To understand the epidemiological and clinical features of patients with non-tuberculous mycobacteria(NTM)lung disease in a hospital for infectious diseases in Xinjiang,and to provide basis for prevention and control of NTM in Xinjiang.The strain distribution,epidemiological features and clinical features of 78 patients with NTM lung disease in the Sixth People′s Hospital of Xinji-ang Uygur Autonomous Region were analysed from June 2021 to June 2024,and a comparative analysis of the clinical features of 156 patients with pulmonary tuberculosis in this hospital during the same period was performed.Among 78 patients with NTM lung disease,the bacteria identified by molecular biology accounted for the top three cases:24 cases of Mycobacterium avium intracellulare complex,16 cases of Mycobacterium Kansaii and 11 cases of Mycobacterium Gordonae.There was no statistically significant difference in gender(χ2=0.009),age(χ2=2.670),smoking history(χ2=0.064),and BMI(χ2=0.896)between the NTM lung disease group and the pulmonary tuberculosis group(P>0.05).However,there were statistically significant differences in the combined bronchiectasis(χ2=19.068),immune-related indicators CD4(Z=-3.498)and CD3(Z=-3.187),and chest CT cavities on imaging(χ2=9.308)be-tween the two groups(P<0.05).There was no statistically significant difference in clinical symptoms such as cough(χ2=0.188)and expectoration(χ2=0.044)between the two groups(P>0.05).The common underlying diseases of NTM lung disease were diabetes mellitus(23.08%),hypertension(21.79%),bronchiectasis(20.51%)and others.The common clinical symptoms of NTM lung disease include cough,sputum,fatigue,poor appetite and others.The common manifestations of chest CT in NTM lung disease were Patchy cord shadows(62.82%),nodule(51.28%),pleural thickening(46.15%),calcification(41.03%)and others.Multivariate Logistic regression analysis showed that bronchiectasis(OR=8.019)is risk factor for NTM lung disease.The dominant strains of NTM in this study were My-cobacterium avium intracellulare complex,Mycobacterium kansasii and Mycobacterium Gordonae.NTM lung disease and pulmonarytuber-culosis have similar clinical manifestations and are difficult to distinguish,especially for patients with bronchiectasis,it is necessary to actively investigate NTM lung disease,provide basis for early diagnosis and treatment of NTM lung disease,and gradually form a system-atic and standardized NTM lung disease diagnosis and treatment system according to local conditions.

Objective:To establish a stable rat model of sequelae of pelvic inflammatory disease(SPID)with clinical characteristics,and to provide a reliable experimental model for the study of the pharmcological effect and mechanism of SPID.Methods:Twenty-four 7-week-old SD rats were divided into sham operation group,model-A(108 cfu/mL mixed bacterial solution,0.2 mL),model-B(109 cfu/mL mixed bacterial solution 0.2 mL),and model-C(108 cfu/mL E.coli 0.2 mL).The weight of the rat's uterine was weighed and the uterine index was calculated.The automatic hematology analyzer was used to detect the blood routine;hematoxylin-eosin staining(HE)and masson staining were used to detect uterine pathlogical changes in rats.Enzyme-linked immunosorbent assay(ELISA)was used to detect interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in rat uterine tissue homogenates.Western blot was used to detect the expression of proteins related to NF-κB signaling pathway.Results:Compared with the sham operation group,the uterine index of model-A,model-B,and model-C were significantly increased(P＜0.05,P＜0.01).The levels of WBC and NE in the model-A increased significantly(P＜0.01).The level of LY in model-B decreased significantly(P＜0.01).The levels of IL-1β,TNF-α in model-A,model-B,and model-C were significantly increased(P＜0.01).The levels of IL-6 in model-A and model-B were significantly increased(P＜0.05,P＜0.01).The collagen volume fraction of model-A and model-B were significantly increased(P＜0.01).Mechanism study indicates that the expression levels of p-IKKβ/IKKβ,p-IκBα/IκBα and p-p65/p65 in model-A were significantly increased(P＜0.01),and the expression levels of IκBα/β-actin were significantly decreased(P＜0.01).The expression level of p-IKKβ/IKKβ in model-B was significantly increased(P＜0.01).Conclusions:A stable rat model of SPID that conforms to clinical characteristics can be successfully constructed by combining 0.2 mL of mixed bacterial solution with a concentration of 108 cfu/mL and mechanical injury.This modeling method intervened in the expression of the NF-κB inflammatory signaling pathway.

Aim Mouse model of myocardial hypertro-phy was established via intraperitoneal injection of iso-proterenol(ISO)in mice.This approach allows for an in-depth investigation into the pharmacological effects and mechanisms of action of emodin,offering novel in-sights and directions for the improvement of myocardial hypertrophy.Methods The mice were randomly di-vided into the following groups:control group(CON),emodin group(EMO),MAPK activator control group(EMO+Ani),model group(ISO),treatment group(ISO+EMO),and activator intervention group(ISO+EMO+Ani).After treatment with emodin and inter-vention with MAPK activator,the heart weight ratio and cardiac size of each group were observed.Hematoxy-lin-eosin(HE)staining was used to observe the patho-logical changes in cardiac tissue,and kits were utilized to measure the levels of GSH,LDH,and MDA in the serum.Western blot was employed to detect the protein expression levels of inflammatory and oxidative factors,as well as p-p38,p-ERK,p38,and ERK in cardiac tis-sue.Results Emodin can significantly inhibit the production of myocardial inflammatory and oxidative factors induced by ISO,thereby effectively alleviating the degree of myocardial hypertrophy and fibrosis.Af-ter the p38/ERK signaling pathway was specifically ac-tivated by farnesol,the improvement effect of emodin on myocardial hypertrophy was weakened.Further comparison revealed that,compared with the myocardi-al hypertrophy pathological model group,the pathologi-cal protein expression levels in the farnesol-treated group showed no significant difference,and were even higher in some indicators.Conclusion Emodin can effectively inhibit the release of inflammatory factors and improve the state of oxidative stress by modulating the p38/ERK signaling pathway,thereby exerting an ameliorative effect on myocardial hypertrophy.

Objective:To explore the construction of an evaluation model for aortic root anatomy and calcium burden in patients with bicuspid aortic valve (BAV) stenosis before transcatheter aortic valve replacement (TAVR) based on deep learning (DL) algorithms.Methods:A retrospective collection of 362 BAV stenosis patients who underwent TAVR from September 2023 to May 2024 was performed. All patients underwent cardiac CT angiography. The patients were divided into training group ( n=104), internal validation group ( n=206), and external validation group ( n=52). A DL model was trained on the training dataset to assess aortic root anatomy and calcification burden. The evaluation included the segmentation accuracy of the algorithm, the measurement performance of key anatomical structures (i.e., valve leaflets and type-1 and type-2 fusion raphe), and calcification burden, as well as the measurement efficiency. Overall segmentation performance was assessed using the average Dice coefficient (ADC). The fine-scale segmentation quality was validated by the 95th-percentile Hausdorff distance (HD-95) and the average symmetric surface distance (ASSD). The consistency of the measurement results was assessed using the Pearson correlation coefficient and the intraclass correlation coefficient ( ICC) with a two-way mixed model for absolute agreement. In addition, the total time and total mouse movement distance required for manual assessment versus the DL model on the validation datasets were recorded and compared. Results:The algorithm demonstrated excellent segmentation performance on aortic root anatomical targets, achieving outstanding consistency within both internal and external validation datasets (0.955

OBJECTIVE:To systematically evaluate the clinical effectiveness of rehabilitation robots in treating lower limb motor dysfunction in patients with cerebral palsy,and to compare the differences in therapeutic effects among different robots.METHODS:PubMed,Web of Science,Embase,Cochrane Library,CNKI,CBM,VIP and WanFang databases were searched to collect randomized controlled trials on rehabilitation robotics for the treatment of motor dysfunction in patients with cerebral palsy,published from database inception to April 10,2024.The main outcome indicators included muscle strength,muscle tension,balance function,step speed,step frequency,step length,walking endurance,lower limb motor function,and activities of daily living.The above indicators were coded according to the International Classification of Functioning,Disability and Health.Meta-analysis was performed to evaluate the clinical efficacy and compare the therapeutic efficacy of different rehabilitation robots.Literature search and screening were performed by two researchers,and the quality of the included literature was evaluated using the Cochrane 5.1.0 risk of bias assessment tool.Meta-analysis was performed using RevMan 5.4 software and Stata 16.0 software.RESULTS:(1)Fifteen articles were finally included,involving 512 patients with 260 in the experimental group and 252 in the control group.(2)The Meta-analysis results showed that rehabilitation robots could improve body structure and function[standardized mean difference=0.41,95%confidence interval(CI):0.24-0.58,P<0.05],activities(standardized mean difference=0.53,95%CI:0.41-0.65,P<0.05)and participation ability(mean difference=7.86,95%CI:1.54-14.18,P<0.05).In particular,the rehabilitation robot improved lower limb muscle strength,balance function,step speed,walking endurance,lower limb gross motor function,and activities of daily living in patients with cerebral palsy,but showed insignificant effects on step frequency,step length,and muscle tension.(3)The network Meta-analysis results showed that:step speed:Innowalkpro>Gait Trainer>Lokomat>3DCalt;6-minute walk test score:Gait Trainer>Lokomat>Lokohelp>Innowalkro;Gross Motor Function Measure-88D score:Lokohelp>Lokomat>KidGo>Innowalkpro>3DCalt;Gross Motor Function Measure-88E score:Lokomat>Lokohelp>KidGo>3DCalt>Innowalkpro.CONCLUSION:Based on the International Classification of Functioning,Disability,and Health,rehabilitation robot training can improve the lower limb motor function and activities of daily living in patients with cerebral palsy.The Innowalkpro robot was more effective in improving step speed;the Gait trainer robot was more effective in improving 6-minute walk test scores;the Lokohelp robot was more effective in improving Gross Motor Function Measure-88D zone scores;and the Lokomat robot was more effective in improving Gross Motor Function Measure-88E zone scores.

Objective To explore the effects of dodecanoylcarnitine(DA)and myristoleic acid(MA)on the function of mouse alveolar epithelial cell line MLE-12 and their underlying mechanisms.Methods An inflammatory model was established by stimulating MLE-12 cells with IL-4.The expression levels of DA,MA,and sphingosine-1-phosphate(S1P)in the cell supernatant were detected by ELISA.MLE-12 cells were separately intervened with DA and MA.RT-PCR and flow cytometry were used to detect the expression changes of inflammatory factors IL-6 and tumor necrosis factor-α(TNF-α)and the level of intracellular reactive oxygen species(ROS).Additionally,Western blot was performed to detect the expression of key proteins such as p38 mitogen-activated protein kinase(p-38 MAPK)and src homology 2 domain-containing phosphatase 1(SHP-1).To explore the role of S1PR2 in the effects of DA and MA,MLE-12 cells were pretreated with the S1PR2 inhibitor JTE-013,and the above experiments were repeated.Results IL-4 stimulation significantly upregulated the levels of DA,MA,and S1P in MLE-12 cells(P<0.05).DA/MA treatment groups exhibited significantly increased expression of IL-6 and TNF-α compared with the control group(P<0.05),along with elevated ROS levels(P<0.05).Western blot analysis revealed that DA/MA promoted SHP-1 dephosphorylation and phosphorylated p38 MAPK activation in MLE-12 cells.Notably,JTE-013 pre-treatment completely reversed these effects(P<0.05).Conclusion Asthma-related metabolites DA and MA exacerbate the inflammatory and oxidative stress responses of MLE-12 cells by activating the S1PR2 receptor,promoting the dephosphorylation of SHP-1 and the activation of the p-p38 MAPK pathway.This study reveals the core regulatory role of S1PR2 in this pathway as well.

Objective:To establish a stable rat model of sequelae of pelvic inflammatory disease(SPID)with clinical characteristics,and to provide a reliable experimental model for the study of the pharmcological effect and mechanism of SPID.Methods:Twenty-four 7-week-old SD rats were divided into sham operation group,model-A(108 cfu/mL mixed bacterial solution,0.2 mL),model-B(109 cfu/mL mixed bacterial solution 0.2 mL),and model-C(108 cfu/mL E.coli 0.2 mL).The weight of the rat's uterine was weighed and the uterine index was calculated.The automatic hematology analyzer was used to detect the blood routine;hematoxylin-eosin staining(HE)and masson staining were used to detect uterine pathlogical changes in rats.Enzyme-linked immunosorbent assay(ELISA)was used to detect interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)in rat uterine tissue homogenates.Western blot was used to detect the expression of proteins related to NF-κB signaling pathway.Results:Compared with the sham operation group,the uterine index of model-A,model-B,and model-C were significantly increased(P＜0.05,P＜0.01).The levels of WBC and NE in the model-A increased significantly(P＜0.01).The level of LY in model-B decreased significantly(P＜0.01).The levels of IL-1β,TNF-α in model-A,model-B,and model-C were significantly increased(P＜0.01).The levels of IL-6 in model-A and model-B were significantly increased(P＜0.05,P＜0.01).The collagen volume fraction of model-A and model-B were significantly increased(P＜0.01).Mechanism study indicates that the expression levels of p-IKKβ/IKKβ,p-IκBα/IκBα and p-p65/p65 in model-A were significantly increased(P＜0.01),and the expression levels of IκBα/β-actin were significantly decreased(P＜0.01).The expression level of p-IKKβ/IKKβ in model-B was significantly increased(P＜0.01).Conclusions:A stable rat model of SPID that conforms to clinical characteristics can be successfully constructed by combining 0.2 mL of mixed bacterial solution with a concentration of 108 cfu/mL and mechanical injury.This modeling method intervened in the expression of the NF-κB inflammatory signaling pathway.

Aim Mouse model of myocardial hypertro-phy was established via intraperitoneal injection of iso-proterenol(ISO)in mice.This approach allows for an in-depth investigation into the pharmacological effects and mechanisms of action of emodin,offering novel in-sights and directions for the improvement of myocardial hypertrophy.Methods The mice were randomly di-vided into the following groups:control group(CON),emodin group(EMO),MAPK activator control group(EMO+Ani),model group(ISO),treatment group(ISO+EMO),and activator intervention group(ISO+EMO+Ani).After treatment with emodin and inter-vention with MAPK activator,the heart weight ratio and cardiac size of each group were observed.Hematoxy-lin-eosin(HE)staining was used to observe the patho-logical changes in cardiac tissue,and kits were utilized to measure the levels of GSH,LDH,and MDA in the serum.Western blot was employed to detect the protein expression levels of inflammatory and oxidative factors,as well as p-p38,p-ERK,p38,and ERK in cardiac tis-sue.Results Emodin can significantly inhibit the production of myocardial inflammatory and oxidative factors induced by ISO,thereby effectively alleviating the degree of myocardial hypertrophy and fibrosis.Af-ter the p38/ERK signaling pathway was specifically ac-tivated by farnesol,the improvement effect of emodin on myocardial hypertrophy was weakened.Further comparison revealed that,compared with the myocardi-al hypertrophy pathological model group,the pathologi-cal protein expression levels in the farnesol-treated group showed no significant difference,and were even higher in some indicators.Conclusion Emodin can effectively inhibit the release of inflammatory factors and improve the state of oxidative stress by modulating the p38/ERK signaling pathway,thereby exerting an ameliorative effect on myocardial hypertrophy.

Objective To explore the effects of dodecanoylcarnitine(DA)and myristoleic acid(MA)on the function of mouse alveolar epithelial cell line MLE-12 and their underlying mechanisms.Methods An inflammatory model was established by stimulating MLE-12 cells with IL-4.The expression levels of DA,MA,and sphingosine-1-phosphate(S1P)in the cell supernatant were detected by ELISA.MLE-12 cells were separately intervened with DA and MA.RT-PCR and flow cytometry were used to detect the expression changes of inflammatory factors IL-6 and tumor necrosis factor-α(TNF-α)and the level of intracellular reactive oxygen species(ROS).Additionally,Western blot was performed to detect the expression of key proteins such as p38 mitogen-activated protein kinase(p-38 MAPK)and src homology 2 domain-containing phosphatase 1(SHP-1).To explore the role of S1PR2 in the effects of DA and MA,MLE-12 cells were pretreated with the S1PR2 inhibitor JTE-013,and the above experiments were repeated.Results IL-4 stimulation significantly upregulated the levels of DA,MA,and S1P in MLE-12 cells(P<0.05).DA/MA treatment groups exhibited significantly increased expression of IL-6 and TNF-α compared with the control group(P<0.05),along with elevated ROS levels(P<0.05).Western blot analysis revealed that DA/MA promoted SHP-1 dephosphorylation and phosphorylated p38 MAPK activation in MLE-12 cells.Notably,JTE-013 pre-treatment completely reversed these effects(P<0.05).Conclusion Asthma-related metabolites DA and MA exacerbate the inflammatory and oxidative stress responses of MLE-12 cells by activating the S1PR2 receptor,promoting the dephosphorylation of SHP-1 and the activation of the p-p38 MAPK pathway.This study reveals the core regulatory role of S1PR2 in this pathway as well.

OBJECTIVE:To systematically evaluate the clinical effectiveness of rehabilitation robots in treating lower limb motor dysfunction in patients with cerebral palsy,and to compare the differences in therapeutic effects among different robots.METHODS:PubMed,Web of Science,Embase,Cochrane Library,CNKI,CBM,VIP and WanFang databases were searched to collect randomized controlled trials on rehabilitation robotics for the treatment of motor dysfunction in patients with cerebral palsy,published from database inception to April 10,2024.The main outcome indicators included muscle strength,muscle tension,balance function,step speed,step frequency,step length,walking endurance,lower limb motor function,and activities of daily living.The above indicators were coded according to the International Classification of Functioning,Disability and Health.Meta-analysis was performed to evaluate the clinical efficacy and compare the therapeutic efficacy of different rehabilitation robots.Literature search and screening were performed by two researchers,and the quality of the included literature was evaluated using the Cochrane 5.1.0 risk of bias assessment tool.Meta-analysis was performed using RevMan 5.4 software and Stata 16.0 software.RESULTS:(1)Fifteen articles were finally included,involving 512 patients with 260 in the experimental group and 252 in the control group.(2)The Meta-analysis results showed that rehabilitation robots could improve body structure and function[standardized mean difference=0.41,95%confidence interval(CI):0.24-0.58,P<0.05],activities(standardized mean difference=0.53,95%CI:0.41-0.65,P<0.05)and participation ability(mean difference=7.86,95%CI:1.54-14.18,P<0.05).In particular,the rehabilitation robot improved lower limb muscle strength,balance function,step speed,walking endurance,lower limb gross motor function,and activities of daily living in patients with cerebral palsy,but showed insignificant effects on step frequency,step length,and muscle tension.(3)The network Meta-analysis results showed that:step speed:Innowalkpro>Gait Trainer>Lokomat>3DCalt;6-minute walk test score:Gait Trainer>Lokomat>Lokohelp>Innowalkro;Gross Motor Function Measure-88D score:Lokohelp>Lokomat>KidGo>Innowalkpro>3DCalt;Gross Motor Function Measure-88E score:Lokomat>Lokohelp>KidGo>3DCalt>Innowalkpro.CONCLUSION:Based on the International Classification of Functioning,Disability,and Health,rehabilitation robot training can improve the lower limb motor function and activities of daily living in patients with cerebral palsy.The Innowalkpro robot was more effective in improving step speed;the Gait trainer robot was more effective in improving 6-minute walk test scores;the Lokohelp robot was more effective in improving Gross Motor Function Measure-88D zone scores;and the Lokomat robot was more effective in improving Gross Motor Function Measure-88E zone scores.