No abstract available.
Macrophages* ; Phospholipases A2* ; Phospholipases* ; Tumor Necrosis Factor-alpha*

Thermal ablation (TA) procedures, such as radiofrequency ablation and laser ablation, are used for the treatment of benign thyroid nodules. Short-term studies (<2 years) have demonstrated that TA is an effective and safe procedure to improve cosmetic or symptomatic problems. However, studies including a longer follow-up period show that treated thyroid nodules can increase in size after 2 to 3 years. Several studies suggest that this results from regrowth at the undertreated nodule margins. Here, we review current data on regrowth after TA and describe factors related to it and possible approaches to prevent it.
Catheter Ablation ; Follow-Up Studies ; Laser Therapy ; Thyroid Gland ; Thyroid Nodule

No abstract available.
Thyroid Gland ; Thyroid Nodule

Absorption ; Adult ; Animals ; Bicuspid ; Blood Platelets ; Bone Density ; Bone Development ; Centrifugation ; Dogs ; Humans ; Intercellular Signaling Peptides and Proteins ; Osteogenesis ; Peri-Implantitis ; Platelet-Rich Plasma ; Transforming Growth Factor beta ; Transplants

BACKGROUND: CpG DNA plays an important role in immune cell function. This study examined whether the temporal control of toll-like receptor (TLR)9 by CpG DNA can regulate the expression of matrix metalloproteinase-9 (MMP-9). MeETHODS AND MATERIALS: Macrophages were cultured in the presence of 10percent FBS. For the various MMP genes analysis, RT-PCR and real-time PCR were performed. In addition, zymography assay performed for the MMP activity. The phosphorylation assay did for the ERK1/2 and NFkappaB activation, and luciferase promoter assay was for the NFkappaB activity. RESULTS: CpG DNA induced the mRNA expression of MMP-2, MMP-9, and MMP-13, but not of MMP-7, MMP-8, and MMP-12, in a time-dependent manner. Especially, the mRNA expression of MMP-9 was strongly induced by CpG DNA using real-time RT-PCR. The TLR9 inhibitor, chloroquine, suppressed CpG DNA-induced MMP-9 expression and its activity. Moreover, CpG DNA induced the phosphorylation of ERK and the inhibition of ERK by U0126 suppressed CpG DNA-induced MMP-9 expression and its activity. CpG DNA stimulated IkappaB-alpha degradation and luciferase activity. In addition, pretreatment of SN-50, the inhibitor of NFkappaB, strongly blocked the CpG DNA-induced MMP-9 expression and activity. CONCLUSION: These observations suggest that CpG DNA may play important roles in the activation of macrophages by regulating the production of MMP-9 via the sequential TLR9-ERK-NFkappaB signaling pathway.
Chloroquine ; DNA ; Luciferases ; Macrophages ; Matrix Metalloproteinase 9* ; Phosphorylation ; Real-Time Polymerase Chain Reaction ; RNA, Messenger ; Toll-Like Receptors*

BACKGROUND: Toll-like receptors (TLRs) are well-known pattern recognition receptors. Among the 13 TLRs, TLR2 is the most known receptor for immune response. It activates mitogen-activated protein kinases (MAPKs), which are counterbalanced by MAPK phosphatases [MKPs or dual-specificity phosphatases (DUSPs)]. However, the regulatory mechanism of DUSPs is still unclear. In this study, the effect of a TLR2 ligand (TLR2L, Pam3CSK4) on DUSP4 expression in Raw264.7 cells was demonstrated. METHODS: A Raw264.7 mouse macrophage cell line was cultured in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum and 1% antibiotics (100 U/mL penicillin and 100 g/mL streptomycin) at 37degrees C in 5% CO2. TLR2L (Pam3CSK4)-mediated DUSP4 expressions were confirmed with RT-PCR and western blot analysis. In addition, the detection of reactive oxygen species (ROS) was measured with lucigenin assay. RESULTS: Pam3CSK4 induced the expression of DUSP1, 2, 4, 5 and 16. The DUSP4 expression was also increased by TLR4 and 9 agonists (lipopolysaccharide and CpG ODN, respectively). Pam3CSK4 also induced ERK1/2 phosphorylation and ROS production, and the Pam3CSK4-induced DUSP4 expression was decreased by ERK1/2 (U0126) and ROS (DPI) inhibitors. U0126 suppressed the ROS production by Pam3CSK4. CONCLUSION: Pam3CSK4-mediated DUSP4 expression is regulated by ERK1/2 and ROS. This finding suggests the physiological importance of DUSP4 in TLR2-mediated immune response.
Acridines ; Animals ; Anti-Bacterial Agents ; Blotting, Western ; Butadienes ; Cell Line ; Dual-Specificity Phosphatases ; Macrophages ; Mice ; Mitogen-Activated Protein Kinase Phosphatases ; Mitogen-Activated Protein Kinases ; Nitriles ; Penicillins ; Phosphorylation ; Phosphotransferases ; Reactive Oxygen Species ; Receptors, Pattern Recognition ; Toll-Like Receptors

PURPOSE: Matrix metalloproteinases (MMPs) are endogenous peptidases that are capable of degrading various components of the basement membranes. To evaluate the clinical significance of the expressions of MMPs in renal cell carcinomas (RCCs), the MMPs' expression in RCCs and non- neoplastic kidney tissues was examined to evaluate the clinical significance of the expressions of MMPs in renal cell carcinomas (RCCs). MATERIALS AND METHODS: Twenty-two patients with RCCs (the RCC group), and eleven patients with non-neoplastic kidneys (the control group), were enrolled in this study between November 2002 and November 2003. The MMP-2 and MMP-9 activities were estimated using gelatin zymography, and they were quantified using a laser densitometer. The results were compared with the clinicopathological characteristics. RESULTS: The expression of MMP-9 was significantly elevated in the RCC group compared with the control group (p<0.01). There was no difference in MMP-2 activity between the RCC group and the control group (p>0.05). The levels of MMP-9 expression in the RCC patients with a large tumor (>4cm) or vascular invasion were significantly higher than that in the patients without these clinical manifestations (p<0.01). There were also significant differences in the expression of MMP-9 among the T stages (p<0.01). CONCLUSIONS: The present study shows a close relationship between the expression of MMP-9 and the tumor size and tumor stage in RCC. MMP-9 may be used as a prognostic marker and for the development of a novel treatment modality for RCC.
Basement Membrane ; Carcinoma, Renal Cell* ; Gelatin ; Humans ; Kidney ; Matrix Metalloproteinase 2* ; Matrix Metalloproteinase 9* ; Matrix Metalloproteinases ; Peptide Hydrolases