ABSTRACT
INTRODUCTION: Anatomic variants of the hepatic vasculature are common, so precise preoperative donor evaluation, including variations in the vasculature, is essential. We analyzed the anatomic similarity according to the donor-recipient relationship. METHODS: Among the cases who underwent living donor liver transplantations from September 2008 to January 2011 we selected 104 cases with clearly defined hepatic artery and portal vein on preoperative computed tomography. They were classified according to Hiatt et al for the hepatic artery and Cheng for the portal vein. We categorized the 104 cases into three groups: parents-child (n=40), sibling (n=24) and no-relation (n=40), for analysis of the concordance of the hepatic artery and portal vein. RESULT: Anatomic variations were observed in 25% of donors and 23.1% of recipients in the hepatic artery and 6.7% of donors and 10.6% of recipients in the portal vein. There was no significant difference in the distribution of the type of hepatic vasculature. Identical anatomic variations between donors and recipients were observed in 62.5% of the parent-child; 66.7% of the sibling and 52.5% of no-related group (P=.493) in the hepatic artery and 92.5%, 100%, and 77.5% (P=.014) in the portal vein respectively. CONCLUSION: There was no similarity in the anatomic variations of the hepatic artery according to the donor-recipient relationship, but a similarity in portal venous anatomy according to the donor-recipient relationship.
Subject(s)
Hepatic Artery/abnormalities , Liver Transplantation , Living Donors , Portal Vein/abnormalities , Vascular Malformations/diagnosis , Chi-Square Distribution , Family , Genetic Predisposition to Disease , Hepatic Artery/diagnostic imaging , Humans , Pedigree , Phlebography/methods , Portal Vein/diagnostic imaging , Preoperative Care , Republic of Korea , Retrospective Studies , Tomography, X-Ray Computed , Vascular Malformations/diagnostic imaging , Vascular Malformations/geneticsABSTRACT
During the course of hominoid evolution, a new transcript variant of the GSDML (gasdermin-like protein) gene was formed by the integration of the antisense-oriented HERV-H (human endogenous retrovirus) LTR (long terminal repeat) element. To investigate regions that are critical for transcriptional regulation of the GSDML gene, we generated seven deletion mutants from a full-length clone (clone 1/630) that includes the HERV-H LTR sequence and compared their expression levels relative to the full-length parental clone using a transient transfection assay. In the transient transfection assay, deletion of the 5' flanking region (cellular origin) of the HERV-H LTR sequence led to a 4.5-fold increase in expression compared to the full-length clone, while deletion of the U5 region showed a significant decrease in transcriptional activity. Deletion of the 3' flanking region of the LTR sequence (clone 42/451) showed similar transcriptional activity to a clone missing the 5' flanking region of cellular origin (clone 42/630). Taken together, these data indicate that the HERV-H LTR sequence (viral origin) positively regulates transcriptional activity of the GSDML gene and that the 5' flanking region sequence (cellular origin) exerts negative transcriptional regulation.
Subject(s)
Endogenous Retroviruses/genetics , Neoplasm Proteins/genetics , Retroviridae/genetics , Base Sequence , Molecular Sequence Data , Promoter Regions, Genetic , Terminal Repeat Sequences/genetics , Transcription, Genetic , Transcriptional Activation , Virus IntegrationABSTRACT
Using PCR, sequencing, and bioinformatic approaches with the genomic DNAs of Korean pigs (domestic, wild, and hybrid with Yorkshire), twelve solitary PERV long terminal repeat elements were identified and analyzed. Structure analysis of the LTR elements indicated that they have different repeat sequences in the U3 region. The PERV-A6-KWP1 and -KWP2 elements bear seven and eight 39-bp repeats, respectively. The R region of the PERV LTR elements was highly conserved in pig and mouse genomes, suggesting that they seem to have originated from a common exogenous viral element and then evolved independently throughout the course of mammalian evolution.
