CCNI2 plays a promoting role in the progression of colorectal cancer.

Colorectal cancer (CRC) is one of the most common malignancies and most of the patients diagnosed with advanced CRC have unsatisfactory treatment effect and poor prognosis. The purpose of this study was to investigate the effect of CCNI2 on the development of CRC. In this sutdy, immunohistochemical staining was used to detect CCNI2 expression levels in clinical samples, meanwhile, the Kaplan-Meier survival analysis was conducted. Celigo cell counting assay was used for screening shCCNI2s. QPCR and WB were performed to verify knockdown efficiency of CCNI2. Cell proliferation, colony formation, cell cycle, apoptosis, and mechanism investigation of CCNI2 knockdown were investigated by MTT assay, colony formation assay, fluorescence-activated cell sorting, and human apoptosis antibody array, respectively. Otherwise, the mouse model of CCNI2 knockdown was also constructed. The results of immunohistochemical staining and qPCR indicated that CCNI2 had a high expression level in the CRC tissues and cell lines. Kaplan-Meier survival analysis manifested that the high expression of CCNI2 suggested poor prognosis. The expression of CCNI2 was significantly reduced by CCNI2-siRNAs, and the downregulated expression level of CCNI2 inhibited CRC cell proliferation and colony formation, arrested cell cycle in G2 phase, as well as promoted cell apoptosis. The various indexes of solid tumor in mice models indicated that CCNI2 knockdown could suppress the growth of CRC tumor. Based on the comprehensive analysis of the above results, CCNI2 was contributed to the progression of CRC and could serve as a prognostic marker for CRC.

[Expression of glucocorticoid receptors alpha and beta in mononuclear cells of peripheral blood in patients with glucocorticoid-induced ocular hypertension].

OBJECTIVE: To study the expression of glucocorticoid receptors (alpha and beta) in mononuclear cells of peripheral blood (PBMCs) in patients with glucocorticoid-induced ocular hypertension (GIOH) and the relationship between of the expression of GRalpha and GRbeta in PBMCs and its susceptibility to GIOH. METHODS: Case control study. Thirty-two patients with anaphylactic conjunctivitis were enrolled in this study. All of whom were received topical application of 0.1% dexamethasone. The patients with the elevation of intraocular pressure (IOP) over 8 mm Hg(1 mm Hg = 0.133 kPa) or higher within two weeks were defined as GIOH and the others were considered as control group. There were no statistical difference in sex, average age, and baseline IOP between two groups. Each group consisted of sixteen patients. GRalpha and GRbeta mRNA (relative value) in PBMCs were detected with semi-quantitative reverse transcriptional polymerase chain reaction (RT-PCR), GRalpha and GRbeta protein (positive ratio) in PBMCs examined with fluorescent labelling flow cytometry. RESULTS: The GRalpha mRNA/GAPDH ratio of GIOH group was significantly (t = 3.872, P < 0.05) higher than that of control group (1.152 +/- 0.057 vs 1.048 +/- 0.031). The GRbeta mRNA/GAPDH of GIOH group was lower than that of control group's (1.055 +/- 0.034 vs 1.063 +/- 0.035), but was not statistically different (t = 0.419, P > 0.05). GRalpha positive percentage was significantly (t = 8.513, P < 0.01) higher in PBMCs of GIOH group than that of the control group (93.10 +/- 7.35)% vs (46.00 +/- 13.11)%, whereas GRbeta positive percentage was significantly (t = 4.842 P < 0.01) lower in PBMCs of GIOH group than that in control group (12.50 +/- 4.18)% vs (23.83 +/- 3.92)%. CONCLUSIONS: The higher expression of GRalpha in PBMCs in patients may have an implication of susceptibility to GIOH and warrant further investigation.

Abnormal composition of gut microbiota contributes to delirium-like behaviors after abdominal surgery in mice.

AIMS: Anesthesia and surgery can cause delirium-like symptoms postoperatively. Increasing evidence suggests that gut microbiota is a physiological regulator of the brain. Herein, we investigated whether gut microbiota plays a role in postoperative delirium (POD). METHODS: Mice were separated into non-POD and POD phenotypes after abdominal surgery by applying hierarchical clustering analysis to behavioral tests. Fecal samples were collected, and 16S ribosomal RNA gene sequencing was performed to detect differences in gut microbiota composition among sham, non-POD, and POD mice. Fecal bacteria from non-POD and POD mice were transplanted into antibiotics-induced pseudo-germ-free mice to investigate the effects on behaviors. RESULTS: α-diversity and ß-diversity indicated differences in gut microbiota composition between the non-POD and POD mice. At the phylum level, the non-POD mice had significantly higher levels of Tenericutes, which were not detected in the POD mice. At the class level, levels of Gammaproteobacteria were higher in the POD mice, whereas the non-POD mice had significantly higher levels of Mollicutes, which were not detected in the POD mice. A total of 20 gut bacteria differed significantly between the POD and non-POD mice. Interestingly, the pseudo-germ-free mice showed abnormal behaviors prior to transplant. The pseudo-germ-free mice that received fecal bacteria transplants from non-POD mice but not from POD mice showed improvements in behaviors. CONCLUSIONS: Abnormal gut microbiota composition after abdominal surgery may contribute to the development of POD. A therapeutic strategy that targets gut microbiota could provide a novel alterative for POD treatment.