Inflammatory bowel disease (IBD) is a chronic and nonspecific disease affected by both genetic and environmental factors. Ecological and social environmental factors, including air pollutants, heavy metals, industrial pollutants and organic pollutants, diet, and lifestyle, influence the occurrence and development of IBD and regulate IBD gene expression through epigenetics and gut microbiota. This article summarizes the role of environmental factors in IBD and explores the ways in which they influence the regulation of gene expression.

Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disorder with unclear etiology. Existing studies indicate that diet plays an important role in both the pathogenesis and prognosis of IBD. This review summarizes clinical evidence regarding the association between diet and the development of IBD, analyze the current nutritional status of the IBD population at the prognosis level and underlying mechanisms of dietary interventions in disease management, and explores the application of precision nutrition in personalized care. The review ultimately aims to provide guidance for developing more precise and personalized dietary management strategies for IBD patients.

Inflammatory bowel disease (IBD) is a chronic and nonspecific disease affected by both genetic and environmental factors. Ecological and social environmental factors, including air pollutants, heavy metals, industrial pollutants and organic pollutants, diet, and lifestyle, influence the occurrence and development of IBD and regulate IBD gene expression through epigenetics and gut microbiota. This article summarizes the role of environmental factors in IBD and explores the ways in which they influence the regulation of gene expression.

Inflammatory bowel disease (IBD) is a chronic gastrointestinal inflammatory disorder with unclear etiology. Existing studies indicate that diet plays an important role in both the pathogenesis and prognosis of IBD. This review summarizes clinical evidence regarding the association between diet and the development of IBD, analyze the current nutritional status of the IBD population at the prognosis level and underlying mechanisms of dietary interventions in disease management, and explores the application of precision nutrition in personalized care. The review ultimately aims to provide guidance for developing more precise and personalized dietary management strategies for IBD patients.

Objective:To investigate the effect of instantaneous flow rate on the consistency of diagnostic accuracy of severe degenerative mitral regurgitation (DMR) using proximal isovelocity surface area (PISA).Methods:From June 2019 to June 2021, 75 patients with DMR who underwent echocardiography in Department of Echocardiography of Zhongshan Hospital, Fudan University were prospectively enrolled. The instantaneous flow rate of DMR during the systolic phase was calculated using M-mode PISA(PISA M-mode), and a time-integrated curve was plotted. Regurgitant volume (RVol) and effective regurgitant orifice area (EROA) were calculated by traditional PISA (PISA max), pair PISA (PISA pair), and PISA M-mode, respectively. RVol acquired from cardiac magnetic resonance (CMR) volumetric method in 22 patients of the enrolled patients. The correlation and consistency of RVol acquired between the three PISA methods and CMR were compared. Agreement of diagnostic accuracy of severe mitral regurgitation (sMR) acquired between the three PISA methods and multi-parameter algorithm by American Society of Echocardiography (ASE) was analyzed using Cohen′s Kappa analysis. Results:The curve of instantaneous flow rate of DMR showed unimodal pattern with the peak at mid-late systolic phase. The correlation of RVol acquired between PISA methods and CMR was moderate for PISA max and PISA pair ( r=0.77, 0.80, both P<0.001), whereas PISA M-mode presented strong correlation with CMR ( r=0.87, P<0.001). RVol acquired from PISA max was larger than that of CMR[(69.1±37.1) ml vs (49.0±29.0)ml, P=0.002]. Both PISA max and PISA pair were shown moderate agreement of diagnostic accuracy of sMR with ASE multi-parameters algorithm (RVol: κ=0.496, 0.525, both P<0.001; EROA: κ=0.570, 0.578, both P<0.001), while PISA M-mode presented strong agreement (RVol: κ=0.867 and EROA: κ=0.802, both P<0.001). Conclusions:Based on the unimodal pattern of instantaneous flow rate in patients with DMR, PISA max may significantly overestimate RVol, exposing a significant proportion of patients with DMR to unnecessary MR surgery. PISA M-mode presents better correlation and consistency with CMR on the quantification of RVol compared with PISA max and PISA pair, and may improve the diagnostic accuracy of quantification of sMR using PISA.

Objective To observe the changes of inflammatory factors in acute lung injury (ALI) in mice induced by lipopolysaccharide (LPS), and to explore the influence of different doses of LPS on ALI onset and progress at different time points. Methods Intratracheally, LPS at the dosages of 2.5, 5.0, 7.5 and 10.0 mg/kg were administered to a total of 210 C57BL/6 mice, and according to the difference in dosage, they were divided into four groups. The ALI model was replicated by intratracheally dropping of LPS. And a normal control group and a normal saline control group were established (each, n=10). The changes of index of pathological lung tissue and lung tissue wet/dry (W/D) ratio were observed at 1, 2, 4, and 8 hours after injury, and simultaneously, the levels of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and protein in serum and bronchoalveolar lavage fluid (BALF) were detected. Results ①The degree of lung injury induced by LPS was dose-and time-dependent.②With the increase of LPS dosage and prolongation of time, in LPS group, the lung W/D ratio and the index of pathological lung tissue were increased;additionally, the levels of NE, TNF-α, IL-6 and protein in serum or BALF were also significantly increased. The critical occurrence point of acute respiratory distress syndrome (ARDS) with specific characteristics was at 5.0 mg/kg of LPS acting for 4 hours [lung W/D ratio: 4.97±0.41, index of pathological changes of lung tissue (score): 5.60±1.52; serum NE (ng/L): 379.99±27.65, TNF-α (ng/L): 159.15±20.62, IL-6 (ng/L): 177.15±29.13;BALF NE (mg/kg):105.85±13.66, TNF-α(mg/kg):227.22±48.01, IL-6 (mg/kg):251.55±54.08, total protein (g/L):1.59±0.37]. The injury induced by LPS acting for 8 hours in the dosage group 10.0 mg/kg was the most significant in comparisons with other groups of dosages at the same time points [lung W/D ratio:5.10±0.18 vs. 5.01±0.43, 5.01±0.19, 4.91±0.30; index of pathological changes of lung tissue (score): 9.20±1.48 vs. 8.00±1.00, 6.00±1.22, 4.40±0.89;serum NE (ng/L): 447.43±34.63 vs. 419.23±30.62, 391.16±54.91, 372.59±51.52; TNF-α(ng/L): 205.99±31.31 vs. 181.01±25.11, 161.01±13.98, 138.83±28.95; IL-6 (ng/L): 233.76±34.84 vs. 206.21±26.68, 186.58±26.54, 156.99±28.83;BALF NE (mg/kg):190.82±41.75 vs. 153.30±35.42, 122.64±25.15, 80.23±13.69;TNF-α(mg/kg):305.24±72.99 vs. 292.77±38.07, 249.60±35.20, 193.63±10.83; IL-6 (mg/kg): 354.81±67.79 vs. 303.02±54.24, 272.43±32.34, 197.64±12.35;total protein (g/L):2.31±0.30 vs. 2.02±0.26, 1.62±0.19, 1.10±0.24, P<0.05 or P<0.01]. Conclusions The severity of ALI induced by LPS in mice was positively correlated to LPS dosage and duration of its action. After administration of LPS 5 mg/kg for 4 hours, remarkable characteristic manifestations of ARDS occur in mice, reaching the critical point.

Objective To investigate the association between variable number of tandem repeat(VNTR) polymorphism of endothelial nitric oxide synthase(eNOS) gene and cerebral infarction(CI).Methods The genotypes of 152 patients with CI were detected by polymerase chain reaction(PCR) and compared with control group. Multiple regression analysis was performed to assess the independent roles of the polymorphism of eNOS and other risk factors.Results The ab genotype distribution frequency of eNOS gene in CI group(22.36%) was higher than that in control group(12.28%), and a allele frequency of eNOS gene in CI group(12.5%) was also higher than that in control group(7.0%). Both differences between CI group and control group were significant(all P