• Journal of Chest Surgery
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• v.40 no.7 s.276
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• pp.508-511
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• 2007

The causes of aortic dissection are usually hypertension, connective tissue disease such as Marfan syndrome, congenital valvular abnormality such as bicuspid aortic valve, iatrogenic injury, pregnancy and drugs. Previous studies have shown that 50% of all dissections in women less than 40 years age were associated with pregnancy. Almost all aortic dissections during pregnancy occur during the third trimester or during labor and delivery. Marfan's syndrome is a particularly important predisposing factor for aortic dissection during pregnancy. We report here on a case of surgical treatment for acute type II aortic dissection in a Marfan syndrome patient who was 24 weeks pregnant, and we include a review of literature.

• Molecules and Cells
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• v.41 no.3
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• pp.198-206
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• 2018

Aortic dissection (AD) is a catastrophic disease with high mortality and morbidity, characterized with fragmentation of elastin and loss of smooth muscle cells. Although AD has been largely attributable to polymorphisms defect in the elastin-coding gene, tropoelastin (TE), other undermined factors also appear to play roles in AD onset. Here, we investigated the effects of post-transcriptional control of TE by microRNAs (miRNAs) on elastin levels in aortic smooth muscle cells (ASMC). We found that miR-144-3p is a miRNA that targets TE mRNA in both human and mouse. Bioinformatics analyses and dual luciferase reporter assay showed that miR-144-3p inhibited protein translation of TE, through binding to the 3'-UTR of the TE mRNA. Interestingly, higher miR-144-3p levels and lower TE were detected in the ASMC obtained from AD patients, compared to those from non-AD controls. In a mouse model for human AD, infusion of adeno-associated viruses (serotype 6) carrying antisense for miR-144-3p (asmiR-144-3p) under CAG promoter significantly reduced the incidence and severity of AD, seemingly through enhancement of TE levels in ASMC. Thus, our data suggest an essential role of miR-144-3p on the pathogenesis of AD.

• Journal of Chest Surgery
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• v.47 no.1
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• pp.6-12
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• 2014

Background: Although a residual intimal tear may contribute to the dilatation of the descending aorta following surgical repair of acute type I aortic dissection (AD), its causal relationship has not been elucidated by clinical data due to the limited resolution of imaging modalities. Methods: This study enrolled 41 patients (age, $55.2{\pm}11.9$ years) who were evaluated with dual-source computed tomography (CT) imaging of the whole aorta in the setting of the surgical repair of acute type I AD. Logistic regression models were used to determine the predictors of a composite of the aortic aneurysm formation (diameter >55 mm) and rapid aortic expansion (>5 mm/yr). Results: On initial CT, a distal re-entry tear was identified in 9 patients. Two patients failed to achieve proximal tear exclusion by the surgery. Serial follow-up CT evaluations (median, 24.6 months; range, 6.0 to 67.2 months) revealed that 14 patients showed rapid expansion of the descending aorta or aortic aneurysm formation. A multivariate analysis revealed that the residual intimal tear (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.02 to 19.31) and the patent false lumen in the early postoperative setting (OR, 4.64; 95% CI, 0.99 to 43.61) were predictive of the composite endpoint. Conclusion: The presence of a residual intimal tear following surgery for acute type I AD adversely influenced the expansion of the descending aorta.

• Journal of Chest Surgery
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• v.44 no.2
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• pp.123-130
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• 2011

Background: The aim of the present study was to identify chromosomal loci that contribute to the pathogenesis of aortic dissection (AD) in a Korean population using array comparative genomic hybridization (CGH) and to confirm the results using real-time polymerase chain reaction (PCR). Materials and Methods: Eighteen patients with ADs were enrolled in this study. Genomic DNA was extracted from individual blood samples, and array CGH analyses were performed. Four corresponding genes with obvious genomic changes were analyzed using real-time PCR in order to assess the level of genomic imbalance identified by array CGH. Results: Genomic gains were most frequently detected at 8q24.3 (56%), followed by regions 7q35, 11q12.2, and 15q25.2 (50%). Genomic losses were most frequently observed at 4q35.2 (56%). Real-time PCR confirmed the results of the array CGH studies of the COL6A2, DGCR14, PCSK6, and SDHA genes. Conclusion: This is the first study to identify candidate regions by array CGH in patients with ADs. The identification of genes that may predispose an individual to AD may lead to a better understanding of the mechanism of AD formation. Further multicenter studies comparing cohorts of patients of different ethnicities are warranted.

• Journal of Chest Surgery
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• v.30 no.8
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• pp.752-759
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• 1997

Profound hypothermia protects . cerebral function during total circulatory arrest(TCA) in the surgical treatment of a variety of cardiac and aortic diseases. Despite its importance, there is no ideal technique to monitor the brain injury from ischemia. Since 1994, we have developed compressed spectral array(CSA) of electroencephalography(EEG) and monitored cerebral activity to reduce ischemic injury. The purposes of this study are to analyse the efficacy of CSA and to establish objective criteria to consistently identify the safe level of temperature and arrest time. We studied 6 patients with aortic dissection(AD, n=3) or aortic arch aneurysm(n=3, ruptured in 2). Body temperatures from rectum and esophagus and the EEG were monitored continuously during cooling and rewarming period. TCA with cerebral ischemia was performed in 3 patients and TCA with selective cerebral perfusion was performed in 3 patients. Total ischemic time was 30, 36 and 56 minutes respectively for TCA group and selective perfusion time was 41, 56 and 92 minutes respectively for selective perfusion group. The rectal temperatures for flat EEG were between 16.1 and 22. $1^{\circ}C$ (mean: 18.4 $\pm$ 2.0): the esophageal temperatures between 12.7 and $16.4^{\circ}C$ (mean $14.7\pm1.6).$ The temperatures at which EEG reappeared $5~15.4^{\circ}C$ for esophagus. There was no neurological defic t and no surgical mortality in this series. In summary, the electrical cerebral activity Teappeared within 23 minutes at the temperature less than $16^{\circ}C$ for rectum. It seemed that $15^{\circ}C$ of esophageal temperature was not safe for 20 minutes of TCA and continuous monitoring the EEG with CSA to identify the electrocerebral silence was useful.