OBJECTIVE: To seek pathological features, diagnosis, treatment, prognosis of Epithelial-myoepithelial carcinoma arising in the nasal cavity. METHOD: One case of Epithelial-myoepithelial carcinoma arising in the nasal cavity was analyzed retrospectively and studied with immunohistochemical Staining and light microscopy, as well as review of the literature. RESULT: The clinical feature of epithelial-myoepithelial carcinoma in the nasal cavity was atypical and diagnosis relied on pathologic features. Epithelial-myoepithelial carcinoma consisted of myoepithelial and epithelial cells. Immunohistochemical staining demonstrated that cytokeratin P, cytokeratin L, S-100 protein, a-smooth muscle actin expressed positively. CONCLUSION Epithelial-myoepithelial carcinoma in the nasal cavity is a rare neoplasm. Wide surgical excision with a clear margin is the main therapy,and these tumors have the potential for metastasis and recurrence.
Carcinoma ; pathology ; Humans ; Male ; Middle Aged ; Myoepithelioma ; pathology ; Nasal Cavity ; pathology ; Nose Neoplasms ; pathology

To perform the quality control of deferasirox and establish its quality criterion, three related substances which were determined by analyzing the synthetic route were synthesized, and their structures were confirmed by 1H NMR and MS. These substances were 2-(2-hydroxyphenyl)-4H-benzo［1, 3-e］oxazin-4-one(A), 2-hydroxy-N-(2-hydroxyben-zoyl)-benzamide(B), and methyl-4-［3, 5-bis(2-hydroxyphenyl)- 1H- ［1, 2, 4］triazol-1-yl］-benzoate(C).

Currently, there is still no effective curative treatment for the development of late-stage liver fibrosis. Here, we have illustrated that TB001, a dual glucagon-like peptide-1 receptor/glucagon receptor (GLP-1R/GCGR) agonist with higher affinity towards GCGR, could retard the progression of liver fibrosis in various rodent models, with remarkable potency, selectivity, extended half-life and low toxicity. Four types of liver fibrosis animal models which were induced by CCl₄, α-naphthyl-isothiocyanate (ANIT), bile duct ligation (BDL) and Schistosoma japonicum were used in our study. We found that TB001 treatment dose-dependently significantly attenuated liver injury and collagen accumulation in these animal models. In addition to decreased levels of extracellular matrix (ECM) accumulation during hepatic injury, activation of hepatic stellate cells was also inhibited via suppression of TGF-β expression as well as downstream Smad signaling pathways particularly in CCl₄-and S. japonicum-induced liver fibrosis. Moreover, TB001 attenuated liver fibrosis through blocking downstream activation of pro-inflammatory nuclear factor kappa B/NF-kappa-B inhibitor alpha (NFκB/IKBα) pathways as well as c-Jun N-terminal kinase (JNK)-dependent induction of hepatocyte apoptosis. Furthermore, GLP-1R and/or GCGR knock-down results represented GCGR played an important role in ameliorating CCl₄-induced hepatic fibrosis. Therefore, TB001 can be used as a promising therapeutic candidate for the treatment of multiple causes of hepatic fibrosis demonstrated by our extensive pre-clinical evaluation of TB001.