The objective of the study is to investigate the impact of receiving daily WeChat services on one's cell phone on adherence to corticosteroid nasal spray treatment in chronic rhinosinusitis (CRS) patients after functional endoscopic sinus surgery (FESS). This study was a two-arm, randomized, follow-up investigation. Patients with chronic rhinosinusitis with/without nasal polyps following bilateral FESS were randomised to receive, or to not receive, daily WeChat service on their cell phone to take corticosteroid nasal spray treatment. A prescription of budesonide aqueous nasal spray 128 µg bid was given to all the subjects. Then they returned to the clinic after 30, 60, 90 days. The primary study outcome was adherence to nasal spray treatment, whereas secondary outcomes were change in endoscopic findings and SinoNasal Outcome Test-20 (SNOT-20). On the whole, there was a significant inter-group difference in the change of adherence rate (F = 90.88, p = 0.000). The WeChat group had much higher adherence rate than the control group during the follow-up. In terms of postoperative endoscopic scores and SNOT-20, except granulation score, no significant differences were observed between the two randomization groups. WeChat services are already after a short period of observation associated with improved adherence to corticosteroid nasal spray treatment in CRS patients after FESS.
Curcumin, a natural polyphenol compound, exhibits tumor suppressive activity in a wide spectrum of cancers, including nasopharyngeal carcinoma cells. However, the exact molecular mechanisms governing this tumor suppressive activity remain elusive. Multiple studies have revealed that miRNAs are critically involved in tumorigenesis, indicating that targeting miRNAs could be a therapeutic strategy for treating human cancer. In the current study, we set out to determine whether curcumin regulates miR-7 expression in nasopharyngeal carcinoma cells. We found that curcumin inhibited cell growth, induced apoptosis, retarded cell migration and invasion, and triggered cell cycle arrest in the human nasopharyngeal carcinoma cell lines CNE1 and CNE2. Importantly, we observed that curcumin upregulated the expression of miR-7 and subsequently inhibited Skp2, a direct miR-7 target. Our results identified that upregulation of miR-7 by curcumin could benefit nasopharyngeal carcinoma patients.
Nasopharyngeal carcinoma (NPC) is a kind of head-neck malignant tumor derived from the nasopharyngeal epithelium and is mainly prevalent in Southern China and Southeast Asia countries. Cisplatin (DDP) provides the first-line therapeutic administration in NPC patients. However, chemoresistance has been a main barrier and caused bad treatment outcome in NPC therapy. To understand the molecular mechanism of acquired resistance to DDP, multiple methods were performed to examine the morphocytology and molecular changes in DDP-resistant NPC cells. We found that drug resistance cells displayed epithelial-mesenchymal transition (EMT) characteristics. DDP-resistant NPC cells exhibited enhanced migration and invasion potential. Moreover, overexpression of TAZ, one key gene in Hippo pathway, is closely associated with the DDP resistance of NPC cells and its EMT properties. Depletion of TAZ in DDP-resistant cells reversed EMT phenotypes to MET characteristics and restored chemosensitivity of DDP-resistant cells to DDP treatment. These results suggest that inactivation of TAZ could be a promising approach for the treatment of NPC patients.
Osteoarthritis (OA) is a chronic degenerative joint disorder. Previous studies have shown abnormally increased apoptosis of chondrocytes in patients and animal models of OA. TNF-α and nitric oxide have been reported to induce chondrocyte ageing; however, the mechanism of chondrocyte apoptosis induced by IL-1β has remained unclear. The aim of this study is to identify the role of the c-Jun N-terminal kinase (JNK) - c-Jun pathway in regulating induction of Bim, and its implication in chondrocyte apoptosis. This study showed that Bim is upregulated in chondrocytes obtained from the articular cartilage of OA patients and in cultured mouse chondrocytes treated with IL-1β. Upregulation of Bim was found to be critical for chondrocyte apoptosis induced by IL-1β, as revealed by the genetic knockdown of Bim, wherein apoptosis was greatly reduced in the chondrocytes. Moreover, activation of the JNK-c-Jun pathway was observed under IL-1β treatment, as indicated by the increased expression levels of c-Jun protein. Suppression of the JNK-c-Jun pathway, using chemical inhibitors and RNA interference, inhibited the Bim upregulation induced by IL-1β. These findings suggest that the JNK-c-Jun pathway is involved in the upregulation of Bim during OA and that the JNK-c-Jun-Bim pathway is vital for chondrocyte apoptosis.
Steroid-induced osteonecrosis of the femoral head (SONFH) is a disabling, aseptic and ischemic disease that develops following steroid therapy. The pathogenesis of SONFH is unclear, so the early diagnosis and treatment for this disease is yet to be established. The purpose of the present study was to identify potential biomarkers for SONFH. The differential expression of serum proteins from patients with SONFH and healthy volunteers was analyzed by the proteomics method. The protein samples were labeled and subjected to isoelectric focusing and two-dimensional gel electrophoresis. The resultant protein spots were matched and quantified by an imaging analysis system. The differentially-expressed protein spots were subjected to in-gel trypsin digestion followed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Significantly lower levels of complement component 3 (C3), C4, inter-α-trypsin inhibitor heavy chain H4 and α-2-macroglobulin were found in the serum of patients with SONFH. These proteins are reported to be actively involved in intravascular coagulation, apoptosis and reactive oxygen species imbalance, indicating that multiple pathological reactions occur in SONFH and these proteins may serve as potential biomarkers for the diagnosis of SONFH.
Nasopharyngeal carcinoma (NPC) is a highly invasive head-neck cancer derived from the nasopharyngeal epithelium, mainly prevalent in southern China and Southeast Asia. Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied in the treatment of NPC. However, resistance to chemotherapeutic drugs has recently become more common, resulting in worse treatment outcome for NPC therapy. To elucidate the underlying molecular basis of drug resistance to DDP in NPC cells, we examined the morphocytology, cell motility and molecular changes in DDP-resistant NPC cells with respect to epithelial-mesenchymal transition (EMT) features. We found that EMT is closely associated with DDP-induced drug resistance in NPC cells, as DDP-resistant cells displayed morphological and molecular markers changes consistent with EMT. Wound healing and Transwell Boyden chamber assays revealed an enhanced migration and invasion potential in DDP-resistant NPC cells. Mechanistically, upregulation of NEDD4 was observed to relate to EMT in DDP-resistant cells. More importantly, depletion of NEDD4 in resistant cells led to a partial reversion of EMT phenotypes to MET characteristics. These data suggest that NEDD4 is largely involved in EMT features and chemoresistance of NPC cancer cells. NEDD4 could be a novel therapeutic target to overcome drug resistance in successful administrations of NPC.
Chronic rhinosinusitis without nasal polyps (CRSsNP) is one of the most common otorhinolaryngologic diseases worldwide. However, the underlying mechanism remains unclear. In this study, the expression of glycogen synthase kinase 3 (GSK‐3) was quantitatively evaluated in patients with CRSsNP (n = 20) and healthy controls (n = 20). The mRNA levels of GSK‐3α and GSK‐3β were examined by qPCR, the immunoreactivities of GSK‐3β and nuclear factor‐κB (NF‐κB) were examined by immunohistochemistry (IHC) staining, and the protein levels of GSK‐3β, phospho‐GSK‐3β (p‐GSK‐3β, s9) and NF‐κB were examined using Western blot analysis. We found that GSK‐3 was highly expressed in both CRSsNP and control groups without significant difference in both GSK‐3β mRNA and protein levels. However, when compared with healthy control group, the GSK‐3β activation index, defined as the ratio of GSK‐3β over p‐GSK‐3β, was significantly decreased, whereas the NF‐κB protein abundance was significantly increased in CRSsNP group (P < 0.05). Strikingly, the GSK‐3β activation index, was highly correlated with NF‐κB protein level, as well as CT scores in CRSsNP group (P < 0.05). It was also highly correlated with the mRNA expressions of inflammation‐related genes, including T‐bet, IFN‐γ and IL‐4 in CRSsNP group (P < 0.05). Our findings suggest that GSK‐3β activation index, reflecting the inhibitory levels of GSK‐3β through phosphorylation, may be a potential indicator for recurrent inflammation of CRSsNP, and that the insufficient inhibitory phosphorylation of GSK‐3β may play a pivotal role in the pathogenesis of CRSsNP.
BackgroundOsteoclast formation is closely related to the immune system. FTY720, a new immunosuppressive agent, has some functions in immune regulation. Its main active ingredients become FTY-720P in vivo by phosphorylation modification. The objective of this study was to determine the effects of FTY-720 with various concentrations on osteoclasts in vitro.Material/MethodsRAW264.7 cells and bone marrow-derived mononuclear phagocytes (BMMs) were treated with RANKL to obtain osteoclasts in vitro. To investigate the role of FTY-720 in osteoclast formation, trap enzyme staining was performed and the number of osteoclasts was counted. Bone slices were stained with methylene blue, we counted the number of lacunae after bone slices were placed into dishes together with osteoclasts, and we observed the effect and function of FTY-720 in osteoclasts induced by RAW264.7 cells and BMMs. Then, we used a protein array kit to explore the effects of FTY-720P on osteoclasts.ResultsThe results of enzyme trap staining and F-actin staining experiments show that, with the increasing concentration of FTY-720P, the number of osteoclast induced by RAW264.7 cells and BMMs gradually decreased (P<0.05), especially when the FTY-720P concentration reached 1000 ng/ml, and the number of osteoclasts formed was the lowest (P<0.05). With bone lacuna toluidine blue staining, the results also show that, with the increasing concentration of FTY-720P, the number of bone lacuna gradually decreased (P<0.05), and the number of lacunae is lowest when the concentration reached 800 ng/ml. Finally, protein array results showed that IL-4, IL-6, IL-12, MMP-2, VEGF-C, GFR, basic FGF, MIP-2, and insulin proteins were regulated after FTY-720P treatment.ConclusionsFTY-720P can suppress osteoclast formation and function, and FTY-720P induces a series of cytokine changes.
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