Search

The control of soil nitrous dioxide (N2O) emission is of great importance to deal with climate change. We conducted a meta-analysis to quantify the potential effect of biotic and abiotic factors possibly altering the role of (AM) fungi in reducing soil N2O emission directly and indirectly via NH3 emission in natural and managed ecosystems. Our dataset was built based on 21 studies in both English (15 studies) and Chinese language (5 studies), including experiment-, plant-, AMF-, nutrient- and soil-related moderator variables. We found that the AM fungi reduced soil N2O emission by 11% (overall effect) and this reduction was observed in 84% of all trials. This effect varied largely from 265% decrease to 345% increase. Due to data limitations, it was still unclear that how AM effect was manipulated by these biotic and abiotic factors. We observed that measurement times, P availability and micronutrient addition had a compounding effect. We improved the sensitivity analysis techniques to evaluate the disproportional influence of a single study. In conclusion, AM fungi had a potential role in reducing soil N2O emission and currently, the available data did not support a meta-analysis on factors manipulating this effect. We call for more lab and field research targeting how biotic and abiotic factors alter this AM fungal effect on soil N2O emission.

Background: Methylene tetrahydrofolate reductase (MTHFR) catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a cosubstrate for homocysteine remethylation to methionine. Single nucleotide polymorphisms (SNP) of MTHF rs1801133 C>T can influence susceptibility to colorectal cancer. However, an association between MTHFR rs1801133 C>T polymorphisms and response to 5-Fluorouracil (5-FU) based chemotherapy in patients with colorectal cancer was not clear. Methods: Studies relevant to MTHFR rs1801133 C>T polymorphisms and response to 5-FU based chemotherapy in patients with colorectal cancer were systematic searched in the electronic databases of PubMed, Web of Science, Embase, and China National Knowledge Infrastructure (CNKI). The genotypes of CC, CT, and TT were extracted from each included publication. The genotypes CC, CT, and TT distribution in 5-FU based chemotherapy response and resistance groups were calculated and pooled through random or fixed effect model by the effect size of odds ratio (OR) and 95% confidence interval (95% CI). The publication bias was evaluated through Begg’s funnel plot and Egger’s line regression test. Results: After searching the electronic databases, 16 studies related to MTHFR gene rs1801133 C>T polymorphisms and a response to 5-FU based chemotherapy in patients with colorectal cancer were included in the present meta-analysis. The pooled data showed no statistical difference in tumor response rate between CT+TT and CC groups in the dominant genetic model CT+CC vs CC (OR=1.21, 95% CI: 0.93~1.59, p>0.05) and recessive model TT vs CT+CC (OR=1.37, 95% CI: 0.91~2.06, p>0.05). The grade 3-4 adverse reaction rate between CT+TT and CC groups also had no statistical difference in the dominant genetic model CT+CC vs CC (OR=0.90, 95% CI: 0.76~1.07, p>0.05) and recessive model TT vs CT+CC (OR=1.12, 95% CI: 0.84~1.50, p>0.05). The Begg’s funnel plot and Egger’s line regression test demonstrated no publication bias. Conclusion: The response and adverse reaction of 5-FU based chemotherapy in colorectal patients were not different in terms of MTHFR rs1801133 C>T polymorphisms.

Osteosarcoma (OS) is one of the most common malignancies of bone. This study was aimed to explore the anti-metastatic effect of euxanthone on OS. Adhesion assay and Transwell assay were used to examine the effect of euxanthone on adhesion, migration and invasion of OS cells. COX-2-over-expressing plasmid was applied to transfect OS cells to assess whether COX-2 affects the anti-metastatic function of euxanthone. PDCD4 knockdown and miR-21 mimic were applied to assess whether euxanthone suppresses the transactivation of c-jun via modulating miR-21-PDCD4 signaling. The effect of euxanthone in vivo was also examined by lung metastasis assay. Euxanthone, a xanthone derivative extracted from Polygala caudata, has been found to exhibit anti-neoplastic activities. In present study, our results showed that euxanthone suppressed cell adhesion, migration, and invasion in OS cells. Our experimental data also showed that repression of COX-2 by euxanthone mediated its anti-metastatic activities. Moreover, our findings revealed that euxanthone modulated the COX-2 expression through the miR-21/PDCD4/c-jun signaling pathway. The anti-metastatic activities of euxanthone were also validated in a pulmonary metastasis model. Taken together, our results highlighted the potential of euxanthone to be used in the treatment of OS. Anat Rec, 302:1399-1408, 2019. © 2018 Wiley Periodicals, Inc.

Human oocyte maturation is a precondition for fertilization and ensuing embryonic development. Previously, we identified TUBB8 variants as a genetic determinant of human oocyte maturation arrest and showed that these variants cause variable and mixed phenotypes in oocyte maturation and early embryo development. We also estimated that rare inherited or de novo variants in the TUBB8 gene accounted for 30% of individuals in a small cohort of patients affected by oocyte maturation arrest. In the present study, we recruited a further 87 patients from unrelated families diagnosed with oocyte maturation or early embryonic arrest and identified 30 patients carrying TUBB8 variants. The corresponding phenotypes not only include oocyte maturation arrest, failure of fertilization, and early embryonic arrest, but also extend to the new phenotype of failure of embryo implantation. These observations provide the most detailed mutational and phenotypic spectrum of TUBB8, further extend the spectrum of variants and dysfunctional oocyte and embryo phenotypes caused by TUBB8 variants, and confirm previous findings for a critical role of TUBB8 during oocyte maturation and early embryonic development. Thus, TUBB8 mutation screening might not only be a genetic diagnostic marker for patients with oocyte maturation arrest, but might also have clinical implications for evaluating the competence of patients’ functional oocytes with first polar body (PB1).