Fecal microbiota transplantation (FMT) is a treatment of transplanting a healthy human intestinal flora to the patient's gastrointestinal tract,in order to treat diseases by reconstructing the normal function of the intestinal flora.In recent years,fecal microbiota transplantation attracted more attention since many studies have demonstrated that fecal microbiota transplantation has great clinical value in the treatment of inflammatory bowel disease,autoimmune disease,irritable bowel syndrome,metabolic syndrome and other diseases.Intestinal tract which is an important human intestinal digestive organ has complex immune functions.Normal intestinal flora plays an important role in promoting the development of the immune system,maintaining normal immune function,and synergistically antagonizing pathogens.The fecal microbiota transplantation affects the receptor's immune function by reconstructing disorganized intestinal flora.In this paper,the effect of fecal microbiota transplantation on the intestinal immune system is reviewed.

The levels of total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, apolipoprotein (APO) A1 and APO B were lower in Bai Ku Yao than those in Han nationalities (all P<0.01). There was no significant difference in serum triglyceride levels and the ratio of Apo A1 to Apo B between two nationalities. Dyslipidemia was positively correlated with body mass index, waist circumference, total energy and total fat intakes, and inversely correlated with degree of physical activity and total dietary fiber intake in both ethnic groups. In addition, dyslipidemia was also positively correlated with age and alcohol consumption in Han, but not in Bai Ku Yao.

OBJECTIVE: To explore the genetic basis for a neonate affected with Glutaric aciduria type I (GA-I). METHODS: Targeted capture and high-throughput sequencing was carried out for the proband and her parents. Candidate variants were verified by Sanger sequencing. RESULTS: The proband was found to harbor compound heterozygous variants of the GCDH gene, namely c.523G>A and c.1190T>C, which was derived from her father and mother, respectively. CONCLUSION The compound heterozygous variants of the GCDH gene probably underlay the GA-I in the patient.
Amino Acid Metabolism, Inborn Errors/genetics* ; Brain Diseases, Metabolic/genetics* ; Child ; Female ; Glutaryl-CoA Dehydrogenase/genetics* ; High-Throughput Nucleotide Sequencing ; Humans ; Infant, Newborn ; Mutation

Objective:To understand the clinical phenotype and spectrum of ATP7B gene mutation in children with Wilson’s disease (WD). Methods:A total of 55 cases diagnosed with WD at the Children's Hospital Affiliated to Nanjing Medical University from June 2012 to June 2018 were taken as the research subject. ATP7B gene point mutation was detected by direct sequencing after PCR amplification. Heterozygous mutation in children was discovered by sequencing. Furthermore, the long segment mutation of exon was analyzed by multiplex ligation-dependent probe amplification (MLPA). Results:All 55 WD children had varying degree of liver damage symptoms. Among them, 2 cases had combined neurological symptoms. The positive rates of K-F ring (21%), 24-hour urine copper (97.7%), and ceruloplasmin were all abnormal. The results of ATP7B gene had identified 8 homozygous, 41 compound heterozygous and 6 heterozygous in 55 cases. Direct sequencing method had detected ten cases of ATP7B heterozygotes. In addition, MLPA analysis showed that other allele in four cases had a deletion of the ATP7B gene exon. In all cases, 35 different ATP7B gene mutations were detected, including 23 missense mutations, 3 frameshift mutations, 4 nonsense mutations, 3 exon deletions and 2 splicing changes. The most common allele mutation was c.2333G > T/p.R778L in exon 8, with an allele frequency of 36.54%, followed by c.2975C > T/p.P992L in exon 13, with an allele frequency of 14.42%. Conclusion:ATP7B gene c.2333G > T/p.R778L and c.2975C > T/p.P992L mutations are the most common mutations in children with WD in China. WD patients report shows that there are three long deletion mutations in the exon of the ATP7B gene. For WD children whose DNA sequencing is heterozygous ATP7B gene, it is suggested to further use MLPA method to detect deletion mutations of exons.