Exocrine pancreatic insufficiency(EPI)is a condition caused by a reduction in the secretion or activity of pancreatic juice and its digestive enzymes,particularly pancreatic lipase.EPI can lead to symptoms such as abdominal pain,bloating,steatorrhea,malnutrition,and weight loss,and may even increase the risk of osteoporosis and cardiovascular diseases.Diagnosis mainly relies on direct and indirect functional tests,while treatment is centered on pancreatic enzyme replacement therapy combined with comprehensive management strategies.This article summarizes the research progress on the definition,common causes,diagnostic methods,treatment,and prevention strategies of EPI,aiming to provide insights for optimizing its diagnosis and management.

Exocrine pancreatic insufficiency(EPI)is a condition caused by a reduction in the secretion or activity of pancreatic juice and its digestive enzymes,particularly pancreatic lipase.EPI can lead to symptoms such as abdominal pain,bloating,steatorrhea,malnutrition,and weight loss,and may even increase the risk of osteoporosis and cardiovascular diseases.Diagnosis mainly relies on direct and indirect functional tests,while treatment is centered on pancreatic enzyme replacement therapy combined with comprehensive management strategies.This article summarizes the research progress on the definition,common causes,diagnostic methods,treatment,and prevention strategies of EPI,aiming to provide insights for optimizing its diagnosis and management.

Objective:To evaluate the safety and efficacy of enhanced recovery after surgery(ERAS) in the perioperative period of congenital choledochal cysts in children.Methods:This is a multicenter prospective randomized controlled study. The clinical data of 273 pediatric congenital choledochal cysts(CCC) patients who underwent surgery at 14 medical centers with complete follow-up data were collected through the medical data analysis platform. Among them, 123 cases in ERAS group were managed perioperatively in strict accordance with ERAS mode, and 150 cases in conventional group were managed according to traditional mode. The length of hospital stay,time to first farting, time to complete feeding, the incidence of complications, cost and readmission rate within 30 days,stress indexes and liver function were compared between the two groups.Results:Compared with the conventional group, median time to start farting (2.0 d vs. 3.0 d, P<0.001), median time to complete feeding (5.0 d vs. 7.0 d, P<0.001), median postoperative hospitalization time (6.0 d vs. 9.0 d, P<0.001),the median total length of stay(13.0 d vs. 15.0 d, P<0.001) were shorter,the median hospitalization cost (37,000 yuan vs.43,000 yuan P<0.001) was lower, and stress indexes recovered quickly. The incidence of postoperative hospital stay and readimission rate within 30 d were not statistically different between the two groups. Conclusion:It is safe and feasible to implement ERAS for children with CCC in the perioperative period, which can reduce stress response, speed up recovery,and save medical costs.

Objective To investigate the role of nucleotide-binding oligomerization domain 2(NOD2)modified by palmitoyltransferase(ZDHHC5)in brain injury after cardiopulmonary resuscitation(CPR)in mice.Methods Twenty-four male C57BL/6J mice were divided into the blank group,the control group,the ZDHHC5-si group and the NOD2-si group,with 6 mice in each group.Except for the blank group without any treatment,CPR modeling was performed in the other three groups.At 24 h before CPR,mice in the ZDHHC5-si group and the NOD2-si group were injected with ZDHHC5 siRNA and NOD2 siRNA via tail vein,respectively.The modified neurological deficit scale(mNSS)was used to evaluate the neurological function at 24 h,48 h and 72 h in each group.Blood samples and brain tissue were collected 72 h after modeling.Real-time fluorescent quantitative PCR(qPCR)was used to detect ZDHHC5 and NOD2 in brain tissue.The protein expression levels of IL-1β,TNF-α and IL-6 in plasma were detected by enzyme-linked immunosorbent assay(ELISA).Colorimetric method and thiobarbituric acid(TBA)method were used to detect protein expression levels of MDA and MPO in brain tissue,respectively.Western blot assay was used to detect expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 in brain tissue.HE pathological sections of brain tissue were observed under light microscope.The pathological sections of brain tissue were observed by TUNEL under fluorescence microscope.Results Compared with the blank group,the mNSS score,the expression levels of IL-1β,TNF-α,IL-6,MDA and MPO,and the protein expression levels of Cleaved Caspase-3,ZDHHC5 and NOD2 were significantly increased(P＜0.05),and brain tissue damage and cell apoptosis were aggravated in the other three groups.Compared with the control group,the above indicators were significantly decreased in the ZDHHC5-si group and the NOD2-si group(P＜0.05),and brain tissue damage and cell apoptosis were significantly attenuated.Compared with the NOD2-si group,the above parameters were significantly decreased(P＜0.05),and brain tissue damage and cell apoptosis were further attenuated in the ZDHHC5-si group.Conclusion In the mouse CPR model,NOD2 can produce palmitoylated NOD2 after regulated by ZDHHC5,which further promotes the release of inflammatory factors and causes neuronal apoptosis,ultimately damaging brain tissue and affecting neurological function.

Objective Exploring the relationship between anxiety symptoms and neurometabolism in the ventrome-dial prefrontal cortex(vmPFC)of adolescents with bipolar depression.Methods Thirty-six adolescent patients with bi-polar depression were assessed and grouped by using the 14-item Hamilton anxiety rating scale(HAMA),including 20 pa-tients with anxiety symptoms and 16 patients without anxiety symptoms.The severity of depressive symptoms was assessed using the 24-Hamilton depression scale(HAMD),and 1H-magnetic resonance spectroscopy(1H-MRS)was used.The dif-ference of vmPFC neurometabolism between 2 groups was compared.Results Compared with the group without anxiety symptoms,the HAMD score[24.50(24.00,26.75)vs.23.00(22.00,24.00)]and the proportion of family history(40.0%vs.0)were significantly higher in the group with anxiety symptoms than in the group without anxiety symptoms(P<0.05).The level of mI/Cr was higher in the group with anxiety symptoms than that in the group without anxiety symptoms(0.58±0.12 vs.0.47±0.11),and the difference was significant(P<0.05).Cho/Cr and HAMD scores in patients with anxiety symptoms were positively correlated(r=0.589,P=0.006),and mI/Cr was negatively correlated with disease duration(r=-0.481,P= 0.032).Conclusions Anxiety symptoms in adolescent bipolar depression patients may be related to elevated levels of mI,a neurometabolite in the brain region of vmPFC.

Objective To identify the effect of both high glucose and high insulin on miR-145 level.Methods The human vascular smooth muscle cells ( VSMCs) were cultured and the proliferation of VSMCs was induced by high glucose and high insulin medium.The samples were divided into 4 groups: normal group, high glu-cose group (25 mmol/L), high insulin group (300 mU/L), high glucose and high insulin group.The ex-pression of miR-145 in VSMCs was assayed by real-time PCR.Proliferation of VSMCs was determined by MTT method After 72 h cultivation.The migration of VSMCs was analyzed by cell scratch test .VSMCs in each group was transfected by miR-145 virus ( lentiviral vector ) .Proliferation and migration were assayed after 48 h transfection.Results The expression of miR-145 in VSMCs of other three groups was decreased ( P<0.05 ) , especially the expression in the high glucose and insulin group was the lowest ( P<0.01 ) .Prolifera-tion and migration of VSMCs was promoted by high glucose and/or high insulin medium.Under fluorescent, transfection rate of VSMCs was about 80%after 48 h transfection.Proliferation and migration of VSMCs in each group after transfection were significantly lower than before ( P<0.05 ) .Conclusions High glucose and high in-sulin could decrease the expression of miR-145 in VSMCs, The overexpression of miR-145 may inhibit the prolif-eration and migration of VSMCs .