Objective:To evaluate the efficacy and safety of upadacitinib in the real-world treatment of difficult-to-treat Crohn's disease (DTT-CD) .Methods:This multicenter, retrospective cohort study included patients diagnosed with DTT-CD according to the International Organization for the Study of Inflammatory Bowel Diseases (IOIBD) criteria, and treated at eight Chinese inflammatory bowel disease centers between January 2023 and March 2025. Clinical outcomes were assessed after 12 weeks of induction therapy with upadacitinib (45 mg qd), including clinical remission rate, clinical response rate, and incidence of adverse events.Results:Among 151 enrolled DTT-CD patients, the clinical remission rate was 47.0%, and the clinical response rate was 90.7% after 12 weeks of treatment. Adverse events occurred in 42 cases (27.8%) .Conclusion:Upadacitinib demonstrated favorable efficacy in inducing clinical remission in DTT-CD patients, with a good safety profile at the induction dose (45 mg qd) .

Objective:To evaluate the efficacy and safety of upadacitinib in the real-world treatment of difficult-to-treat Crohn's disease (DTT-CD) .Methods:This multicenter, retrospective cohort study included patients diagnosed with DTT-CD according to the International Organization for the Study of Inflammatory Bowel Diseases (IOIBD) criteria, and treated at eight Chinese inflammatory bowel disease centers between January 2023 and March 2025. Clinical outcomes were assessed after 12 weeks of induction therapy with upadacitinib (45 mg qd), including clinical remission rate, clinical response rate, and incidence of adverse events.Results:Among 151 enrolled DTT-CD patients, the clinical remission rate was 47.0%, and the clinical response rate was 90.7% after 12 weeks of treatment. Adverse events occurred in 42 cases (27.8%) .Conclusion:Upadacitinib demonstrated favorable efficacy in inducing clinical remission in DTT-CD patients, with a good safety profile at the induction dose (45 mg qd) .

Objective To investigate the role of triggering receptor expressed on myeloid cells-1(TREM-1)in ath-erosclerosis induced by chronic intermittent hypoxia(CIH).Methods ApoE-/-mice were randomly divided into blank group,model group and experimental group.The mice in the model group and the experimental group were kept in a hypoxic environment and fed with a high-fat diet.After 4 weeks of high-fat feeding,mice in the experi-mental group were intraperitoneally injected with TREM-1 inhibitor LR12(5 mg/kg)for 8 weeks.After 12 weeks of feeding,the level of serum total cholesterol(TC),low density lipoprotein(LDL),triglyceride(TG),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-10(IL-10)were detected.Histological analysis of aortic TREM-1 expression,plaque area and macrophage level were examined.Results Compared with blank group,the expression of TREM-1 in the aorta of the model group significantly increased(P＜0.05).Com-pared with model group,the aortic plaque,the level of lipids in serum(TC,LDL,TG)and inflammatory factors(TNF-α,IL-1β,IL-10),aortic plaque,the expression of TREM-1 and infiltrating macrophages in aortic plaque of the experimental group were all significantly reduced(P＜0.05).Conclusions TREM-1 is involved in the develop-ment of CIH-induced AS.Inhibition of TREM-1 can alleviate CIH-induced AS and its mechanism is related to the inhibition of macrophage activation.

Background:Identifying missed diagnoses of polyps is significant in reducing the incidence of colorectal cancer.Until now,the role of repeat colonoscopy during colorectal polypectomy in reducing themissed diagnoses of polyps is sparsely studied.Aims:To analyze the value of repeat colonoscopy during colorectal polypectomy in reducing themissed diagnoses of polyps.Methods:One hundred and forty-six patients in the first affiliated hospital of Ningbo University who underwent polypectomy were consecutively recruited for repeat colonoscopy from January 2020 to January 2021.The number,size,and location of missed polyps were recorded and analyzed during colorectal polypectomy.Univariate logistic regression analysis was used to analyze the independent risk factors of missed polyps.Results:There were 86 males and 60 females among the 146 enrolled patients,which aged(55.54±10.51)years.The overall missed polyps'rate was 27.17%.We found that all missed polyps were sessile polyps and<10 mm in size,the difference was significant in the left colon.Univariate logistic regression analysis showed that the endoscopist' experience was an independent risk factor for missed polyps.Conclusions:Endoscopist'experience was an independent risk factor for missed polyps.Repeat colonoscopy could reduce the missed polyps.

Objective:To explore the role of glycoprotein nonmetastatic melanoma protein B (Gpnmb) in chronic intestinal fibrosis of mice induced by dextran sodium sulfate (DSS) .Methods:Twelve BALB/c mice were randomly and equally divided into model group and control group. The mice in model group received water containing 2.5% dextran sodium sulfate (DSS) to establish a chronic intestinal fibrosis model, while the mice in control group were not treated. The body mass, colon length, colonic histomorphology score and histological damage score of mice were calculated. The inflammatory degree of colitis was assessed by HE staining and the degree of colonic fibrosis was assessed by Masson staining. The protein expression of collagen typeⅠ alpha 2 (Col1α2) , Gpnmb and its receptor CD44 in colonic tissues was determined by immunohistochemistry and Western blot. The mRNA expression of Col1α2 and Gpnmb was detected by fluorescent quantitative PCR. The differences of the above indexes between the two groups were compared by t test. Results:Compared with the control group, the colon length of the model group was shorter and the colonic histomorphology score was higher (all P<0.05) . HE staining results showed that the intestinal glands in the colonic mucosa were disorderly arranged, atrophic and reduced, the goblet cells were less, and edema, neutrophil and lymphocyte infiltration were seen in the mucosa and submucosa in the model group. The mucosa of the control group was normal without inflammation. Compared with the control group, the histological damage score of the colon in the model group was higher and the fibrotic area was larger, the protein expression of Col1α2, Gpnmb and CD44 was higher, the mRNA expression of Col1α2 and Gpnmb were higher (all P<0.05) . Conclusion:Gpnmb may promote the occurrence and development of DSS-induced chronic intestinal fibrosis in mice through CD44.

Objective:To explore the role of glycoprotein nonmetastatic melanoma protein B (Gpnmb) in chronic intestinal fibrosis of mice induced by dextran sodium sulfate (DSS) .Methods:Twelve BALB/c mice were randomly and equally divided into model group and control group. The mice in model group received water containing 2.5% dextran sodium sulfate (DSS) to establish a chronic intestinal fibrosis model, while the mice in control group were not treated. The body mass, colon length, colonic histomorphology score and histological damage score of mice were calculated. The inflammatory degree of colitis was assessed by HE staining and the degree of colonic fibrosis was assessed by Masson staining. The protein expression of collagen typeⅠ alpha 2 (Col1α2) , Gpnmb and its receptor CD44 in colonic tissues was determined by immunohistochemistry and Western blot. The mRNA expression of Col1α2 and Gpnmb was detected by fluorescent quantitative PCR. The differences of the above indexes between the two groups were compared by t test. Results:Compared with the control group, the colon length of the model group was shorter and the colonic histomorphology score was higher (all P<0.05) . HE staining results showed that the intestinal glands in the colonic mucosa were disorderly arranged, atrophic and reduced, the goblet cells were less, and edema, neutrophil and lymphocyte infiltration were seen in the mucosa and submucosa in the model group. The mucosa of the control group was normal without inflammation. Compared with the control group, the histological damage score of the colon in the model group was higher and the fibrotic area was larger, the protein expression of Col1α2, Gpnmb and CD44 was higher, the mRNA expression of Col1α2 and Gpnmb were higher (all P<0.05) . Conclusion:Gpnmb may promote the occurrence and development of DSS-induced chronic intestinal fibrosis in mice through CD44.

The resistance to steroid remains a major trouble in the treatment of idiopathic nephrotic syn-drome,and the mechanisms are complicated. Recent studys have shown that multidrug resistance gene l and P-glycoprotein170,glucocorticoid receptor,renal pathology,gene mutation and complications are all closely related to the resistance to steroid. This review is focused on the mechanisms of steroid resistance of children′s idiopath-ic nephrotic syndrome.

Post-traumatic stress disorder in parents of children in neonatal intensive care unit ( NICU) directly influences children′s remedy and development, to which has been paid increasing attention by nurses. The review introduces the basic concept of post-traumatic stress disorder in parents of children in NICU, symptoms, research tools and influencing factors. Based on the results and experience of foreign research, the review provides references for domestic nurses to study post-traumatic stress disorder in parents of children in NICU.

Objective To discuss Si tactic of breathing exercises on the rehabilitation of lung function, dyspnea, distance of 6-minute walk distance (6MWD), respiratory muscle endurance and quality of life in stable patients with chronic obstructive pulmonary disease (COPD). Methods 63 patients with COPD were divided into experimental group with 31 cases and control group with 32 cases according to random digital table method. The experimental group were given routine treatment and nursing care, take Si tactic of breathing exercises. The control group were given routine treatment and nursing care only. Both groups were given treatment for 4 months. The indexes of lung function (FEV1, FEV1%, FEV1/FVC), scores of the Modified Medical Research Council Scale (MMRC), 6MWD, scores of Saint-George′s Respiratory Questionnaire (SGRQ), maximal voluntary ventilation (MVV) changes before and after the therapy were measured. Results After intervention, the lung function as measured by FEV1, MVV, 6MWD showed a significant improvement in the experimental group, and was higher than that in the control group[(1.42±0.43) L vs.(1.22±0.32) L and(1.21±0.45) L,(52.39±14.21) L vs.(47.20±14.59) L and (43.65±11.89) L, (288.36±71.70) m vs.(244.42±71.50) m and (250.56 ±79.25) m, P<0.05]; MMRC scores, SGRQ scores, activities and daily life part score were lower after intervention and was lower than that in the control group [(2.63 ±1.00) points vs. (3.21 ±0.92) points and (3.14±1.12) points, (44.38±5.23) points vs. (54.74±5.73) points and (52.87±5.49) points, (41.25± 6.03) pints vs.(66.48±6.38) points and (64.13±5.34) points, (28.00±7.34) points vs. (44.87±4.86) points and (42.31 ±9.12) points, P<0.05]. Conclusions For COPD patients in stable stage, Si tactic of breathing exercises can improve the pulmonary function and alleviate dyspnea, enhance exercise endurance and respiratory endurance, thereby improve the quality of life of patients, so this is one of the method for comprehensive pulmonary rehabilitation in the future.

Aim To explore the role of heat shock protein 90(Hsp90)in hydrogen sulfide-induced protection against PC12 cells injuries elicited by cobalt chloride(CoCl_2).Methods Hydrogen sulfide preconditioning against CoCl_2-induced injury model was set up in PC12 cells.Cell viability was tested by using cell counter kit-8.Morphological changes in apoptotic PC12 cells were detected by Hoechst 33258 staining and photofluorography.Apoptotic rate was evaluated by propidium iodide(PI)staining and flow cytometry(FCM).The expression of Hsp90 was evaluated by Western blot.Results Hsp90 expression was upregulated after treatment with 400 μmol·L~(-1) sodium hydrosulfide(a H_2S donor),peaking at 3 h,returning to the basal level at 24 h.Furthermore,H_2S preconditioning obviously enhanced the upregulation of Hsp90 expression induced by CoCl_2.H_2S preconditioning markedly protected PC12 cells against injuries induced by CoCl_2,increasing the viability of cells and decreasing the percentage of apoptotic cells.17-allylamino-17-demethoxygeldanamycin(17-AAG),an inhibitor of Hsp90,antagonized H_2S preconditioning-induced Hsp90 activation and the adaptive cytoprotection.Conclusion H_2S can protect PC12 cells against CoCl_2-induced injuries,and upregulating the expression of Hsp90 may be one of the mechanisms underlying cytoprotection induced by H_2S preconditioning.