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.

Fine mapping of a dominant thermo-sensitive genic male sterility gene (BntsMs) in rapeseed (Brassica napus) with AFLP- and Brassica rapa-derived PCR markers.

KEY MESSAGE: A new thermo-sensitive dominant genic male sterility (TSDGMS) line of Brassica napus was found and mapped in this paper. Our result will greatly accelerate the map-based cloning of the BntsMs gene. TE5A is a thermo-sensitive dominant genic male sterility line originating from spontaneous mutation of the inbred line TE5 in Brassica napus and provides a promising system for the development of hybrid cultivars. Genetic analysis has revealed that the BntsMs mutant is controlled by a single, dominant gene. Here, we describe the fine mapping of BntsMs using amplified fragment length polymorphism (AFLP) and intron polymorphism (IP) methodologies. We screened 1,024 primer combinations and then identified five AFLP markers linked to the BntsMs gene, two of which were successfully converted into sequence-characterised amplified region (SCAR) markers. The linkage of the markers was identified by analysing a large BC2 population of 700 recessive-fertility individuals. Two SCAR markers were found in the flanking region of the BntsMs gene at distance of 3.5 and 4.8 cm. Based on sequence information from the previously screened AFLP markers and on genome organisation comparisons of the A genome of Brassica rapa and Arabidopsis, seven IP markers linked to the BntsMs gene were developed. By analysing the 700 recessive-fertility individuals, two IP markers, IP004 and IP470, were localised to the flanking region of the BntsMs gene at a distance of 0.3 and 0.2 cm, respectively. A comparison of the B. rapa and Arabidopsis genomes revealed 27 genes of B. rapa in the flanking region of these two IP markers. It is likely that the molecular markers developed from these investigations will greatly accelerate the positional cloning of the BntsMs gene.

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.