Zanthoxylum bungeanum root-rot associated shifts in microbiomes of root endosphere, rhizosphere, and soil.

Root-rot disease has lead to serious reduction in yields and jeopardized the survival of the economically and ecologically important Zanthoxylum bungeanum trees cultured in Sichuan Province. In order to investigate the interaction between the microbiome and the root-rot disease, a metagenomic analysis was performed to characterize the microbial communities and functions in Z. bungeanum root endosphere, rhizosphere and bulk soil with/without root-rot disease. Soil physicochemical properties, microbial population size and enzyme activities were also analyzed for finding their interactions with the root-rot disease. As results, lower total nitrogen (TN) and available phosphorus (AP) contents but higher pH in rhizosphere and bulk soil, as well as lower substrate-induced respiration (SIR) and higher protease activity in bulk soil of diseased trees were found, in comparison with that of healthy trees. Microbial diversity and community composition were changed by root-rot disease in the endosphere, but not in rhizosphere and bulk soils. The endophytic microbiome of diseased trees presented higher Proteobacteria abundance and lower abundances of Bacteroidetes, Firmicutes and dominant fungal phyla. The relative abundances of nitrogen cycle- and carbon cycle-related genes in endophytic microbiomes were different between the diseased and healthy trees. Based on ANOSIM and PCoA, functional profiles (KEGG and CAZy) of microbiomes in rhizosphere and bulk soil shifted significantly between the diseased and healthy trees. In addition, soil pH, TN, AP, SIR, invertase and protease were estimated as the main factors influencing the shifts of taxonomic and functional groups in microbiomes of rhizosphere and bulk soil. Conclusively, the imbalance of root and soil microbial function groups might lead to shifts in the root endosphere-rhizosphere microenvironment, which in turn resulted in Z. bungeanum root-rot.

[Cuscuta chinensis flavonoids reduce the expression of GM-CSF in the testis of oligozoospermia rats].

OBJECTIVE: To investigate the effect of Cuscuta chinensis flavonoids (CCF) on the expression of the granulocyte-macrophage colony-stimulating factor (GM-CSF) in the testis of the rat with oligozoospermia (OZ). METHODS: Thirty SD male rats were randomly divided into three groups of equal number, blank control, OZ model control and CCF intervention. The OZ model was established in the latter two groups by intraperitoneal injection of cyclophosphamide at 30 mg/kg qd for 5 successive days. From the 6th day, the rats in the CCF intervention group were treated intragastrically with mixed suspension of CCF at 5 mL/kg and those in the other two groups with normal saline, all for 4 weeks. The epididymal sperm concentration and motility and the testicular morphology were examined and the expression of GM-CSF in the testis tissue detected with the SELDI Protein Chip. RESULTS: Compared with the rats in the blank control and CCF intervention groups, the OZ model controls showed dramatically decreased epididymal sperm concentration and motility (both P < 0.01) and significant morphological changes in the testis with deformed seminiferous tubules and reduced number and disordered arrangement of spermatogenic cells. Normal testicular morphology was observed in the CCF intervention group and there were no statistically significant differences in sperm concentration and motility between the CCF intervention and blank control groups (P > 0.05). The expression of GM-CSF was significantly up-regulated in the testis tissue of the OZ model controls but lower than the minimum value obtained with the SELDI Protein Chip in the blank control and CCF intervention groups. CONCLUSIONS: Cuscuta chinensis flavonoids can significantly down-regulate the expression of GM-CSF in the testis of the rats with cyclophosphamide-induced oligozoospermia.

Prognostic Significance of Monosomal Karyotype in Adult Patients With Acute Myeloid Leukemia Treated With Risk-Adapted Protocols.

BACKGROUND: The monosomal karyotype (MK) is a well-known adverse prognostic factor and has been found to be related to poor outcome in patients with acute myeloid leukemia (AML). However, the outcome in MK-positive AML patients undergoing different therapies has not been well investigated. PATIENTS AND METHODS: We retrospectively analyzed clinical and laboratory features in 225 MK-positive AML patients. Clinical outcome of overall survival (OS) and disease-free survival (DFS) was evaluated in patients according to age group and in patients who received different therapy protocols. RESULTS: The proportion of MK-positive patients increased along with age. Also, patients who were treated with high-dose cytarabine (HD-Ara-C) as consolidation therapy followed by allogeneic hematopoietic stem cell transplantation (allo-HSCT) demonstrated longer OS and DFS compared to allo-HSCT or HD-Ara-C alone. Patients treated with allo-HSCT alone exhibited longer DFS compared to patients treated with HD-Ara-C alone. No difference in OS was discovered between these 2 single protocols. CONCLUSION: MK was associated with a lower complete remission rate. HD-Ara-C therapy followed by allo-HSCT could improve the prognosis of MK-positive AML patients.

Imatinib and bortezomib induce the expression and distribution of anaphase-promoting complex adaptor protein Cdh1 in blast crisis of chronic myeloid leukemia.

Anaphase promoting complex cofactor Cdh1 plays a critical role in tumor suppression and genomic stability in cancer. However, its role in chronic myeloid leukemia (CML) remains unclear. We treated both wild-type and imatinib-resistant K562 cells with imatinib or nilotinib and bortezomib, respectively. The siRNAs of Cdh1 and Skp2 were designed and transiently transfected with HiPerFect transfection reagent into CML cells. Expression of Cdh1-Skp2-p27 pathway proteins were detected by Western blotting. Cell cycle, cell apoptosis and cellular morphology were detected by flow cytometry and Wright staining. Our study revealed that Cdh1 was expressed at lower levels in imatinib-resistant CML blast crisis (BC) patients than imatinib-sensitive ones. Moreover, imatinib and bortezomib induced cell cycle quiescence or arrest, upregulation and nuclear relocation of Cdh1 in CML cells. Furthermore, nilotinib and bortezomib resulted in upregulation of Cdh1 in imatinib-resistant CML cells. Conversely, Cdh1 silencing resulted in stabilization of Skp2 and Cdc20, subsequently promoting G1-S transition and formation of multinucleated cells. Our study shows that TKIs and bortezomib can regulate the cell cycle and cell apoptosis via regulation of the expression and redistribution of Cdh1 in CML-BC, which sheds light on the orchestration of crosstalk between TKIs and bortezomib in imatinib-resistant CML-BC. Additionally, Cdh1 tends to play an important role in maintenance of genomic stability, the detailed mechanisms deserve further study.