Turtle peptide and its derivative peptide ameliorated DSS-induced ulcerative colitis by inhibiting inflammation and modulating the composition of the gut microbiota.

Ulcerative colitis (UC) is a recurrent intestinal disease with an increasing incidence worldwide that seriously affects the life of patients. Turtle peptide (TP) is a bioactive peptide extracted from turtles that has anti-inflammatory, antioxidant and anti-aging properties. However, studies investigating the effect of TP on the progression of UC are lacking. The aim of this study was to investigate effects and underlying mechanisms of TP and its derivative peptide GPAGPIGPV (GP-9) in alleviating UC in mice. The results showed that 500 mg/kg TP treatment significantly ameliorated colitis symptoms and oxidative stress in UC mice. TP alleviated intestinal barrier damage in UC mice by promoting mucosal repair and increasing the expression of tight junction proteins (ZO1, occludin and claudin-1). TP also modulated the composition of the gut microbiota by increasing the abundance of the beneficial bacteria Anaerotignum, Prevotellaceae_UCG-001, Alistipes, and Lachno-spiraceae_NK4A136_group and decreasing the abundance of the harmful bacteria Prevotella_9 and Parasutterella. Furthermore, we characterized the peptide composition of TP and found that GP-9 ameliorated the symptoms of dextran sodium sulfate (DSS)-induced colitis in mice by inhibiting the TLR4/NF-κB signaling pathway. In conclusion, TP and its derivative peptides ameliorated DSS-induced ulcerative colitis by inhibiting the expression of inflammatory factors and modulating the composition of the intestinal microbiota; this study provides a theoretical basis for the application of TP and its derivative peptides for their anti-inflammatory activity.

Review of DNA repair enzymes in bacteria: With a major focus on AddAB and RecBCD.

DNA recombination repair systems are essential for organisms to maintain genomic stability. In recent years, we have improved our understanding of the mechanisms of RecBCD/AddAB family-mediated DNA double-strand break repair. In E. coli, it is RecBCD that plays a central role, and in Firmicute Bacillus subtilis it is the AddAB complex that functions. However, there are open questions about the mechanism of DNA repair in bacteria. For example, how bacteria containing crossover hotspot instigator (Chi) sites regulate the activity of proteins. In addition, we still do not know the exact process by which the RecB nuclease or AddA nuclease structural domains load RecA onto DNA. We also know little about the mechanism of DNA repair in the industrially important production bacterium Corynebacterium glutamicum (C. glutamicum). Therefore, exploring DNA repair mechanisms in bacteria may not only deepen our understanding of the DNA repair process in this species but also guide us in the targeted treatment of diseases associated with recombination defects, such as cancer. In this paper, we firstly review the classical proteins RecBCD and AddAB involved in DNA recombination repair, secondly focus on the novel helical nuclease AdnAB found in the genus Mycobacterium.

Neuropilin-1 is associated with the prognosis of cervical cancer in Henan Chinese population.

Objective: Neuropilin-1 has been reported to be a valuable diagnostic biomarker in patients with cervical intraepithelial neoplasia (CIN) and early cervical cancer. The aim of this study was to investigate the association between Neuropilin-1 and the prognosis of cervical cancer in Henan Chinese population. Methods: Tissues were collected in The Third Affiliated Hospital of Zhengzhou University between 2010 and 2012, determining the level and expression of Neuropilin-1 in different cervical lesions by immunohistochemistry. The cell proliferation assay, wound-healing assays and Transwell assay were performed to explore the ability of proliferation, migration and invasion for Hela and Caski cells after NRP-1 was knocked down by shRNA transfection. Western blotting was performed to investigate the role of NRP-1 in endothelial-to-mesenchymal transition (EndMT). Tumor xenografts model was used to evaluate the effect of NRP-1 on the tumor growth. Results: The expression of NRP-1 was upregulated in the tumor tissues compared with the CIN and normal tissues (P<0.0001). The overall survival time of the high NRP-1 expression group was significantly shorter than that of the low NRP-1 expression group (P<0.0001); NRP-1-depleted cells had dramatically lower rate of proliferation, migration and invasion compared to control cells (all P<0.05). Depletion of NRP-1 significantly suppressed the growth of CaSki xenograft tumor in nude mice. Conclusions: The current study demonstrated that NRP-1 expression is significantly correlated with the progression of CC. Notably, high NRP-1 expression is correlated with a poorer survival in patients with CC, and has been shown to be an independent prognostic factor.

Efficacy and Safety of Chemotherapy Combined with Stereotactic Radiotherapy in the Treatment of Nasopharyngeal Carcinoma.

BACKGROUND The aim of this study was to investigate the efficacy and safety of chemotherapy (CT) combined with stereotactic radiotherapy (SRT) in the treatment of nasopharyngeal carcinoma (NPC). MATERIAL AND METHODS A total of 329 NPC patients without any previous treatment were included in this study between January 2009 and November 2013. These patients were divided into three groups: CT group (n=114), SRT group (n=109), and CT + SRT group (n=106). Contrast-enhanced nasopharyngeal computed tomography (CT)/magnetic resonance (MR) scan was performed on the third month after treatment. Short-term efficacy was evaluated according to the Response Evaluation Criteria in Solid Tumors (RECIST). Toxicity was graded according to the Acute Radiation Morbidity Scoring Criteria (RTOG) and the World Health Organization (WHO) toxicity grading scale. Overall survival (OS), progression free survival (PFS), and incidence rate of acute toxicity (grade ≥3) were calculated after a 24 month follow-up. RESULTS Total response rate of all patients was 85.41%. Compared with the CT group and the SRT group, the CT + SRT group showed a substantially improved efficacy in NPC treatment. The incidence rate of the acute toxicity in the CT + SRT group was slightly higher than in the CT group and the SRT group, but the difference was not statistically significant. No treatment-related deaths were observed. The CT + SRT group had the highest two-year OS and PFS, followed by the CT group and the SRT group. CONCLUSIONS It was shown that NPC patients treated with CT + SRT had better short- and long-term efficacy than those treated with CT or SRT alone.

In Vivo and In Vitro Effects of ATM/ATR Signaling Pathway on Proliferation, Apoptosis, and Radiosensitivity of Nasopharyngeal Carcinoma Cells.

AIM: The study investigated the ability of ataxia-telangiectasia mutated (ATM)/Rad3-related (ATR) signaling pathway to influence the proliferation, apoptosis, and radiosensitivity of nasopharyngeal carcinoma (NPC) cells. MATERIALS AND METHODS: NPC tissues and corresponding adjacent normal tissues were collected from 143 NPC patients. The NPC CNE2 cells were assigned into a control group, X-ray group, CGK-733 group, and X-ray+CGK-733 group. The mRNA levels of ATM and ATR were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) and the protein levels of ATM and ATR using western blotting. The positive expression of ATM and ATR in tissues and nude mouse tumor tissues was determined by immunohistochemistry. Cell proliferation, migration, invasion, and apoptosis rates were analyzed by the 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, scratch test, transwell assay, and flow cytometry, respectively. A nude mouse model of NPC was established to observe tumor volume and growth. RESULTS: The mRNA levels of ATR and ATM and the expression of ATR and ATM protein in NPC tissues were significantly higher than those in adjacent normal tissues. The colony formation assay showed that the colony-forming rate decreased, showing radiation dose-dependent and CGK-733 concentration-dependent manners. Expression of ATM, ATR, Chk1, and Chk2 was evidently increased in the X-ray, CGK-733, and X-ray+CGK-733groups compared with the control group, and the aforementioned expression was highest in the X-ray+CGK-733 group among the four groups. The cell proliferation, invasion, and migration were decreased, tumor volume decreased and cell apoptosis increased in the X-ray, CGK-733, and X-ray+CGK-733 groups compared with the control group; the X-ray+CGK-733 group exhibited lowest cell proliferation, invasion and migration, smallest tumor volume, and highest cell apoptosis among the four groups. CONCLUSIONS: Inhibition of ATM/ATR signaling pathway reduces proliferation and enhances apoptosis and radiosensitivity of NPC cells.

[Application of fourier transform infrared spectroscopy to non-invasive detection of pleomorphic adenoma of salivary gland in vivo].

In the present work, 20 patients with salivary pleomorphic adenoma were recruited for FTIR spectroscopic measurement. These obtained FTIR spectra were analyzed and compared. It was found that there were significant differences in the spectral features of the skin covering normal salivary gland, pleomorphic adenoma, and carcinoma change of pleomorphic adenoma, such as the changes in peak position, band shape and relative intensity of the bands in the ranges of 1000-1800 cm(-1) and 2800-3000 cm(-1). Pathological diagnosis demonstrated that 2 of the 20 patients suffered actually carcinoma change of pleomorphic adenoma, which is in good agreement with the result of FTIR spectroscopicmeasurement. FTIR spectroscopic m ethodsuggested that pleomorphic adenoma is the intermediate between normal salivary gland and carcinoma change of pleomorphic adenoma.