Definitive surgical correction is safe and effective, with good results. Therefore, it should be considered even in asymptomatic patients because of the risk of future complications.

One hour after implantation, only 50% of smooth muscle cells remained in the implanted area. Some implanted cells deposited in other tissue. Implanted cell survival progressively decreased during the 4-week study.

OBJECTIVES:The objective of this study was to assess prospectively the diagnostic accuracy of computer-assisted computed tomographic colonography (CTC) in the detection of polypoid (pedunculated or sessile) and nonpolypoid neoplasms and compare the accuracy between gastroenterologists and radiologists.METHODS:This nationwide multicenter prospective controlled trial recruited 1,257 participants with average or high risk of colorectal cancer at 14 Japanese institutions. Participants had CTC and colonoscopy on the same day. CTC images were interpreted independently by trained gastroenterologists and radiologists. The main outcome was the accuracy of CTC in the detection of neoplasms ≥6 mm in diameter, with colonoscopy results as the reference standard. Detection sensitivities of polypoid vs. nonpolypoid lesions were also evaluated.RESULTS:Of the 1,257 participants, 1,177 were included in the final analysis: 42 (3.6%) were at average risk of colorectal cancer, 456 (38.7%) were at elevated risk, and 679 (57.7%) had recent positive immunochemical fecal occult blood tests. The overall per-participant sensitivity, specificity, and positive and negative predictive values for neoplasms ≥6 mm in diameter were 0.90, 0.93, 0.83, and 0.96, respectively, among gastroenterologists and 0.86, 0.90, 0.76, and 0.95 among radiologists (P<0.05 for gastroenterologists vs. radiologists). The sensitivity and specificity for neoplasms ≥10 mm in diameter were 0.93 and 0.99 among gastroenterologists and 0.91 and 0.98 among radiologists (not significant for gastroenterologists vs. radiologists). The CTC interpretation time by radiologists was shorter than that by gastroenterologists (9.97 vs. 15.8 min, P<0.05). Sensitivities for pedunculated and sessile lesions exceeded those for flat elevated lesions ≥10 mm in diameter in both groups (gastroenterologists 0.95, 0.92, and 0.68; radiologists: 0.94, 0.87, and 0.61; P<0.05 for polypoid vs. nonpolypoid), although not significant (P>0.05) for gastroenterologists vs. radiologists.CONCLUSIONS:CTC interpretation by gastroenterologists and radiologists was accurate for detection of polypoid neoplasms, but less so for nonpolypoid neoplasms. Gastroenterologists had a higher accuracy in the detection of neoplasms ≥6 mm than did radiologists, although their interpretation time was longer than that of radiologists.

Cell transplantation prevents cardiac dysfunction after myocardial infarction. However, because most implanted cells are lost to ischemia and apoptosis, the benefits of cell transplantation on heart function could be improved by increasing cell survival. To examine this possibility, male Lewis rat aortic smooth muscle cells (SMCs; 4 ϫ 10 6 ) were pretreated with antiapoptotic Bcl-2 gene transfection or heat shock and then implanted into the infarcted myocardium of anesthetized, syngenic female rats (n ϭ 23 per group). On the first day after transplantation, apoptotic SMCs were quantified by using transferase-mediated dUTP nick-end labeling staining. On days 7 and 28, grafted cell survival was quantified by using real-time PCR, and heart function was assessed with the use of echocardiographyandtheLangendorffapparatus.SMCsgivenantiapoptotic pretreatments exhibited improvements in each measure relative to controls. Apoptosis was reduced in Bcl-2-treated cells relative to all other groups (P Ͻ 0.05), whereas survival (P Ͻ 0.01) was increased. Heat shock also significantly decreased apoptosis and increased survival relative to control groups (P Ͻ 0.05 for group effect), although these effects were less pronounced than in the Bcl-2-treated group. Further, scar areas were reduced in both Bcl-2-and heat shock-treated groups relative to controls (P Ͻ 0.05), and fractional area change and cardiac function were greater (P Ͻ 0.05 for both measures). These results indicate that antiapoptosis pretreatments reduced grafted SMC loss after transplantation and enhanced grafted cell survival and ventricular function, which was directly related (r ϭ 0.72; P ϭ 0.002) to the number of surviving engrafted cells. cell therapy; Bcl-2; heat shock; ventricular modulation; angiogenesis SKELETAL MYOBLAST TRANSPLANTATION prevents scar thinning and ventricular dilatation after a myocardial infarction and has been associated with improved regional and global function in both animal experimentation (5,17,26) and the initial clinical trials of this intervention (6, 15). The mechanism responsible for this beneficial effect has not been elucidated but may include angiogenesis, altering the elasticity of the ventricular wall, and/or modifying matrix remodeling. These mechanisms were suggested because none of the myriad of implanted cells have been demonstrated to differentiate into functioning cardiomyocytes, nor have they been demonstrated to beat synchronously with the remaining recipient cardiomyocytes. Therefore, the goal of cell transplantation is to establish a graft of viable cells within the infarct region to modify ventricular remodeling and prevent congestive heart failure. If the grafted cells could contribute to the contractility of the infarct scar, the beneficial effect would be enhanced. In the present study, our first aim was to evaluate the efficacy of smooth muscle cell (SMC) transplantation to augment cardiac function, because these cells routinely induce angiogenesis and matrix remodeling and might be ideally suited to efficient...

The functional benefit of cell transplantation after a myocardial infarction is diminished by early cell losses. IGF-1 enhances cell proliferation and survival. We hypothesized that IGF-1-transfected smooth muscle cells (SMCs) would enhance cell survival and improve engraftment after cell transplantation. The IGF-1 gene was transfected into male SMCs and compared with SMCs transfected with a plasmid vector (vector control) and nontransfected SMCs (cell control). IGF-1 mRNA ( n = 10/group) and protein levels ( n = 6/group) were higher ( P < 0.05 for all groups) at 3, 7, and 14 days compared with controls. VEGF was also increased in parallel to enhanced IGF-1 expression. IGF-1-transfected cells demonstrated greater cell proliferation, stimulated angiogenesis, and decreased caspase-3 activity after simulated ischemia and reperfusion ( P < 0.05 for all groups compared with vector or cell controls). A uniform left ventricular injury was produced in female rats using a cryoprobe. Three weeks later, 2 × 106 cells from three groups were implanted into the scar. One week later, IGF-1-transfected SMCs had increased myocardial IGF-1 and VEGF levels, increased Bcl2 expression, limited cell apoptosis, and enhanced vessel formation in the myocardial scar compared with the two control groups ( P < 0.05 for all groups). The proportion of SMCs surviving in the implanted region was greater ( P < 0.05) in the IGF-1-transfected group than in the vector or cell controls. Gene enhancement with IGF-1 improved donor cell proliferation, survival, and engraftment after cell transplantation, perhaps mediated by enhanced angiogenesis and reduced apoptosis.