Soo Jin Na Choi

Changes in suprarenal and infrarenal aortic angles after endovascular aneurysm repair

Purpose We investigated whether suprarenal and infrarenal aortic angles change after the endovascular aneurysm repair (EVAR) procedure and during follow-up, and investigated the correlation between infrarenal aortic angle after EVAR and type Ia endoleaks. Methods Data collected on 70 EVAR procedures for a fusiform infrarenal aortic aneurysm performed between May 2006 and December 2012 were supplemented with a retrospective review of charts and radiographs. Results The greater the preoperative infrarenal aortic angle, the greater the suprarenal aortic angle (r = 0.72, P < 0.001). The infrarenal aortic angle decreased after the EVAR procedure and continued to decrease slowly thereafter (all P < 0.001). Suprarenal aortic angle decreased immediately after the EVAR procedure and continued to decrease during the first month (P < 0.001). No differences in angulation were observed based on stent graft type. Type Ia endoleaks occurred with significantly greater incidence in patients with a larger post EVAR infrarenal angle (P = 0.037). Conclusion The infrarenal aortic angle decreased significantly immediately after the EVAR procedure and continued to decrease slowly thereafter. Suprarenal aortic angle decreased immediately after the EVAR procedure and continued to decrease during the first month. We found a correlation between infrarenal and suprarenal aortic angle. Type Ia endoleaks occurred with greater incidence in patients with a larger infrarenal angle immediately after EVAR.

A de novo SOX10 mutation in a patient with Waardenburg syndrome type IV

To the Editor:Waardenburg syndrome type IV (WS4), a rare congenital disorder caused by defective functioning of the embryonic neural crest, is characterized by a combination of pigmentary abnormalities of the skin, eyes, and hair; sensorineural deafness; and Hirschsprung disease (HD). SOX10 is a key transcription factor in the development of 2 neural crestederived lineages, melanocytes and neurons of the myenteric ganglia. To date, only 3 nontruncating missense mutations of SOX10 are known in WS4: p. Ala157Val, p. Arg106Trp, and p. Leu145Pro. The clinical spectrum as a result of SOX10 mutation has different syndromes manifesting variable combination ofphenotypes, includingdepigmentation,hearing loss, peripheral and central neuropathy, and HD. However, the genotype-phenotype correlations according to specific mutation location and type are not clear. Here, the propositus, an 8-year-old boy, presented with a white forelock, white hair, and depigmented patches over almost his entire body. The depigmented patches developed immediately after birth and spread symmetrically on the trunk and on the inner aspects of the upper and lower extremities (Fig 1, A and B). In his history, he had been diagnosed with HD based on clinical symptoms such as a distended abdomen and constipation, and the results of a rectal biopsy and abdominal imaging with colonic contrast, which showed a huge colon (Fig 1, C ). At the age of 2 years, he was treated with a

Anatomical Features and Early Outcomes of Endovascular Repair of Abdominal Aortic Aneurysm from a Korean Multicenter Registry.

Purpose: To introduce a nation-based endovascular aneurysm repair (EVAR) registry in South Korea and to analyze the anatomical features and early clinical outcomes of abdominal aortic aneurysms (AAA) in patients who underwent EVAR. Materials and methods: The Korean EVAR registry (KER) was a template-based online registry developed and established in 2009. The KER recruited 389 patients who underwent EVAR from 13 medical centers in South Korea from January 2010 to June 2010. We retrospectively reviewed the anatomic features and 30-day clinical outcomes. Results: Initial deployment without open conversion was achieved in all cases and procedure-related 30-day mortality rate was 1.9%. Anatomic features showed the following variables: proximal aortic neck angle 48.8±25.7° (mean±standard deviation), vertical neck length 35.0±17.2 mm, aneurysmal sac diameter 57.2±14.2 mm, common iliac artery (CIA) involvement in 218 (56.3%) patients, and median right CIA length 34.9 mm. Two hundred and nineteen (56.3%) patients showed neck calcification, 98 patients (25.2%) had neck thrombus, and the inferior mesenteric arteries of 91 patients (23.4%) were occluded. Conclusion: Anatomical features of AAA in patients from the KER were characterized as having angulated proximal neck, tortuous iliac artery, and a higher rate of CIA involvement. Long-term follow-up and ongoing studies are required.

Mycophenolic acid mediated mitochondrial membrane potential transition change lead to T lymphocyte apoptosis.

Purpose This study demonstrated that apoptosis induced by mycophenolic acid (MPA) is mediated by mitochondrial membrane potential transition (MPT) changes in Jurkat cells. Methods Cell viability and MPT changes were measured by flow cytometry. Western blotting was performed to evaluate the expression of Bcl-2 family proteins, Bid, truncated Bid (tBid), cytochrome c, voltage dependent anion channel (VDAC), poly ADP-ribose polymerase (PARP), and protein kinase C-δ (PKC-δ). The catalytic activity of caspase-9 and -3 was also measured. Results Cell viability was decreased in time- and dose-dependent manners. Bcl-2 protein expression was decreased, but Bax protein expression was identified. A decreased Bcl-XL /Bcl-XS ratio was also noted. The expression of tBid protein also increased in a time-dependent manner in Jurkat cells treated with MPA. While normal MPT appeared as orange fluorescence, abnormal MPT corresponded to green fluorescence. Green fluorescence increased as orange decreased in the MPA-treated cells. Significantly increased concentrations of MPA induced the release of cytosolic cytochrome c. MPA also augmented the catalytic activity of caspase-9 and caspase-3 in Jurkat cells. Our findings demonstrated that MPA-induced apoptosis is mediated by MPT changes accompanied by decreased Bcl-XL expression and the appearance of tBid protein. The release of cytosolic cytochrome c from mitochondria and increased catalytic activity of caspase-9 and caspase-3 were observed in MPA-treated Jurkat cells. Conclusion These results suggest that mitochondrial dysfunction caused by MPA induces human T lymphocyte apoptosis.

Long Term Outcomes of Living Renal Donor Undergoing Nephrectomy

Background Kidney donation is a relatively safe procedure with minimal adverse effects. But some reports have described the development of proteinuria and hypertension after donation. There are number of reports about safety and good quality of life after living donor kidney transplantation overseas but not enough reports have been published in domestic studies. We evaluated the physiologic and psychosocial impacts after kidney donation in this study. Methods Between April 1988 and April 2010, we performed 201 living donor nephrectomies and obtained information on only 88 (43.7%) donors. We measured the estimated glomerular filtration rate (GFR), blood pressure, body mass index, hemoglobin, cholesterol and assessed prevalence of hypertension and proteinuria. And questionnaire consisted of health status and psychosocial outcomes of donors. Results The average time after donation was 95.05±85.45 months (range, 6-261). The left kidney was used in 76 patients (86%). There was a total complication rate of 8% but serious complication was absent. Proteinuria was found in 9 patients (10%), hypertension in 11 patients (11%). Glomerular filtration rate decreased from 103.65±25.02ml/min to 76.12±19.90ml/min (P<0.001) and hemoglobin decreased from 13.91±1.62g/dl to 13.01±1.72g/dl (P<0.001). Five patients (6%) developed a postdonation GFR between 40 and 60ml/min and two patients developed below 20ml/min. In questionnaire, most donors did not have problems in a routine life and economic activities. Their satisfaction about donation was very high (92%). Conclusions Living kidney donation resulted in reduced GFR in the donors. Follow-up of living kidney donors is essential to determine risk factors for deterioration of residual kidney function.

Vascular Complications Related to Posterior Lumbar Disc Surgery

Purpose To evaluate patients who underwent surgical or endovascular treatment after vascular injury related to posterior lumbar disc surgery. Materials and Methods We retrospectively reviewed seven cases of vascular injuries (four lacerations, one arteriovenous fistula [AVF], and two pseudoaneurysms) related to lumbar disc surgery by a posterior approach from January 1997 to December 2016 at Chonnam National University Hospital. Information of patient characteristics, diagnosis, treatment strategies, and outcomes were analyzed. Results Five out of seven cases were inhospital cases. In three laceration cases, each patient instantly became hypotensive and a life-threatening arterial injury was suspected. Therefore, the patient was immediately turned to the supine position and surgical repair was performed. The patients with pseudoaneurysm and AVF were treated by endovascular intervention. Remaining two were referred cases under the impression of vascular injuries. One laceration case of them was in preshock condition, and the left common iliac artery was surgically repaired. The other referred patient showed pseudoaneurysm which was treated with stent graft insertion. There was no surgery or endovascular intervention related death and none of the patients suffered any sequela related to vascular injury. Conclusion Vascular injury associated with posterior lumbar disc surgery is not common, but can be fatal. Early recognition, diagnosis, and prompt treatment are essential to prevent fatal outcomes. Recently, endovascular intervention is increasingly and preferably used because of its low morbidity and mortality. However surgery is still the best option for the patients with unstable vital sign and endovascular approach can be applied to stable patients.

Colon perforation due to embolization coil for internal iliac aneurysm

Coil migration is an extremely rare but hazardous complication of aneurysmal coil embolization. Only 1 case report has described coil migration following endovascular exclusion to gastrointestinal (GI) tract. We report the experience of a case of colon penetration caused by embolization coil placed for internal iliac aneurysm. A 66-year-old man visited the Emergency Department for hematochezia that had persisted for 3 months. Stent insertion and coil embolization of left internal iliac artery aneurysm had been performed on the patient 18 months ago. Colonoscopy was performed. It suggested penetration of sigmoid colon by embolization coil and diverticulum. Angiography revealed extravasation of contrast media at left internal iliac artery. Covered stent deployment was done in the left internal iliac artery. One week after the stent insertion, the patient underwent anterior resection, aneurysm resection, and coil removal. The patient recovered without complications. He was discharged at 2 weeks after the operation.

MicroRNA profiling of tacrolimus-stimulated Jurkat human T lympocytes

Purpose This study investigated the Jurkat T cell line expresses cytotoxicity when treated with different concentrations of FK506, and analyzed the expression pattern of microRNA when stimulated by FK506 using the microRNAs microarray, as well as the expression pattern of a gene that is related to the differentiation, activation and proliferation of T cells after being affected by the change of microRNAs. Methods To investigate the effects of FK506 on microRNA expression, we purified total RNA of Jurkat cells treated with 20 µM FK506 for 72 hours and used to analyze microRNA profiling by using Agilents chip. Results These results demonstrated that treatment with FK506 markedly induced the down-regulation of 20 microRNAs as well as the up-regulation of 20 microRNAs in a time-dependent manner. The genes that down-regulated by FK506 include let-7a*, miR-20a*, and miR-487a. Otherwise miR-202, miR-485-5p, and miR-518c* are gradually up-regulated in expression. Sanger Institute and DAVIDs bioinformatics indicated that microRNAs regulated the several transcriptomes including nuclear factor of activated T cell-related, T cell receptor/interleukin-2 signaling, and Ca2+-calmodulin-dependent phosphatase calcineurin pathways. Conclusion As a result of treating FK506 to a Jurkat cell line and running the microRNA microarray, it was found that FK506 not only took part in the suppression of T cell proliferation/activation by inhibiting calcineurin in Jurkat apoptosis, but also affected the microRNAs that are involved in the regulation of various signal transduction pathways.

MYCOPHENOLIC ACID INDUCED APOPTOSIS IN HUMAN JURKAT CELLS VIA GENERATION OF ROS AND REGULATION HO-1 EXPRESSION: 180

Introduction Mycophenolic acid (MPA) is a selective inhibitor of inosine monophosphate dehydrogenase. Heme oxygenase-1(HO-1), the rate-limiting enzyme of heme catabolism, is known to modulate apoptosis in stress-related conditions. This study demonstrated that pharmacologic induction of HO-1 along with catalytic activation significantly modulated apoptosis of Jurkat cells induced by MPA. Methods We observed, cell viability, measurement of H2O2 generation, intracellular accumulations of Ca2+ and NO, and western blottings of apoptotic pathway proteins, such as caspases, Bcl-2, and Bax proteins. Mitochondrial membrane potential determination by JC-1 staining was performed. Results Cells were cultured with the presence or absence of FK506.MPA induced apoptotic cell death showing nuclear fragmentation and sub G0/G1 phase arrest in Jurkat cells. Caspase-3 proteases expression on MPA treated-Jurkat cells in a time-dependent manner. Treatment of MPA resulted in reactive oxygen species (ROS) generation in Jurkat cells. Decreased HO-1 expression on MPA treated-Jurkat cells after 36 hours. Change of mitochondrial membrane potential transition (MPT) was also noted. Expression of Bax proteins was identified. CoPPIX, HO-1 inducer, induced expression of HO-1 proteins in MPA treated Jurkat cells. CoPPIX inhibited generation of H2O2. CoPPIX, significantly inhibited the MPA induced apoptosis. Summaries were as follows. 1.Pharmacologic induction of HO-1 along with catalytic activation significantly modulated apoptosis of Jurkat cells induced by MPA. 2.MPA induced apoptotic cell death showing nuclear fragmentation and sub G0/G1 phase in Jurkat cells. CoPPIX, HO-1 inducer, significantly inhibited the cisplatin-induced apoptosis. 3.Treatment of MPA resulted in ROS generation in Jurkat cells. CoPPIX attenuated ROS production and mitochondrial permeability transition in MPAtreated cells. Conclusion The protective mechanism of HO-1 on MPA-induced apoptosis is associated with direct inhibition of ROS generation and mitochondrial permeability transition.