Alteration of the faecal microbiota composition in patients with constipation: evidence of American Gut Project.

There is limited information is known about the composition difference of the gut microbiota in patients with constipation and healthy controls. Here, the faecal 16S rRNA fastq sequence data of microbiota from the publicly available American Gut Project (AGP) were analysed. The tendency score matching (PSM) method was used to match in a 1:1 manner to control for confounding factors age, gender, body mass index (BMI), and country. A total of 524 participants including 262 patients with constipation and 262 healthy controls were included in this analysis. The richness and evenness of the gut microbiota in the constipation group were significantly lower than those in the control group. The dominant genera in the constipation group include Escherichia_Shigella, Pseudomonas, and Citrobacter. The dominant genera in the control group include Faecalibacterium, Prevotella, Roseburia, Clostridium_XlVa, and Blautia. The abundance of three butyrate production-related pathways were significantly higher in the constipation group than in the control groups. There was no significant difference in the diversity and gut microbiota composition in patients with constipation at different ages. In conclusion, patients with constipation showed gut microbiota and butyrate metabolism dysbiosis. This dysbiosis might provide a reference for the diagnosis and clinical therapy of diseases.

Clostridium butyricum promotes intestinal motility by regulation of TLR2 in interstitial cells of Cajal.

OBJECTIVE: Clostridium butyricum (C. butyricum) as a probiotic has been reported to have an important role in the pathogenesis of gastrointestinal diseases. However, the effects of C. butyricum on regulation of intestinal motility of ulcerative colitis (UC) remain unclear. Our study aimed to explore the cross-regulation effect of C. butyricum and toll-like receptor 2 (TLR-2) on UC. MATERIALS AND METHODS: Interstitial cells of Cajal (ICCs) were treated by C. butyricum for 2 h, the mRNA and protein levels of TLR-2, IL-6, and IL-8 were detected by RT-qPCR and Western blot. Then, TLR2-specific small interfering RNA (si-TLR2) was transfected into ICCs, and the relative expressions of IL-6 and IL-8, SCF, cell viability, ghrelin, SP, and ET were measured by RT-qPCR, Western blot, CCK-8, and ELISA. Besides, the signal pathways of NF-κB and JNK were determined by Western blot. RESULTS: C. butyricum significantly increased TLR2, IL-6, and IL-8 expressions in ICCs. However, TLR2 silence alleviated C. butyricum-induced IL-6 and IL-8 expressions. Moreover, TLR2 silence significantly inhibited C. butyricum-induced cell viability in ICCs. Additionally, C. butyricum significantly increased SCF expression and promoted the secretion of ghrelin and SP. However, a significant reduction in the levels of SCF, ghrelin, and SP was evident in the silence of TLR2 expression. Besides, TLR2 silence reduced C. butyricum-activation NF-κB and JNK signal pathways in ICCs. CONCLUSIONS: These findings revealed that C. butyricum promoted intestinal motility by regulation of TLR2 in ICCs, which contributed to understand the molecular mechanisms of C. butyricum on UC.

Effects of miR-223 on colorectal cancer cell proliferation and apoptosis through regulating FoxO3a/BIM.

OBJECTIVE: Colorectal cancer is a common malignant tumor of the digestive tract. It frequently occurs at the junction of the rectum and sigmoid colon. It is characterized by high mortality and poor prognosis. Bcl-2 interacting mediator of cell death (BIM) plays a role in the regulation of cell proliferation and apoptosis, and involves in the pathogenesis of colorectal cancer. The transcription factor forkhead, transcription factor O subfamily 3a (FoxO3a) plays a role in the regulation of BIM expression and is associated to the pathogenesis of colorectal cancer. Bioinformatics analysis suggests that there is a targeted relationship between FoxO3a and microRNA-223 (miR-223). This study aims to investigate effects of miR-223 on the regulation of FoxO3a/BIM signaling pathway and colorectal cancer cell proliferation and apoptosis. MATERIALS AND METHODS: Colorectal cancer cell line SW620 and normal colorectal epithelial cell line NCM460 were cultured in vitro. Dual luciferase reporter assay was used to validate the relationship between miR-223 and FoxO3a. Flow cytometry was adopted to detect apoptosis. EdU staining was applied to test cell proliferation. Western blot was selected to determine FoxO3a and BIM protein expressions. RESULTS: There was targeted regulatory relationship between miR-223 and FoxO3a. MiRa-223 up-regulated, FoxO3a and BIM expressions reduced, and cell proliferation was enhanced in SW620 cells compared with NCM460 cells. MiR-223 inhibitor or pIRES2-FoxO3a transfection significantly increased FoxO3a and BIM expressions, attenuated cell proliferation, and enhanced cell apoptosis. CONCLUSIONS: MiR-223 targeted inhibited expression of FoxO3. Down-regulating the expression of miR-223, it increased the expressions of FoxO3a and BIM, weakened SW620 cells proliferation and induced apoptosis.

Predictive role of cytokines IL-10, IL-12 and TNF-α gene polymorphisms for the development of osteonecrosis of the femoral head in the Chinese Han population.

The progressive neurodegenerative process in osteonecrosis of the femoral head (ONFH) is accompanied by chronic inflammation, including activation of microglia and astrocytes that express pro-inflammatory cytokines. Up to now, numerous studies of genetic epidemiology have assessed the association of anti- and pro-inflammation cytokines gene polymorphisms and risk of ONFH in different populations, but contradictory results were obtained due to the genetic heterogeneity of in different populations. In the study, 250 ONFH patients and 228 matched healthy controls from Shandong Province were recruited to evaluate the influence of interleukin-10 (IL-10) rs1800872, IL-12 rs3212227 and tumor necrosis factor-(TNF-α) rs1800629 polymorphism in ONFH. Single nucleotide polymorphism (SNP) locus was genotyped using the PCR-RFLP method. The genotypic and allele frequencies of TNF-α and IL-10 did not show significant difference between ONFH patients and normal controls. However, the frequencies of wild (AA) and homozygous mutant (CC) genotype of IL-12 rs3212227 in controls were more than that in ONFH patients, but that of the heterozygous genotype was more in patients with ONFH. Thus, our findings indicate that IL-12 rs3212227 AC genotype confer genetically susceptibility to ONFH in the Chinese Han population.

[Follicular thyroid carcinoma metastatic to the lung and bone and cutaneous: one case report].

Follicular thyroid carcinoma usually metastasizes through a hematogenous route, the most frequent sites of distant metastases are bone and lung, cutaneous metastasis is exceptionally rare. In this paper, we report a patient with lung, bone and subcutaneous metastasis of well-differentiated forms of follicular thyroid carcinoma, 19 years after resection of thyroid tumor.

[Protective effect of tetrandrine on pancreatic islet cells damaged by alloxan in rats].

Tetrandrine (TET, 100 mg/kg) injected intraperitoneally could prevent rats from diabetes induced by alloxan. After 48 h of injection of alloxan, the blood sugar of the preventive group decreased from the control value of 25.46 +/- 1.21 mmol/L to 7.63 +/- 0.44 mmol/L (P < 0.001) while the serum insulin level increased to 11.33 +/- 1.97 microU/ml and the plasma glucagon concentration to 66.85 +/- 5.07 pg/ml respectively from the control group's value of 7.13 +/- 0.45 microU/ml and 90.35 +/- 8.33 pg/ml. In glucose tolerance test, TET 100 mg/kg showed that the abnormal glucose tolerance induced by alloxan could be improved. The blood sugar area under the glucose tolerance curve of the preventive group decreased from the control groups level of 113.28 +/- 5.02 mmol.h/L to 29.45 +/- 1.63 mmol.h/L (P < 0.001). Immunohistochemical observation of islet beta cells confirmed that TET could markedly prevent beta cells from injuries induced by alloxan and there was no obvious change in the appearance of islet beta cells in the preventive group. The above results suggested that TET could protect pancreatic islet beta cells from injuries caused by Alloxan.