ABSTRACT
PURPOSE: The aim of this study was to measure the cortical bone thickness of the infrazygomatic crest area in individuals with unilateral cleft lip and palate using cone beam computed tomography for placement of miniplates used for bone anchored maxillary protraction. MATERIALS AND METHODS: CBCT scans were obtained from 31 non-syndromic UCLP children diagnosed with maxillary hypoplasia (17 males, 14 females, mean age: 11.9 years). 5 horizontal and 5 vertical reference planes were drawn at the infrazygomatic crest area. The cortical bone thickness at 25 intersection points on the cleft side and the non-cleft side was measured. RESULTS: The mean cortical bone thickness of the 25 measured points was 1.19 mm on the cleft side and 1.17 mm on the non-cleft side with no significant difference. The greatest cortical bone thickness was found to be at the most superior, posterior point (H+6, V+0), which was 1.49 mm on the cleft side and 1.47 mm on the non-cleft side. The thinnest mean cortical bone thickness was measured at the most inferior, anterior point (H-2, V-8), which was 0.94 mm on the cleft side and 0.95 mm on the non-cleft side. There was no significant difference between males and females.
Subject(s)
Cleft Lip/diagnostic imaging , Cleft Palate/diagnostic imaging , Adolescent , Child , Cone-Beam Computed Tomography/methods , Cortical Bone/diagnostic imaging , Female , Humans , Imaging, Three-Dimensional , MaleABSTRACT
We found that LTR-directed transcription of the human endogenous retrovirus K can be induced by HSV-1 infection. The effect was mediated by the action of a HSV-1 immediate early protein, ICP0 and required the AP-1 binding site present on the HERV-K LTR. In addition, ICP0 could up-regulate AP-1 activity, suggesting that ICP0 increases transcription of HERV-K through AP-1 site. This effect might be important to understand both HERV-K- and HSV-1-mediated pathogenesis because HERV-K LTR represents an important class of retrotranspositional mutagens and also could provide a new regulatory element for the linked DNA sequences.
Subject(s)
Immediate-Early Proteins/physiology , Retroviridae/genetics , Terminal Repeat Sequences/genetics , Transcription, Genetic/genetics , Transcriptional Activation/physiology , Herpesvirus 1, Human/chemistry , Humans , Luciferases/genetics , Luciferases/metabolism , Retroviridae/classification , Tumor Cells, CulturedABSTRACT
Co-infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) is common and is associated with a more severe liver disease and increased frequency in the development of hepatocellular carcinoma (HCC). Here, we demonstrated that HBV X protein (HBx) and HCV core protein additively repress the universal cyclin-dependent kinase inhibitor p21 gene at the transcription level. The transforming growth factor-beta responsive element and Sp1 site of the p21 promoter were responsible for the effect of HCV core and HBx, respectively. Furthermore, cell growth was additively stimulated by them, suggesting that additive repression of the p21 might be important to understand the cooperative development of HCC by HBV and HCV.