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NF‐YA is considered as a crucial regulator for the maintenance of cancer stem cell (CSC) and involved in various types of malignant tumours. However, the exact function and molecular mechanisms of NF‐YA in the progression of cervical cancer remains poorly understood. Here, the expression of NF‐YA detected by immunohistochemistry was gradually increased from normal cervical tissues, to the high‐grade squamous intraepithelial lesions, and then to cervical cancer tissues. NF‐YA promoted the cell proliferation and tumorigenic properties of cervical cancer cells as well as tumorsphere formation and chemoresistance in vitro. The luciferase reporter assay combined with mutagenesis analyses and Western blotting showed that NF‐YA trans‐activated the expression of SOX2 in cervical cancer. Furthermore, quantitative chromatin immunoprecipitation (qChIP) and electrophoretic mobility shift assay (EMSA) confirmed that NF‐YA protein directly bound to the CCAAT box region located upstream of the SOX2 promoter. Together, our data demonstrated that NF‐YA was highly expressed in cervical cancer and promoted the cell proliferation, tumorigenicity and CSC characteristic by trans‐activating the expression of SOX2.

Understanding the interaction between biomaterials and the immune system has become increasingly important. Mineralized collagen (MC) has the same chemical components and microstructures to natural bone tissue, and is considered as a better biomaterial for bone prostheses compared to hydroxyapatite (HA). However, there is little information about how MC affects inflammatory responses. In this study, we investigate the inflammatory responses to MC and HA by culturing RAW264.7 cells on their surfaces. We observed that MC increases CD206+ staining and IL-10 (M2 macrophages), whereas HA shows cells expressing more CD86 and secreting more TNF-α. This result indicates that MC may attenuate inflammatory responses to implanted bone prostheses.

Liposomes containing phosphatidylserine (PSL) produce PGE2 after being phagocytosed by microglia, but the precise underlying mechanism behind it still remains unclear. Here, we showed that liposomes consisting of phosphatidylserine and lysophosphatidylcholine, a lipolysis product of phosphatidylcholine by PLA2, were phagocytosed by microglia, but failed to induce secretion of PGE2. Furthermore, PSL-induced PGE2 secretion was significantly inhibited by MJ33, an aiPLA2 inhibitor, but not by AACOCF3, a cPLA2 inhibitor. PSL also produced PGD2 and 15d-PGJ2 in microglia. We thus hypothesize that free arachidonic acid is supplied through aiPLA2-mediated lipolysis of phagocytosed phosphatidylcholine, leading to the production of PGH2 and its downstream metabolites.

On the basis of gas chromatography (GC) coupled with a short capillary column and an electron capture detector (ECD), a simple and rapid method for the determination of five haloacetic acids(HAAs) in drinking water was developed by the optimization of derivation conditions and the modification of gas chromatographic program. HAAs formation potential (HAAFP) of the reaction of humic acid with chlorine was determined via this method. The major advantages of the method are the simplicity of chromatographic temperature program and the short run time of GC. Dichloroacetic acid(DCAA) and Trichloroacetic acid(TCAA), which were detected in the determination of HAAFP, were rapidly formed in the first 72 h of the reaction of humic acid with chlorine. HAAFP of the reaction of humic acid with chlorine increased with the increase in the concentrations of humic acid and chlorine. The average HAAFP of the reaction of humic acid with chlorine was 39.9 μg/mg TOC under the experimental conditions. When the concentration of humic acid was 4 mg/L, the concentration of HAAs, which were produced in the reaction of humic acid with chorine, may exceed MCL of 60 μg/L HAAs as the water quality standards for urban water supply of China and the first stage of US EPA disinfection/disinfection by-products (D/DBP) rule; when the concentration of humic acid was 2 mg/L, the concentration of HAAs may exceed MCL of 30 μg/L HAAs for the second stage of US EPA D/DBP rule. When humic acid was reacted with chlorine dioxide, only DCAA was detected with a maximum concentration of 3.3 μg/L at a humic acid content of 6 mg/L. It was demonstrated that the substitution of chlorine dioxide for chorine may entirely or partly control the formation of HAAs and effectively reduce the health risk associated with disinfected drinking water.

BACKGROUND/AIMS A large number of studies have shown that function constipation (FC) has an extremely high incidence of mental and psychological disorders. Cranial electrotherapy stimulation (CES) was applied to the treatment of psychological disorders such as anxiety and depression. We explored the effects of CES combined with biofeedback therapy (BFT) on the psychological state, clinical symptoms, and anorectal function in patients with FC. METHODS A total of 74 patients with FC were randomly divided into 2 groups. The control group received BFT. CES combined with BFT was carried out in the experiment group. All patients were assessed using the self-rating anxiety scale (SAS), self-rating depression scale (SDS), and Wexner constipation score at baseline and the end of each course. Anorectal manometry and balloon expulsion tests were performed before and after treatment. RESULTS After treatment, the participants in the experiment group had significantly lower score SAS, SDS, and Wexner constipation scores than the control group (all P < 0.05). The number of successful expulsion in the experiment group was larger than the control group (P = 0.016). CONCLUSIONS CES combined with BFT was effective in improving the psychological status of anxiety, depression, and bowel symptoms in patients with FC.

Phosphatidylserine (PS)-containing liposomes (PSLs) strongly inhibit inflammatory bone loss in adjuvant arthritic (AA) rats. This effect was attributed to the inhibition of osteoclastogenesis through the secretion of prostaglandin E(2) and transforming growth factor-β1 by osteoclast precursors after the phagocytosis of PSLs. However, infiltrated macrophages are considered to secrete anti-inflammatory mediators after phagocytosis of PSLs, which also contribute to inhibiting osteoclastogenesis. In the present study, we have attempted to elucidate the effects of PSLs on the phenotype of infiltrated macrophages during inflammatory bone loss. In AA rats, the ankle joints swelled with the infiltration of both macrophages and helper T cells into the synovium after a complete Freund's adjuvant injection. In the ankle joints of AA rats, approximately half of the infiltrated macrophages underwent a phenotypic change from interleukin (IL)-1β-producing to IL-10-producing cells after the phagocytosis of PSLs. In lipopolysaccharide (LPS)-stimulated macrophages, PSLs also significantly decreased IL-1β production, but increased IL-10 production. Moreover, PSLs inhibited the rapid activation of p38 mitogen-activated protein kinases (MAPK) and nuclear factor (NF)-κB, but enhanced the delayed activation of extracellular signal-regulated kinase (ERK) in LPS-stimulated macrophages. PSL-induced different influence on the activities of p38 MAPK and ERK is a likely underlying mechanism for phenotypic change of infiltrated macrophages after the phagocytosis of PSLs. This phenotypic change may be responsible for a significant decrease in the mean mRNA level of the receptor activator of NF-κB (RANK) and the RANK ligand (RANKL) in the ankle joint of PSL-treated AA rats, resulting in the inhibition of inflammatory bone loss.

Liposomes containing phosphatidylserine (PS) are engulfed by phagocytes including macrophages, microglia, and dendritic cells. PS liposomes (PSLs) mimic the effects of apoptotic cells on these phagocytes to induce the secretion of anti-inflammatory molecules and to inhibit the maturation of dendritic cells. However, the effects of PSLs on osteoclasts, which are also differentiated from the common myeloid precursors, remain to be determined. This study investigated the effects of PSLs on the osteoclastogenesis. In the rat bone marrow culture system, osteoclast precursors phagocytosed PSLs to secrete TGF-β1 and PGE2, which in turn inhibited osteoclastogenesis through the downregulation of receptor activator for NF-κB ligand, receptor activator of NF-κB, ICAM-1, and CD44. Consistent with these in vitro observations, i.m. injection of PSLs significantly increased the plasma level of TGF-β1 and PGE2 and decreased the expression of receptor activator for NF-κB ligand, receptor activator of NF-κB, and ICAM-1 in the skeletal tissues of ankle joints of rats with adjuvant arthritis (AA). A quantitative analysis using microcomputed tomography revealed that PSLs as well as TGF-β1 together with PGE2 significantly inhibited AA-induced trabecular bone loss. These observations strongly suggest that PSLs generate TGF-β1 and PGE2 release, leading to inhibit osteoclastogenesis and AA-induced trabecular bone loss. Because PS is a component of the cell membrane, PSLs therefore can be a potentially effective pharmacological intervention against abnormal bone loss, such as osteoporosis without deleterious side effects.