Objective:To compare the effects of different surgical treatment of chronic rhinitis-sinusitis difference,and its impact on transport function of maxillary sinus mucociliary,provide a clinical-surgical sinusitis preferably reference about the treatment of chronic nasal formulation for.Methods:From 2013.9-2014.12,otorhinolaryngology clinic in our hospital,160 cases were diagnosed as chronic nose-as research subjects were randomly divided into four groups of patients with sinusitis were treated from 1 to 4,60 cases in each group;treatment groupl receiving the maxillary sinus ostium augmentation,treatment group 2 received fenestration,treatment group 3 through tears crypt before maxillary sinus surgery,treatment 4 group receiving the maxillary sinus balloon dilatation;after covering the nasal mucosa observed and compared four groups of patients about edema,vesicle formation,bone exposure,scarring,etc.,as well as internal maxillary sinus secretions traits,volume situation,and compared patients after four groups line maxillary sinus cavity and perioral saccharin test biopsy cases three months and six months.Results:The four groups were made after surgery better clinical efficacy,and group efficacy 4 with the other three groups,the effect is most significant (all P ＜0.05),the difference was statistically significant,and after three months and six months,group 4 compared with other surgical group,the Lund-Kernedy score were also lower,MMT time were also lower,the difference was more significant (all P ＜0.05);in the maxillary sinus biopsy aspects:the number of postoperative inflammatory cells and dendritic cells and glandular cell morphology and submucosal edema improved submucosal structures also in the group of four most significant (P＜0.05).Conclusion:Maxillary sinus balloon dilatation treatment chronic nasal sinusitis curative effect is higher,which can effectively improve the cell and submucosal gland cell morphology and sinus mucosa edema,sinus unobstructed drainage effect,and high safety.

OBJECTIVETo explore the role of annexin A2 (ANXA2) expression in the intestinal mucosa in the pathogenesis of inflammatory bowel disease (IBD).

METHODSIntestinal or colonic mucosal biopsy samples were obtained from 54 patients with ulcerative colitis (UC), 37 with Crohn's disease (CD), and 15 healthy control subjects. Immunohistochemistry was employed to examine the expression of ANXA2 in the intestinal mucosa, and mRNA expression of ANXA2 was detected using real-time PCR.

RESULTSImmunohistochemistry showed a ANXA2 positivity rate of 83.3% (45/54) in patients with UC, 27.0% (10/37) in patients with CD, and 53.3% (8/15) in the control subjects. ANXA2 expression in the intestinal or colonic mucosa was significantly up-regulated in patients with UC compared with the patients with CD and healthy control subjects, but was significantly lower in patients with CD than in the healthy controls (P<0.05). The expression levels of ANXA2 were strongly associated with the severity of clinical manifestations and the histopathological grades of UC (P<0.05). Compared with the healthy controls and patients with CD, patients with UC showed a significantly increased ANXA2 mRNA expression level in the inflamed mucosa of UC (P<0.05).

CONCLUSIONANXA2 can serve as a marker for differential diagnosis of IBD, and its up-regulated expression is closely related to the pathogenesis of UC.

Annexin A2 ; metabolism ; Case-Control Studies ; Colitis, Ulcerative ; metabolism ; pathology ; Crohn Disease ; metabolism ; pathology ; Female ; Humans ; Inflammatory Bowel Diseases ; metabolism ; pathology ; Intestinal Mucosa ; metabolism ; pathology ; Male

Background The association between serum nickel (Ni) and oral cancer incidence is unclear and most of the previous studies were observational studies that did not control for confounding factors between groups. Objective To assess the correlation of serum Ni with oral cancer incidence based on propensity score matching (PSM) and inverse probability of treatment weighting (IPTW). Methods A cohort of 456 newly diagnosed oral cancer patients was recruited from the First Hospital of Fujian Medical University during November 2011 to May 2019, and residents ordered their health check-up in hospitals or local community health centers over the same period were selected as a control group, which included a total of 1410 participants. Serum Ni was evaluated by inductively coupled plasma mass spectrometry. Case-control pairs were selected using a 1:1 PSM (caliper value of 0.02), and the study subjects in the case group and control group were weighted for subsequent analysis by IPTW. The general characteristics of the study subjects were tested for equilibrium before and after matching by chi-square test and standardized mean difference (SMD). This was followed by exploring the potential nonlinear dose-response relationship between serum Ni and oral cancer using restricted cubic splines as well as analyzing the association between serum Ni and oral cancer incidence by conditional logistic regression and weighted logistic regression. Results After controlling for between-group covariates by PSM and IPTW, the dose-response curves demonstrated that the risk of developing oral cancer tended to decline and then increase with the increasing serum Ni level. The outcome of the analysis using PSM demonstrated that as compared to the control group, the risk of developing oral cancer in the 0.09-16.80 μg·L⁻¹ serum Ni group was negatively correlated with serum Ni level (OR=0.36, 95%CI: 0.24-0.54), whereas the risk of developing oral cancer in the >16.80 μg·L⁻¹ serum Ni group was positively correlated with serum Ni level (OR=5.43, 95%CI: 2.76-10.68). After applying IPTW, a negative association was found between the risk of oral cancer and serum Ni concentration within a serum Ni window ranging from 0.09 to 20.55 μg·L⁻¹ (OR=0.39, 95%CI: 0.29-0.52), while a positive association with an OR and 95%CI of 5.54 (3.62-8.49) for the Ni concentration > 20.55 μg·L⁻¹. Conclusion In this study, a J-shaped relationship between serum Ni concentration and the risk of developing oral cancer is found, which shows that high serum Ni concentration (>20.55 μg·L⁻¹) may be a risk factor for oral cancer.

Inflammatory orofacial pain, in which substance P (SP) plays an important role, is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs). SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms, including glial fibrillary acidic protein (GFAP) activation, phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways, and cytokine upregulation. However, in the TG, the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown. In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process. In the present study, complete Freund's adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo. SP was administered to SGC cultures in vitro to confirm the effect of SP. Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist), U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2), and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia. In addition, SP promoted SGC activation, which was proven by increased GFAP, p-MAPKs, IL-1β and TNF-α in SGCs under inflammatory conditions. Moreover, the increase in IL-1β and TNF-α was suppressed by L703, 606, U0126 and SB203580 in vivo and in vitro. These present findings suggested that SP, released from TG neurons, activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs, contributing to inflammatory orofacial pain associated with peripheral sensitization.