ABSTRACT
Ulcerative colitis （UC） is a common inflammatory bowel disease （IBD） in clinical practice， characterized by symptoms such as abdominal pain， diarrhea， and bloody mucus in the stool. It is difficult to cure and has a high recurrence rate. The pathogenesis of UC is related to abnormal immune response， oxidative stress in intestinal tissues， and inflammatory reactions. As reported， the abnormal activation of the NOD-like receptor pyrin domain-containing protein 3 （NLRP3） inflammasome is involved in the pathological process of UC. This activation triggers pathological mechanisms such as oxidative stress， pyroptosis， and inflammation in intestinal epithelial cells. Therefore， blocking the abnormal activation of NLRP3 is beneficial for alleviating UC. Currently， western medicine treatment for UC mainly includes salicylic acid derivatives， corticosteroids， and biologics， but the overall efficacy is unsatisfactory. Traditional Chinese medicine （TCM） treatment of this disease has the advantages of significant efficacy and low recurrence rate. In recent years， great advances have been made in the basic research of using TCM methods to treat UC. Studies have found that TCM intervention targeting the NLRP3 inflammasome can significantly promote intestinal mucosal healing and treat UC， and the mechanism of action involves multiple targets， levels， and pathways. This article summarized the experimental research on the impact of TCM targeting the NLRP3 inflammasome on UC in recent years， and found that NLRP3 interacted with factors such as Caspase-1 and nuclear factor-κB （NF-κB）， thereby promoting the release of pro-inflammatory factors and cell pyroptosis in intestinal epithelial cells. This activation triggered oxidative stress， inflammatory reactions， and other pathological mechanisms. TCM acted on the NLRP3 inflammasome and its upstream and downstream factors to block the pathological process of UC， inhibit the pathological damage to the intestinal mucosa， and thereby alleviate colonic ulcers. The findings of this study provide a theoretical basis for the prevention and treatment of UC and further drug development.
ABSTRACT
OBJECTIVE@#To explore the genetic characteristics of a child with Focal segmental glomerulosclerosis and neurodevelopmental syndrome (FSGSNEDS).@*METHODS@#A child with FSGSNEDS who had visited Shengli Oilfield Central Hospital on September 15, 2019 was selected as the study subject. Clinical data of the child was collected, and trio-whole exome sequencing (trio-WES), Sanger sequencing, chromosomal karyotyping analysis, and copy number variation sequencing (CNV-seq) were used to analyze the child and his parents.@*RESULTS@#The child, a 3-year-old boy, had manifested developmental delay, nephrotic syndrome, and epilepsy. Trio-WES and Sanger sequencing showed that he has carried a heterozygous c.1375C＞T (p.Q459*) variant of the TRIM8 gene, for which both his parents were of the wild type. Based on guidelines from the American College of Medical Genetics and Genomics (ACMG), the variant was predicted to be pathogenic. No abnormality was found in the chromosomal karyotyping and CNV-seq results of the child and his parents.@*CONCLUSION@#The child was diagnosed with FSGSNEDS, for which the c.1375C＞T variant of the TRIM8 gene may be accountable.
Subject(s)
Male , Humans , Child , Child, Preschool , DNA Copy Number Variations , Glomerulosclerosis, Focal Segmental/genetics , Genomics , Heterozygote , Karyotyping , Carrier Proteins , Nerve Tissue ProteinsABSTRACT
Objective:To investigate the efficacy of atenolol combined with perindopril in the treatment of chronic heart failure in older adult patients and its effects on ventricular function, serum connective tissue growth factor (CTGF), and nexin.Methods:120 older adult patients with chronic heart failure who received treatment in the Department of Cardiology, the First People's Hospital of Fuyang District from January 2016 to January 2018 were included in this study. They were randomly assigned to receive either basic treatment + atenolol treatment (control group, n = 60) or atenolol combined with perindopril treatment (observation group, n = 60). Clinical efficacy and clinical symptom, serum CTGF, nexin level and ventricular function pre- and post-treatment, as well as adverse reactions were compared between the control and observation groups. Results:After treatment, effective rate in the observation group was significantly higher than that in the control group (91.6% vs. 78.3%, χ2 = 4.183, P = 0.041). After treatment, CTGF and nexin levels in the control and observation groups were decreased compared with before treatment (both P < 0.05). After treatment, CTGF and nexin levels in the observation group were (4.42 ± 0.46) μg/L and (0.82 ± 0.03) μg/L, respectively, which were significantly lower than those in the control group [(4.82 ± 0.51) μg/L, (0.98 ± 0.04) μg/L, t = 18.153, 4.511, 19.335, 24.787, all P < 0.05]. After treatment, left ventricular end diastolic diameter and left ventricular end systolic diameter in the control and observation groups were deceased compared with before treatment (both P < 0.05). After treatment, left ventricular end diastolic diameter and left ventricular end systolic diameter in the observation group were (48.73 ± 4.41) mm and (41.13 ± 4.15) mm, respectively, which were significantly lower than those in the control group [(56.01 ± 4.67) mm, (47.45 ± 4.17) mm, t = 5.700, 8.799, 8.317, 8.351, all P < 0.05]. After treatment, left ventricular ejection fraction in the control and observation groups was significantly increased compared with before treatment. After treatment, left ventricular ejection fraction in the observation group was significantly higher than that in the control group [(44.86 ± 4.59) % vs. (39.05 ± 4.69) %, P < 0.05]. Conclusion:Atenolol combined with perindopril in the treatment of older adult patients with chronic heart failure can reduce clinical symptoms, improve ventricular function, decrease serum CTGF and nexin levels and is highly safe. Therefore, this method is worthy of clinical application.