Objective To determine if differences exist in the timing of cleft palate repair with respect to sex, race, income, and geographical location within the United States. Design Retrospective cross-sectional study using the Kids’ Inpatient Database (KID) from 1997 to 2009. Setting Inpatient. Patients Children with cleft palate with or without cleft lip undergoing inpatient cleft palate repair. Main outcome measures Age at the time of palatoplasty (in months) by sex, race, income quartile, and geographic location. Results A total of 7,218 children with cleft palate underwent repair at a mean age of 12.1 months (95% CI 12.0-12.3). Females underwent palatoplasty at an older age (13.6 months) than males (13.2 months), a difference of 0.47 months (SE: 0.19, p=0.015). White children underwent surgery at an earlier age (12.1 months) than Black (12.9 months) (difference: 0.73 months, SE: 0.37, p=0.045), Hispanic (12.7 months) (difference: 0.57 months, SE 0.25, p=0.025), and Asian children (15.7 months) (difference: 3.60 months, SE 0.49, p<0.0001). Asian children were also found to undergo repair later than Hispanic (difference 3.03 months, SE 0.51, p<0.0001) and Black (difference: 2.87 months, SE 0.59, p<0.0001) children. Patients born into the highest income brackets were repaired 0.75 months earlier than those in the lowest bracket (SE: 0.26, p=0.005). Patients in the Midwest underwent palatoplasty later (14.3 months) than in the Northeast (12.9 months) (difference: 1.36 months, SE: 0.31, p<0.0001), South (13.2 months) (difference: 1.05 months, SE: 0.36, p=0.004), and West (13.2 months) (difference: 1.09 months, SE: 0.32, p=0.0007). Conclusions After controlling for confounding factors, our results suggest that in recent history, Black, Hispanic, and Asian children with cleft palate were repaired later than their White counterparts. In addition, children of affluent families were repaired earliest, and economically disadvantaged children were repaired later than their peers.
Introduction Angiogenin-1 (Ang1) and angiogenin-4 (Ang4) are 14-kDa ribonucleases with potent angiogenic and antimicrobial properties. The role of Ang1 and Ang4 in chronic colitis and colitis-associated cancer has not been previously studied. Methods Wild-type (WT) and angiogenin-1 knock-out (Ang1-KO) C57BL/6 mice were given azoxymethane, a colon carcinogen, 2 days in advance of three cycles of 3.5% dextran sodium sulfate (DSS). Disease activity index (DAI) was recorded, a colonoscopy was performed after each DSS treatment, and mice were euthanized (colitis, recovery, cancer) with tissue evaluated by histopathology. Ang1, Ang4, TNF-α, Il-1F062, IL-6, IL-10, IL-23, IL-33 mRNA levels were analyzed by RT-PCR. Results Ang1-KO mice exhibited more severe colitis compared to WT mice during both the acute (P<0.05) and recovery (P<0.05) phases of each DSS cycle. Consistent with these results, colonic TNF-α, IL1-β, IL-6, IL-10, and IL-33 mRNA levels were significantly upregulated in Ang1-KO mice (P<0.05). While Ang4 increased to similar levels in both WT and Ang1-KO mice during colitis and recovery phases, WT mice were distinguished by a significant upregulation of Ang1. Interestingly, despite the reduced colitis, WT mice developed significantly more tumors compared to Ang1-KO mice (P<0.05). 134 tumors formed in WT mice (4.6 tumors/mouse) while only 46 tumors formed (1.5 tumors/mice) in Ang1-KO mice, which were also characterized by a 34-fold decrease in Ang4 compared to WT mice and the complete absence of Ang1. Conclusions In a mouse model of colitis-associated cancer, Ang1-KO mice develop more severe colitis, but fewer tumors compared to WT mice. Ang1 levels correlate with the severity of colitis and the development of colitis-associated cancer, while Ang4 was upregulated during both colitis and cancer. Ang1 and Ang4 play important regulatory roles in the response to chronic colitis and the development of colitis-associated cancer and may serve as novel therapeutic targets.
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