,the principals in charge of the infection control department who had the qualifications for senior professional and technical position and engaged in infection control for more than 5 years are very scarce.It is necessary to further optimize the structure of the infection control professionals.

Objective To explore the mechanism of total saponin from Panax japonicus(TSPJ)in alleviating neuroinflammation in experimental autoimmune encephalomyelitis(EAE)based on the activation of microglia mediated by MAPK signaling pathway.Methods In vivo experiments,mice were divided into normal group,model group and TSPJ low-and high-dosage groups.EAE mouse model was induced by myelin oligodendrocyte glycoprotein polypeptide.Each medication group was gavaged with corresponding drug solution once a day for 28 days.The number of Iba-1-positive cells was assessed using immunofluorescence,the protein expressions of tumor necrosis factor-α(TNF-α),interleukin(IL)-6,IL-1β and MAPK signaling pathway related factors were detected by Western blot.In vitro experiments,murine microglia BV2 were divided into normal group,model group and TSPJ low-and high-dosage groups.LPS+IFN-γ was used to induce M1 polarization of BV2 cells,medication groups were given TSPJ intervention,the content of nitric oxide(NO)in cell supernatant,the expression of M1 microglia markers and MAPK signaling pathway related factors were detected,and ERK and JNK signaling pathway inhibitors were further used to clarify the molecular mechanism of TSPJ antagonizing neuroinflammation.Results The results of in vivo experiments showed that compared with the normal group,the cell body and number of microglia in cerebral cortex of the model group mice increased significantly(P<0.01),and the protein expressions of TNF-α,IL-6,IL-1β,p-p38/p38,p-JNK/JNK,p-ERK1/2/ERK1/2 significantly increased(P<0.05,P<0.01);compared with the model group,the number of microglia in cerebral cortex of TSPJ low-and high-dosage groups significantly decreased(P<0.01),the expressions of TNF-α,IL-6,p-p38/p38,p-JNK/JNK,p-ERK1/2/ERK1/2 protein significantly decreased(P<0.05,P<0.01),and the expression of IL-1β protein in TSPJ high-dosage group significantly decreased(P<0.05).The results of in vitro experiments showed that compared with the normal group,the content of NO in cell supernatant of the model group significantly increased(P<0.01),the protein expressions of CD16,CD86,p-p38/p38,p-JNK/JNK,p-ERK1/2/ERK1/2 significantly increased(P<0.01);compared with the model group,the content of NO in cell supernatant of TSPJ low-and high-dosage groups significantly decreased(P<0.01),and the protein expressions of CD16,CD86,p-p38/p38,p-JNK/JNK,p-ERK1/2/ERK1/2 significantly decreased(P<0.05,P<0.01).TSPJ combined with ERK and JNK pathway inhibitors could further inhibit the expressions of TNF-α and IL-6,but there was no significant difference compared with inhibitors alone.Conclusion TSPJ can inhibit the activation of microglia by regulating MAPK signaling pathway,thereby reducing EAE induced central nervous inflammation.

Objective To explore the pathological features of bronchiolar adenoma(BA)and its specific high-resolution computed tomography(HRCT)signs,and to differentiate BA from minimally invasive adenocarcinoma(MIA)using a non-invasive preoperative method.Methods A total of 80 patients with BA and 130 patients with MIA were retrospectively selected,and the clinical information and HRCT features were compared.All cases were divided into development set and test set at a 7︰3 ratio.Logistic regression analysis was used to screen the independent predictors of MIA and construct a model.Results There were significant differences in age,lobe distribution,density,vacuole sign,tumor-related vessels number(TVN),and distance to pleura(DTP)between BA and MIA patients(P<0.05).Age,density,TVN,DTP and long diameter were identified as independent predictors of MIA.A model was constructed,with area under the curve(AUC)of 0.887 and 0.884 in the development and test sets,respectively.Conclusion The model based on HRCT morphological features of BA and MIA demonstrates superior diagnostic performance compared to individual CT morphological features.