NaHCO3-Buffered Lidocaine Gel for Outpatient Rigid Cystoscopy in Men.

PURPOSE: The purpose of this study was to explore the effect of NaHCO3-buffered lidocaine gel as a topical anesthetic agent for pain relief for rigid cystoscopy. DESIGN: Prospective randomized controlled trial. METHODS: ASA I-II male patients undergoing rigid cystoscopy randomly received 10 mL 2% Carbocaine lidocaine gel with 1 mL 0.9% saline (group 1) or 1 mL 5% NaHCO3 solution (group 2). After 3 minutes exposure, the cystoscope was inserted into the urethra. On receiving the gel, cystoscope insertion, and intravesical observation, pain score was recorded using the visual analog scale. FINDINGS: The gel pH with or without NaHCO3 was 7.20 and 6.41, respectively. The concentration of soluble lidocaine in the gel was stable for 24 hours or more. The visual analog scale score in group 2 was significantly lower (1.3 ± 0.9) than in group 1 (5.28 ± 1.99). No adverse effects were recorded. CONCLUSION: Alkalized lidocaine gel resulted in successful analgesia for rigid cystoscopy in men without adverse effects.

Carcinoembryonic antigen interacts with TGF-{beta} receptor and inhibits TGF-{beta} signaling in colorectal cancers.

As a tumor marker for colorectal cancers, carcinoembryonic antigen (CEA) enhances the metastatic potential of cancer cells. CEA functions as an intercellular adhesion molecule and is upregulated in a wide variety of human cancers. However, the molecular mechanisms by which CEA mediates metastasis remain to be understood. Transforming growth factor-ß (TGF-ß) signaling regulates both tumor suppression and metastasis, and also contributes to the stimulation of CEA transcription and secretion in colorectal cancer cells. However, it remains unknown whether CEA, in turn, influences TGF-ß functions and if a regulatory cross-talk exists between CEA and the TGF-ß signaling pathway. Here, we report that CEA directly interacts with TGF-ß receptor and inhibits TGF-ß signaling. Targeting CEA with either CEA-specific antibody or siRNA rescues TGF-ß response in colorectal cancer cell lines with elevated CEA, thereby restoring the inhibitory effects of TGF-ß signaling on proliferation. CEA also enhances the survival of colorectal cancer cells in both local colonization and liver metastasis in animal study. Our study provides novel insights into the interaction between CEA and TGF-ß signaling pathway and establishes a negative feedback loop in amplifying the progression of colon cancer cells to more invasive phenotypes. These findings offer new therapeutic opportunities to inhibit colorectal cancer cell proliferation by cotargeting CEA in promoting tumor-inhibitory action of the TGF-ß pathway.