The development of inflammatory bowel diseases (IBD) is associated with genetics, environment, immune abnormalities, and intestinal flora, including ulcerative colitis (UC) and Crohn′s disease (CD). Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that promotes the expression of multiple genes in response to the hypoxic environment, and its roles in regulating intestinal barrier function, intestinal metabolism, and inflammatory and immune responses are research hotspots. This article reviews the role of HIF-1α in IBD by analyzing the relationships between HIF-1α and intestinal epithelial barrier and inflammatory response to provide new ideas for the clinical treatment of IBD.

The development of inflammatory bowel diseases (IBD) is associated with genetics, environment, immune abnormalities, and intestinal flora, including ulcerative colitis (UC) and Crohn′s disease (CD). Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that promotes the expression of multiple genes in response to the hypoxic environment, and its roles in regulating intestinal barrier function, intestinal metabolism, and inflammatory and immune responses are research hotspots. This article reviews the role of HIF-1α in IBD by analyzing the relationships between HIF-1α and intestinal epithelial barrier and inflammatory response to provide new ideas for the clinical treatment of IBD.

OBJECTIVE To preliminary predict and analyze the quality marker(Q-markers)of Platycodonis Radix decoction based on the validity and measurability of traditional Chinese medicine Q-marker. METHODS The fingerprints of 20 batches of Platycodonis Radix samples were established, and the similarity was evaluated. At the same time, a "component-target-pathway" network diagram was constructed through network pharmacology to predict the potential active components of Platycodonis Radix. Mathematical analysis methods such as principal component analysis and orthogonal partial least-squares discrimination analysis were used to screen differential components; the content of candidate components were determined. RESULTS There were 19 common peaks in the established fingerprint, and 8 common components were identified as candidate active components for network pharmacology analysis. Network pharmacology indicated that 6 compounds were screened out with a high degree of connectivity. Based on the comprehensive consideration of Q-marker principle:traceability and transmissibility, specificity, efficacy, and measurability, luteolin, syringin, chlorogen acid, platycoside D, platycoside D3 and platycoside E were preliminarily predicted as potential Q-markers of platycodon. CONCLUSION The prediction analysis of Platycodonis Radix Q-marker provides a reference for the comprehensive control of the quality of Platycodonis Radix medicinal materials, and also lays a foundation for the research and exploration of the substance basis and mechanism of action of Platycodonis Radix.

This article reports the prenatal diagnosis of 22q11.2 deletion syndrome (22q11.2 DS) in two consecutive pregnancies of a woman. Echocardiography on the first fetus at 24 +4 gestational weeks identified the right aortic arch, and right-sided ductus arteriosus with aberrant left subclavian artery. Subsequently, an amniocentesis was performed, and chromosomal microarray analysis (CMA) of amniotic fluid revealed a 2.181 Mb heterozygous microdeletion of 22q11.21, which indicated the presence of 22q11.2 DS in the fetus. After genetic counseling, the pregnant woman decided to terminate the pregnancy and declined genetic testing. During her second pregnancy, ultrasound at 21 +5 weeks detected interrupted aortic arch type B with aberrant left subclavian artery, ventricular septal defect, and enlarged posterior fossa in the fetus and further CMA of amniotic fluid indicated fetal 22q11.2 DS. CMA was performed on peripheral blood of the woman, which found the same deletion on 22q11.21. The woman had nasal sounds and velopharyngeal insufficiency with normal phenotype. Following the genetic counseling regarding the risk of recurrence, the pregnant woman opted to terminate the pregnancy and was suggested to undergo preimplantation genetic diagnosis in future pregnancies. One year after the second pregnancy termination, the woman's father developed heart failure at the age of 53 and was also found to have nasal sounds. Low-depth whole genome copy number variation sequencing in venous blood confirmed 22q11.2 DS in her father. For those with a prenatal diagnosis of 22q11.2 DS, genetic testing of the fetal parents is recommended to help assess the risk of recurrence and facilitate genetic counseling.

Objective To explore the relationship between the expression of M2 pyruvate kinase(PKM2)and E-cad-herin(E-cadherin)in tumor tissues and the clinicopathology and prognosis of breast cancer patients.Methods 447 patients with breast cancer admitted from February 2020 to February 2022 were selected as the objects of this study.Breast cancer tissues and adjacent tissues of patients were taken,and patients were divided into good prognosis group(261 cases)and poor prognosis group(186 cases)according to the prognosis of patients.Immunohistochemistry was used to determine the expression of PKM2 and E-cadherin in the tissues of the patients,and the patients were followed up for 6 months.The patients were divided into groups according to whether the patients had recurrence and metastasis,and the relationship between the expression of PKM2 and E-cadherin in the breast cancer tissues of the patients and the clinicopathology was explored.The expression of PKM2 and E-cad-herin protein between breast cancer tissue and adjacent tissue,and between good prognosis group and poor prognosis group were compared,and the correlation between PKM2 and E-cadherin protein expression and poor prognosis of patients was explored.Results There were no differences in the expression of PKM2 and E-cadherin in breast cancer patients with different ages,tumor sites and tumor sizes(P＞0.05).The positive rate of PKM2 protein expression was higher and the positive rate of E-cadherin protein expression was lower in postmenopausal,middle and highly differentiated,stage I to II and no lymph node metastasis(P＜0.05).The positive rate of PKM2 in patients with poor prognosis was 94.62%,higher than 81.23%in patients with good prognosis;The positive rate of E-cadherin in patients with poor prognosis was 30.65%,which was lower than 46.36%in patients with good prognosis(P＜0.05).By Spearman correlation coefficient analysis,poor prognosis was positively correlated with the positive rate of PKM2 in breast cancer tissues(r=0.195,P＜0.001),and negatively correlated with the positive rate of E-cad-herin protein(r=-0.158,P=0.001).Conclusion PKM2 and E-cadherin protein expression in tumor tissues of breast canc-er patients has some link with the clinicopathology of patients,and there is some correlation with patient prognosis.

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory disease, mainly including ulcerative colitis (UC) and Crohn′s disease (CD). With the in-depth study of the role of regulated cell death (RCD) in IBD, more and more evidences show that autophagy, ferroptosis, pyroptosis, apoptosis and necroptosis are closely related to the progress and prognosis of IBD. This article reviews the pathogenesis and therapeutic prospects of RCD represented by autophagy in IBD, providing a reference for the treatment of IBD.

Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory disease, mainly including ulcerative colitis (UC) and Crohn′s disease (CD). With the in-depth study of the role of regulated cell death (RCD) in IBD, more and more evidences show that autophagy, ferroptosis, pyroptosis, apoptosis and necroptosis are closely related to the progress and prognosis of IBD. This article reviews the pathogenesis and therapeutic prospects of RCD represented by autophagy in IBD, providing a reference for the treatment of IBD.

Objective:To analyze the phenotypic and genomic characteristics of Salmonella isolates recovered from meat products in Beijing wholesale markets. Methods:A total of 336 Salmonella strains from meat products collected from wholesale markets in Beijing were tested for antimicrobial resistance to 25 antimicrobial compounds by micro-broth dilution method; whole genome data were sequenced, followed by the serotype and ST type prediction by Seqsero2 and SISTR software, and the drug resistance genes and virulence factors were also predicted with CARD and VFDB databases of Abricate software; Salmonella serotyping assay kit and serum agglutination method were used for serotype confirmation of some isolates with different genome prediction results. Results:The resistance rates to Nalidixic acid and Ampicillin were 62.5% (210/336) and 55.1% (185/336), respectively, and all isolates were susceptible to Tigecyclin, Cefoxitin and Carbapenem antimicrobial compounds; 207 isolates (61.6%, 207/336) were multi-drug resistant, some could even be resistant to ten categories of drugs at the same time, and the most common antimicrobial resistance spectrum was NAL-AMP-SAM. A total of 24 serotypes were detected with predominant serotypes of Enteritidis (34.5%, 116/336), Derby (17.3%, 58/336) and Indiana (10.4%, 35/336). A total of 27 ST types were detected, the dominant type was ST11; ST types were in good consistency with serotypes; The detection rates of resistant genes referred to aminoglycosides, fluoroquinolones, β-lactams, sulfonamides and tetracyclines are more than 48%, and the first two reached 100%. The prediction of drug resistance genes was consistent with the results of antimicrobial resistance phenotype. A total of 122 virulence genes were predicted, 74 of which existing among all isolates.Conclusion:Salmonella in meat from the wholesale markets of Beijing has a high proportion of multiple drug resistance, a complex drug resistance spectrum, a variety of serotypes and ST types, and a high carrying rate of drug resistance gene and virulence gene; drug resistance phenotype and genotype are relatively consistent.

Objective:To analyze the phenotypic and genomic characteristics of Salmonella isolates recovered from meat products in Beijing wholesale markets. Methods:A total of 336 Salmonella strains from meat products collected from wholesale markets in Beijing were tested for antimicrobial resistance to 25 antimicrobial compounds by micro-broth dilution method; whole genome data were sequenced, followed by the serotype and ST type prediction by Seqsero2 and SISTR software, and the drug resistance genes and virulence factors were also predicted with CARD and VFDB databases of Abricate software; Salmonella serotyping assay kit and serum agglutination method were used for serotype confirmation of some isolates with different genome prediction results. Results:The resistance rates to Nalidixic acid and Ampicillin were 62.5% (210/336) and 55.1% (185/336), respectively, and all isolates were susceptible to Tigecyclin, Cefoxitin and Carbapenem antimicrobial compounds; 207 isolates (61.6%, 207/336) were multi-drug resistant, some could even be resistant to ten categories of drugs at the same time, and the most common antimicrobial resistance spectrum was NAL-AMP-SAM. A total of 24 serotypes were detected with predominant serotypes of Enteritidis (34.5%, 116/336), Derby (17.3%, 58/336) and Indiana (10.4%, 35/336). A total of 27 ST types were detected, the dominant type was ST11; ST types were in good consistency with serotypes; The detection rates of resistant genes referred to aminoglycosides, fluoroquinolones, β-lactams, sulfonamides and tetracyclines are more than 48%, and the first two reached 100%. The prediction of drug resistance genes was consistent with the results of antimicrobial resistance phenotype. A total of 122 virulence genes were predicted, 74 of which existing among all isolates.Conclusion:Salmonella in meat from the wholesale markets of Beijing has a high proportion of multiple drug resistance, a complex drug resistance spectrum, a variety of serotypes and ST types, and a high carrying rate of drug resistance gene and virulence gene; drug resistance phenotype and genotype are relatively consistent.

Objective:To study the types of pathogenic gene mutations and their main clinical characteristics in children with glucose-6-phosphate dehydrogenase (G6PD) deficiency in Zunyi area.Methods:Children with clinical manifestations of "yellow staining" or "suspected yellow staining" who were admitted to Guizhou Children's Hospital, Affiliated Hospital of Zunyi Medical University, from September 13, 2018 to September 13, 2020 were selected for G6PD gene mutation detection by multicolor probe melting curve analysis, and the pathogenic gene mutation types and clinical characteristics of children with G6PD deficiency were analyzed.Results:The results of G6PD gene mutation detection showed that among the 1 740 children tested, 119 were positive for gene mutation, and the positive detection rate was 6.84%. The proportion of male infants was higher than that of female infants, and the difference was statistically significant (91 males and 28 females, χ 2 = 15.10, P < 0.001); infancy accounted for 63.87% (76/119), and early childhood accounted for 18.49% (22/119). A total of 11 known pathogenic gene mutation types and 1 unknown mutation were detected. Among the top 4 pathogenic gene mutations, the overall was c.1024 C>T, c.1376 G>T, c.1388 G>A and c.95 A>G, male was c.1376 G>T, c.1388 G>A, c.1024 C>T and c.95 A>G; female was c.1024 C>T, c.95 A>G, c.1388 G>A and c.519 C>T. Among the 119 children with G6PD gene mutation, 90 cases had varying degrees of jaundice, including 36 cases of severe and more severe jaundice (including 2 cases of extremely severe neonatal bilirubin encephalopathy), and 54 cases of mild to moderate jaundice; 37 cases had anemia of different degrees, including 6 cases of mild anemia, 12 cases of moderate anemia, and 19 cases of severe or more severe anemia (including 1 case of extremely severe anemia). Conclusions:There are 12 types of gene mutations in children with G6PD deficiency in Zunyi area, and the most common mutation types are c.1024 C>T, c.1376 G>T, c.1388 G>A and c.95 A>G. Children with G6PD deficiency are often accompanied by varying degrees of jaundice and anemia.