Bronchoscopes ; Bronchoscopy ; instrumentation ; methods ; Child ; China ; Humans

Cervical cancer is one of the most common and deadliest cancers in females worldwide. Despite the treatment methods of surgery, radiotherapy and chemotherapy are maturing, the prognosis of patients with recurrent, advanced or metastatic cervical cancer remains poor. Molecular targeted therapy provides new hope for these patients. This review focuses on the advances in agents targeting vascular endothelial growth factor pathway, epidermal growth factor receptor, mammalian target of rapamycin, histone deacetylases and cyclooxygenase-2 in cervical cancer.

Objective To investigate the effect and mechanism of Src kinase in renal interstitial fibrosis of unilateral ureteral obstruction (UUO) mice.Methods Male C57BL/6J mice were randomly divided into 4 groups,including sham operation group (n=8),sham operation+PP2 group (n=8),UUO operation group (n=8) and UUO operation+PP2 group (n=8).The mice were injected 2 mg/kg PP2 by intraperitoneal everyday after surgery in sham+PP2 group and UUO+PP2 group.PP2 dissolved in 1％ DMSO (formulated with normal saline).Sham and UUO group were given equal 1％ DMSO.The mice were sacrificed at 7th day.Renal collagen was observed with Sirius red stain.The activities of Src,protein kinase B (PKB,AKT),p38 mitogen-activated protein kinase (p38 MAPK),extracellular signal-regulated kinase (ERK) and the protein expressions of α-smooth muscle actin (α-SMA) and fibronectin (FN) were detected by Western blotting.The expression of collagen I (COL [) was detected by immunohistochemistry and the expressions of matrix metalloprotein 9 (MMP-9),tissue inhibitor of metalloproteinase 1 (TIMP-1),transforming growth factor-β31 (TGF-β31),monocyte chemotactic protein-1(MCP-1),interleukin-6 (IL-6) were measured by ELISA.Resuts Compared with sham mice,UUO mice on 7th day displayed obvious renal fibrosis.Meanwhile,UUO mice had increased expressions of COL Ⅰ and FN,and activities of AKT,ERK and p38 MAPK (all P ＜ 0.05).Their renal expressions of α-SMA,TGF-β1,MMP-9,TIMP-1,MCP-1 and IL-6 were also raised (all P ＜ 0.05).Compared with those in UUO group,in UUO + PP2 group the activities of Src,AKT,p38 MAPK and ERK,and expressions of TGF-β1,MCP-1 and IL-6 decreased (all P ＜ 0.05).Additionally,expressions of COL Ⅰ,FN and α-SMA,collagen deposition and renal fibrosis receded in UUO + PP2 group (all P ＜ 0.05).However,the expressions of MMP-9 and TIMP-1 were not influenced by PP2 treatment.Conclusions Src kinase promotes myofibroblasts accumulation and inflammatory reaction through activating its downstream signaling pathway in the progressing of renal interstitial fibrosis.

Carcinoma ; Cytological Techniques ; Humans ; Nasopharyngeal Neoplasms ; pathology ; Neoplastic Stem Cells ; cytology ; Oncogenes

Adult ; Humans ; Orthodontics, Corrective ; methods ; Temporomandibular Joint Disorders ; therapy

Desensitization, Immunologic ; trends ; Humans

Bronchial Diseases ; diagnosis ; surgery ; Bronchoscopy ; Child ; Humans ; Tuberculosis ; diagnosis ; surgery

Aged ; Humans ; Lung Diseases, Fungal ; complications ; microbiology ; Male ; Pneumoconiosis ; complications

Mitogen-activated protein kinase (MAPK) s a serine/tyrosine kinase which s expressed widely and regulates various signal transduction pathways in mammalian cell. As one of the key branches of MAPK pathway, p38 MAPK signaling pathway plays an important role in various physiological and pathological processes, such as cell proliferation, differentiation, apoptosis and cell cycle regulation. In recent years, the research on p38MAPK signaling pathway in cell growth, metabolism and function of osteoclast, osteoblast and chondrocyte related to bone metabolism has attracted increasing attention. This article reviews the relationship beween p38MAPK and bone metabolism, in order to investigate the mechanism of action of p38MAPK in bone metabolism related diseases.

Objective:The study aims to investigate whether phosphorothioate-modified antisense vascular endothelial growth factor oligodeoxynucleotides(VEGF ASODN)micro-encapsulated in cationic liposome could inhibit angiogenesis and metastasis of lung cancer.Methods:The phosphorothioate-modify VEGF ASODN, VEGF SODN(sense oligodeoxynucleotides) and VEGF MODN(mismatch oligonucleotides)micro-encapsulated in cationic liposome were added into in vitro culture of Lewis lung carcinoma(LLC ) cells,respectively. Expression of VEGF protein was detected by immunohistochemistry staining. And the inhibitory effects on bovine aortic endothelial cell proliferation by conditioned media obtained from LLC cells treated with ODN were observed. 40 mice of Lewis lung cancer models were established and subsequently were randomized into 4 groups: control group, ASODN group, SODN group,and MSODN group. Liposome, ASODN, SODN or MODN were given by twice a week for 4 weeks,respectively.The weights of subcutaneous tumors were measured. The rates of lung metastasis were detected, while the microvessel density(MVD) in tumor mass was detected by imuunohistochemistry staining. Peak systolic flow velocity(PS) and resistance index(RI) were measured with a sonographic scanner.Results:ASODN downregulated the expression of VEGF in LLC cells at the level of protein in vitro. The conditioned media obtained from LLC cells treated with ASODN significantly inhibited the proliferation of bovine aortic endothelial cells. ASODN significantly suppressed the growth of subcutaneous tumors and lung metastasis. MVD, PS and RI of VEGF ASODN group were remarkably different from those of other 3 groups(P