Objective To investigate the clinical value of the polymerase chain reaction (PCR) technique in detection of pediatric helicobacter pylori(HP) infection.Methods A total of 130 children with different digestive tract symptoms received esophagogastroduodenoscopy,and 120 children between 3 and 17 years old were enrolled.The gastric antrum mucosa was taken under the gastroscope for 2 blocks,and the gastric juice was absorbed as the specimen.One block of gastric antrum mucosa was examined histopathologi-cally,and the other block of gastric antrum mucosa and gastric juice were examined by PCR.We used the primers UreC,HP-16s,CSTP to detect HP,and then used the primers Cag750 and Cag595 to detect CagA. Results A total of 28 cases(23.33%) of upper gastrointestinal ulcer were detected by gastroscopy,and HP was detected by histopathological method in 26 cases(21.67%),and 41 cases(34.17%) were detected by PCR method.The detection rate of HP by PCR was significantly higher than that of HP in pathological method (χ2= 4.659,P = 0.031). By pathological examination of HP,14 cases (50%) and 12 cases (13.04%) with peptic ulcers and no peptic ulcers were detectd,and the difference in detection rate was statistically significant(χ2=17.275,P<0.001).Samples of children with peptic ulcers and no peptic ulcers were detected in 16 cases(57.14%) and 25 cases (27.17%) by PCR,and the difference in detection rate was statistically significant (χ2=8.572,P=0.003).The CagA were detected in 7 cases of peptic ulcers and 7 cases of non peptic ulcers by PCR,and the difference in detection rate was statistically significant(25.00%vs 7.61%,χ2=6.300,P=0.012).Conclusion The PCR method could quickly and sensitively detect the HP and its CagA gene,and the detection of gastric mucosa and gastric juice by PCR could improve the detection rate of HP.A combination of PCR and pathological method is suggested as the detection method for children′s HP infection.

Objective To investigate the effects of Helicobacter pylori( HP) on gut microbiota in children by comparing the difference of gastric microbiota between HP-positive and HP-negative individuals. Methods Genome was extracted from excrements of 8 HP-positive cases and 8 HP-negative cases. After genomic extraction,the hypervariable region of 16S rRNA gene were amplified and a small fragment library was constructed,and high-throughput sequencing was carried out, then the data of the lower machine was effectively sequenced by biological information processing. We could seek for the species that have changed significantly due to HP infection by comparing the differences in the composition of intestinal flora between the two groups. Results Compared with HP-negative group,HP-positive group showed less OTUs. The dif-fenece of biodiversity between them was conspicuous. The Caproiciproducens,Enterobacteriaceae,Enterobac-teriales,Blautia-obeum,Esherichia-albertli,human-gut-metagenome and Dorea in HP-positive group were sig-nificantly higher than HP-negative group,while the Bacteroides-uniformis, Bacteroidaceae and Bacteroides in HP-negative group were significantly higher than HP-positive group. Conclusion HP could significantly affect the structure and composition of gut microbiota in children.

Ureaplasma is a common pathogen in the human reproductive tract and consists of two distinct biotypes: biotype 1 and biotype 2. In 2002, based on the differences between biotypes, biotype 1 was further classified to a separate species named Ureaplasma parvum (Up), whereas biotype 2 is referred to as Ureaplasma urealyticum (Uu). Uu infection is associated with various urogenital diseases including infertility, preterm birth, and urethritis, while the pathogenicity of Up remains controversial. Researches have shown that different serotypes showed distinct pathogenicity and drug resistance in different diseases and populations, highlighting the importance of clinical tests of serotype and biotype for Ureaplasma. This article reviews the factors that may be associated with Ureaplasma infection, and the current status of the diagnosis and treatment in clinical practice, aiming to provide insights into the clinical significance and necessity of biotypes and serotype tests for Ureaplasma-positive cases and to serve as a reference for the clinical diagnosis and treatment of related diseases.

Cancer stands as one of the predominant causes of mortality globally, necessitating ongoing efforts to develop innovative therapeutics. Historically, natural products have been foundational in the quest for anticancer agents. Bulbocodin D (BD) and Bulbocodin C (BC), two bibenzyls derived from Pleione bulbocodioides (Franch.) Rolfe, have demonstrated notable in vitro anticancer activity. In human lung cancer A549 cells, the IC_50s for BD and BC were 11.63 and 11.71 μmol·L^-1, respectively. BD triggered apoptosis, as evidenced by an upsurge in Annexin V-positive cells and elevated protein expression of cleaved-PARP in cancer cells. Furthermore, BD and BC markedly inhibited the migratory and invasive potentials of A549 cells. The altered genes identified through RNA-sequencing analysis were integrated into the CMap dataset, suggesting BD's role as a potential signal transducer and activator of transcription 3 (STAT3) inhibitor. SwissDock and MOE analyses further revealed that both BD and BC exhibited a commendable binding affinity with STAT3. Additionally, a surface plasmon resonance assay confirmed the direct binding affinity between these compounds and STAT3. Notably, treatment with either BD or BC led to a significant reduction in p-STAT3 (Tyr 705) protein levels, regardless of interleukin-6 stimulation in A549 cells. In addition, the extracellular signal-regulated kinase (ERK) was activated after BD or BC treatment. An enhancement in cancer cell mortality was observed upon combined treatment of BD and U0126, the MEK1/2 inhibitor. In conclusion, BD and BC emerge as promising novel STAT3 inhibitors with potential implications in cancer therapy.
Humans ; Lung Neoplasms/metabolism* ; STAT3 Transcription Factor/metabolism* ; Antineoplastic Agents/chemistry* ; A549 Cells ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation