Objective To explore the mechanism of the gut microbiota-short-chain fatty acid axis in the heterogeneity of lactose intolerance(LI)in infants.Methods A total of 138 children diagnosed with LI due to diarrhea in the Affiliated Hospital of Xuzhou Medical University from June 2024 to April 2025 were selected as the research subjects.According to the severity of LI,they were divided into the mild LI group(n=68)and the severe LI group(n=70),and then 50 healthy children who received health care during the same period were selected as the healthy control group.The structure of the intestinal flora was analyzed by 16S rRNA gene sequencing,the content of short-chain fatty acids in feces was quantified by gas chromatography-mass spectrometry(GC-MS),and an infant intestinal organoid model was established to verify the functional mech-anism of key short-chain fatty acids.Results Compared with the healthy control group,the Shannon index,the abundance of Bifidobacterium,and the ratio of Bifidobacterium to Escherichia coli abundance(B/E)in the mild LI group and the severe LI group were lower,and the severe LI group was lower than the mild LI group(P<0.05).Compared with the healthy control group,the Escherichia coli/Shigella abundance was higher in the mild LI group and the severe LI group,and the severe LI group was higher than the mild LI group(P<0.05).Compared with the healthy control group,the levels of total short-chain fatty acids,acetic acid,propionic acid and butyric acid in the mild LI group and the severe LI group were lower,and those in the severe LI group were lower than those in the mild LI group(P<0.05).The multiple linear regression predic-tion model showed that the frequency of diarrhea=6.80-0.17×butyric acid+0.25×Escherichia coli-0.31×Bifidobacterium.The area under the curve of the prediction efficacy of this model was 0.89(95%CI:0.83-0.94).Compared with the control intestinal cells,the levels of transepithelial layer resistance(TEER)and tight junction protein(Claudin)-3 in the intestinal cells treated with lactose were lower,and the level of IL-8 was higher.However,the levels of TEER and Claudin-3 in the intestinal cells treated with lactose+bu-tyric acid were higher than those in the intestinal cells treated with lactose,and the level of IL-8 was lower(P<0.05).Conclusion The imbalance of intestinal flora and butyric acid deficiency jointly lead to the differ-ences in LI symptoms in infants and young children.

Objective To explore the correlation between eosinophils(EOS),interleukin-17A(IL-17A),tumor necrosis factor α(TNF-α)and vascular endothelial growth factor(VEGF)in peripheral blood and my-coplasma pneumoniae infection with wheezing in children.Methods A total of 98 children with mycoplasma pneumoniae infection diagnosed and treated in the hospital from January 2022 to May 2023 were selected as the study group.The study group was divided into wheezing group(32 cases)and non-wheezing group(66 ca-ses)according to whether they were accompanied by wheezing,and 30 children with lobar pneumonia without wheezing who were examined by fiberoptic bronchoscopy during the same period were selected as the control group.The levels of EOS,IL-17A,TNF-α and VEGF in peripheral blood of different groups were compared,and the correlation between the four indexes and mycoplasma pneumoniae infection with wheezing in children was analyzed.Results The levels of EOS,IL-17A,TNF-α and VEGF in peripheral blood of the study group were significantly higher than those of the control group,and the differences were statistically significant(P＜0.05).The differences in the levels of EOS,IL-17A,TNF-α and VEGF in the peripheral blood of the three groups were statistically significant(P＜0.05).Specifically,the levels of EOS,IL-17A,TNF-α and VEGF in the wheezing group were significantly higher than those in the non-wheezing group and the control group,and the differences were statistically significant(P＜0.05),and the levels of EOS,IL-17A,TNF-α and VEGF in the non-wheezing group were significantly higher than those in the control group,and the differences were sta-tistically significant(P＜0.05).Pearson correlation analysis showed that the levels of EOS,IL-17A,TNF-α and VEGF in peripheral blood were positively correlated with mycoplasma pneumoniae infection with wheez-ing in children(P＜0.05).Using wheezing as a state variable and plotting the receiver operating characteristic(ROC)curve,it was found that the area under the curve of peripheral blood EOS,IL-17A,TNF-α and VEGF for distinguishing mycoplasma pneumoniae infection with wheezing in children was 0.658,0.960,0.948,and 0.937.Conclusion Peripheral blood EOS,IL-17A,TNF-α,The level of VEGF is positively correlated with Mycoplasma pneumoniae infection with wheezing in children,which could be used for clinical differentiation of mycoplasma pneumoniae infection with wheezing in children.

Objective: To investigate the methods for qualitative pathological assessment of dynamic changes in liver fibrosis/cirrhosis after antiviral therapy in patients with chronic hepatitis B (CHB), since antiviral therapy can partially reverse liver fibrosis and cirrhosis caused by hepatitis B and semi-quantitative, rather than qualitative, pathological assessment is often used for the research on liver fibrosis regression. Methods: Previously untreated CHB patients with liver fibrosis and cirrhosis were enrolled, and liver biopsy was performed before treatment and at 78 weeks after the antiviral therapy based on entecavir. The follow-up assessment was performed once every half a year. Based on the proportion of different types of fibrous septum, we put forward the new qualitative criteria called P-I-R classification (predominantly progressive, predominantly regressive, and indeterminate) for evaluating dynamic changes in liver fibrosis. This classification or Ishak fibrosis stage was used to evaluate the change in liver fibrosis after treatment and Ishak liver inflammation score was used to evaluate the change in liver inflammation after treatment. Results: A total of 112 CHB patients who underwent liver biopsy before and after treatment were enrolled, and among these patients, 71 with an Ishak stage of ≥3 and qualified results of live biopsy were included in the final analysis. Based on the P-I-R classification, 58% (41/71) were classified as predominantly progressive, 29% (21/71) were classified as indeterminate, and 13% (9/71) were classified as predominantly regressive; there were no significant differences between the three groups in alanine aminotransferase, aspartate aminotransferase, albumin, HBeAg positive rate, HBV DNA, and liver stiffness (P < 0.05). After treatment, the proportion of predominantly progressive, indeterminate, or predominantly regressive patients changed to 11% (8/71), 11% (8/71), and 78% (55/71), respectively. Among the 35 patients who had no change in Ishak stage after treatment, 72% (25/35) were classified as predominantly regressive and had certain reductions in the Laennec score, percentage of collagen area, and liver stiffness. Conclusion This new P-I-R classification can be used to assess the dynamic changes in liver fibrosis after antiviral therapy in CHB patients.

Objective To study the expression of basic ifbroblast grouth factor (bFGF) and transforming growth factorβ1 (TGF-β1) in different stages of myocardial ifbrosis (CFs). Methods CFs of neonatal Sprague-Dawley rats were isolated with the method of trypsin digestion and differential anchoring velocity, then cultured in vitro. The generation 2-4 of CFs were used for the experiment and randomly divided into 2 groups:the control group were cultured without AngII , and the test group were cultured with AngII 10-6 mol/L. The test group were cultured for 12, 24, 48, and 72 h respectively, and then the synthesis of col agen were measured by ELISA, the bFGF, TGF-β1-mRNA expression was measured by RT-PCR, and the bFGF and TGF-β1 protein expression was measured by western blot analyses. Results Compared with those of control group, the expressions of bFGF and TGF-β1 both in gene and in protein in the test groups increased gradual y with the timing (P?

s:Objective To investigate the possible role of basic ifbroblast growth factor (bFGF) and transforming growth factorβ1 (TGF-β1) in mice with Coxsackie viral myocarditis and their relationship. Methods Eighty male BALB/c mice, 4 weeks old, were divided randomly into study group (n=40) and control group (n=40). The study group was repeated intraperitoneally injected with Coxasckie viral B3 to establish the model of viral myocarditis, while the control group was injected with virus-free Eagle’s medium in the same period. On the 7th, 14th, 28th and 42th day after the ifrst injection, 8 alive mice selected randomly from each group were sacriifced to examine the myocardial collagen volume fraction (CVF) by Masson dyeing, and to detect the protein and mRNA expression of bFGF and TGF-β1 by RT-PCR and immunohistochemistry. The correlations were analyzed. Results At each time point, the expressions of protein and mRNA of bFGF and TGF-β1 both in study group were signiifcantly higher than those in control group (P<0.01), and gradually increased over time. The expressions of protein and mRNA of bFGF and TGF-β1 were positively correlated with CVF (r=0.86~0.95, all P<0.01). In addition, the expressions of protein and mRNA of bFGF also had positive correlation with the expression of protein and mRNA of TGF-β1 (r=0.94, 0.92, P<0.01). Conclusion bFGF and TGF-β1 may promote the occurrence and development of myocardial ifbrosis in viral myocarditis, which may provide a new target for future treatment of myocardial ifbrosis.

Objective To study the role of transforming growth factor-β1 (TGF-β1),connective tissue growth factor (CTGF)and endothelin-1 (ET-1) in myocardial tissues of the mice with myocardial fibrosis induced by coxsachievirus B3 (CVB3) and the effect of Carvedilol intervention for it in acute stage and chronic phase of viral myocarditis.Methods Forty male BALB/c mice were randomly divided into 4 groups (10 cases in each group):control group,model group,Carvedilol acute phase intervention group,the chronic phase intervention group.Mice in model group and Carvedilol intervention groups were inoculated with CVB3 (100TCID50/0.1 mL) by peritoneal injection fortnightly.Mice in control group were given normal saline(NS) instead equivalently.Mice were poured Carvedilol (10 mg/kg per day for 2 weeks) from the second day in acute phase intervention group and from the fourth week in the chronic phase intervention group,while mice of control group and model group were poured with equivalent NS instead.At the end of 6 weeks,mice were sacrificed.Heart weight index (HWI) was determined.The collagen volume fraction (CVF) of left ventricular myocardial tissue were examined after Masson staining.Expressions of ET-1,TGF-β1 and CTGF were detected by enzyme linked immunosorbent assay and immunohistochemistry staining respectively; the mRNA expression was tested by reverse transcription-polymerase chain reaction.Results Compared with the control group,HWI and CVF of model group increased significantly(all P ＜ 0.01),those of the intervention groups decreased than those of the model group(all P ＜ 0.01),and in the acute phase those of the intervention group were significantly lower than those in chronic phase intervention group(all P ＜ 0.05).The expressions of TGF-β1,CTGF,ET-1 and their mRNA in model group were increased significantly than those in the control group(all P ＜0.01),and were decreased in acute and the chronic phase intervention group than those in model group(all P ＜0.01),while those were significantly lower in acute phase intervention group than those in chronic phase intervention group (all P ＜ 0.01).Conclusions TGF-β1,CTGF and ET-1 may be involved in myocardial fibrosis induced by CVB3.Compared with the chronic phase intervention,the acute phase intervention of Carvedilol can reduce myocardial fibrosis more efficiently by down-regulating the excessive expression of inflammatory factors.