Mycotic Abdominal Pseudoaneurysm due to Psoas Abscess after Spinal Fusion.

A 36-year-old man, who had undergone thoracoscopic anterior spinal fusion using the plate system and posterior screw fusion three months previously, presented to our hospital with left flank pain and fever. Computed tomography indicated the presence of a psoas muscle abscess. However, after two days of percutaneous catheter drainage, a mycotic abdominal aortic pseudoaneurysm was detected via computed tomography. We performed in situ revascularization using a prosthetic graft with omental wrapping. Methicillin-resistant Staphylococcus aureus was identified on blood and pus culture, and systemic vancomycin was administered for one month. Although the abscess recurred, it was successfully treated with percutaneous catheter drainage and systemic vancomycin administration for three months, without the need for instrumentation removal. The patient remained asymptomatic throughout two years of follow-up.

Repositioning Potential of PAK4 to Osteoclastic Bone Resorption.

Drug repositioning is a rational approach for expanding the use of existing drugs or candidate drugs to treat additional disorders. Here we investigated the possibility of using the anticancer p21-activated kinase 4 (PAK4)-targeted inhibitor PF-3758309 to treat osteoclast-mediated disorders. PAK4 was highly expressed in bone marrow cells and was phosphorylated during their differentiation into osteoclasts, and osteoclast differentiation was significantly inhibited by the dominant negative form of PAK4 and by PF-3758309. Specifically, PF-3758309 significantly inhibited the fusion of preosteoclasts, the podosome formation, and the migration of preosteoclasts. PF-3758309 also had in vivo antiresorptive activity in a lipopolysaccharide-induced bone erosion model and in vitro antiosteoclastogenic activity in the differentiation of human bone marrow-derived cells and peripheral blood mononuclear cells into osteoclasts. These data demonstrate the relevance of PAK4 in osteoclast differentiation and the potential of PAK4 inhibitors for treating osteoclast-related disorders.

The role of autophagy induced by pemetrexed in lung adenocarcinoma cells.

Autophagy is known as an important regulatory mediator for cell survival or death and its important role in cancer. Pemetrexed (PTX) has been used in chemotherapy for lung cancer. However, the underlying molecular mechanisms have not been fully clarified. To investigate the role of autophagy induced by PTX in A549 cells, we performed MTT assay, acridine orange staining, western blotting, Annexin V/PI by using the 3-MA autophagy inhibitor. PTX induced autophagy after 48 h treatment in A549 cells. Furthermore, PTX showed acidic vesicular organelles (AVOs) and expressed LC3-II in A549 cells. The induction of autophagy by PTX was inhibited by 3-MA which was confirmed by reduced AVOs. When the autophagy was inhibited, Annexin V was increased. In addition, PARP cleavage was increased as shown by western blotting. Taken together, PTX induced autophagy in A549 cells and these cellular events possibly cause the apoptotic and/or necrotic cell death of A549 cells.

Aortic valve leaflet replacement with bovine pericardium to preserve native dynamic capabilities of the aortic annulus.

Valve replacement is typically the most appropriate option for treating aortic valve stenotic insufficiency. However, neither mechanical nor bioprosthetic replacement components preserve the circumferential expansion and contraction of a native aortic annulus during the cardiac cycle, because the prosthetic ring is affixed to the annulus. A 64-year-old man presented with a bicuspid and stenotic aortic valve, and the native annulus was too small to accommodate a porcine replacement valve. We fashioned new aortic leaflets from bovine pericardium with use of a template, and we affixed the sinotubular junction with use of inner and outer stabilization rings. Postoperative echocardiograms revealed coaptation of the 3 new leaflets with no regurgitation. At the patient's 5.5-year follow-up examination, echocardiograms showed flexible leaflet movement with a coaptation height of 7 mm, and expansion and contraction of the aortic annulus similar to that of a normal native annulus. The transvalvular pressure gradient was insignificant. If long-term durability of the new leaflets is confirmed, this method of leaflet replacement and fixation of the sinotubular junction might serve as an acceptable alternative to valve replacement in the treatment of aortic valve stenosis. We describe the patient's case and present our methods and observations.

Autophagy induction by low-dose cisplatin: the role of p53 in autophagy.

The majority of chemotherapy treatments for lung cancer use cisplatin; however, its use is limited as it has several side-effects. Autophagy (or type II cell death) is an important mechanism by which programmed cell death occurs. The purpose of this study was to determine whether low-dose cisplatin treatment induces autophagy in lung cancer cells. We also examined whether autophagy inhibition results in p53-mediated apoptosis. NCI-H460 (wild-type p53) and NCI-H1299 (null-type p53) cells were treated with 5 or 20 µM cisplatin for 12, 24 or 48 h. An MTT assay was performed to measure the cell viability following cisplatin treatment. To detect cisplatin-induced autophagy, cell morphology (autophagic vacuole) and LC3 localization were examined. The outcome of autophagy inhibition was determined using 3-methyladenine (3-MA) to detect Annexin V (+), propidium iodide (PI) (-) and acridine orange (+) cells by FACS analysis. To determine whether cisplatin induced autophagy, we examined the role of p53 as a cell survival regulator in autophagy. Low-doses of cisplatin (5 µM) induced cell death and this was augmented by 3-MA in both cell lines. Autophagic vacuoles and cytoplasmic LC3 formation was more evident in H460 cells than in H1299 cells. The induction of autophagy by low-dose cisplatin was increased by 2-fold in H460 compared to H1299 cells. However, the tests for apoptosis showed no difference between the 2 cell lines. Following 3-MA pretreatment, cisplatin-induced autophagy was found to be markedly reduced (a 3-fold reduction) in wild-type p53 compared to null-type p53 cells. However, cisplatin-induced apoptosis increased in wild-type p53 compared to null-type p53 cells. Autophagy induction and apoptotic shift after autophagy inhibition may be mediated by p53 activation in lung cancer cells treated with low-dose cisplatin.

Rupture of the left atrial roof due to blunt trauma.

Cardiac rupture after blunt trauma is rare and associated with high mortality. The anatomic pattern of blunt cardiac rupture has been demonstrated with the right cardiac chambers more frequently affected than the left. Furthermore, left atrial injury is usually restricted to the atrial appendage and the pulmonary vein-atrial junction. Herein, we report the first case of a 61-year old man with a rupture of the left atrial roof after blunt trauma with minimal thoracic injury.

Predictive factors of sustained sinus rhythm and recurrent atrial fibrillation after the maze procedure.

BACKGROUND: We examined perioperative predictors of sustained sinus rhythm (SR) in patients undergoing the Cox maze operation and concomitant cardiac surgery for structural heart disease. MATERIALS AND METHODS: From October 1999 to December 2008, 90 patients with atrial fibrillation (AF) underwent the Cox maze operation and other concomitant cardiac surgery. Eighty-nine patients, all except for one postoperative death, were followed-up with serial electrocardiographic studies, 24-hour Holter monitoring tests, and regular echocardiographic studies. RESULTS: Eighty-nine patients undergoing the maze operation were divided into two groups according to the presence of SR. At the time of last follow-up (mean follow-up period, 51.0±30.8 months), 79 patients (88.8%) showed SR (SR group) and 10 patients (11.2%) had recurrent AF (AF group). Factors predictive of sustained SR were the immediate postoperative conversion to SR (odds ratio, 97.2; p=0.001) and the presence of SR at the 6th month postoperatively (odds ratio, 155.7; p=0.002). Duration of AF, mitral valve surgery, number of valves undergoing surgery, left atrial dimension, and perioperative left ventricular dimensions and ejection fractions were not predictors of postoperative maintenance of SR. CONCLUSION: Immediate postoperative SR conversion and the presence of SR at the 6th postoperative month were independent predictors of sustained SR after the maze operation.

Early experience of thoracic endovascular aortic repair: a local single hospital experience.

PURPOSE: The purpose of this retrospective study was to evaluate the short- to mid-term results of thoracic endovascular aortic repair (TEVAR) in Wonkwang University School of Medicine & Hospital. METHODS: Between February 2009 and May 2011, 8 consecutive patients had undergone endovascular stent-grafting for thoracic aortic diseases. Five patients were treated for traumatic thoracic aortic injuries, two patients were treated for thoracic aneurysms and one patient was treated for a pseudoaneurysm due to penetrating aortic ulcers. Attempted stent-graft deployment was performed electively in 6 patients and emergently in 2. Follow-up was performed at 1-month, 6-month, 1-year, and annually thereafter. RESULTS: Technical success rates were achieved in 87.5% and the 30-day mortality rate was 0%. Mean hospital length of stay after TEVAR was 30 days in traumatic thoracic aortic injuries and 10 days in thoracic aneurismal diseases. Intra-operative Type I endoleak due to migration at deflation was visualized in 1 patient, which was treated by insertion of another stent-graft. During follow-up, a major complication was encountered in one patient who received carotid-subclavian bypass to relieve left arm ischemia. After 5 months he was treated with arch replacement for aortic arch aneurysm with type I endoleak at proximal site after endovascular treatment. The 30-day mortality rate was 0%. However, 1 case of mortality (12.5%) was observed during the follow-up period. CONCLUSION: The short and mid-term results of endovascular repair of thoracic aortic diseases are promising. TEVAR is an effective procedure in the management of thoracic aortic diseases.

Inhibitory regulation of osteoclast differentiation by interleukin-3 via regulation of c-Fos and Id protein expression.

Interleukin-3 (IL-3) is produced under various pathological conditions and is thought to be involved in the pathogenesis of inflammatory diseases; however, its function in bone homeostasis under normal conditions or nature of the downstream molecular targets remains unknown. Here we examined the effect of IL-3 on osteoclast differentiation from mouse and human bone marrow-derived macrophages (BMMs). Although IL-3 can induce osteoclast differentiation of multiple myeloma bone marrow cells, IL-3 greatly inhibited osteoclast differentiation of human BMMs isolated from healthy donors. These inhibitory effects of IL-3 were only observed at early time points (days 0 and 1). IL-3 inhibited the expression of c-Fos and NFATc1 in BMMs treated with RANKL. However, IL-3-mediated inhibition of osteoclast differentiation was not completely reversed by ectopic expression of c-Fos or NFATc1. Importantly, IL-3 induced inhibitor of DNA binding/differentiation (Id)1 in hBMMs, while Id2 were sustained during osteoclast differentiation of mBMMs treated with IL-3. Ectopic expression of NFATc1 in Id2-deficient BMMs completely reversed the inhibitory effect of IL-3 on osteoclast differentiation. Furthermore, inflammation-induced bone erosion was markedly inhibited by IL-3 administration. Taken together, our results suggest that IL-3 plays an inhibitory role in osteoclast differentiation by regulating c-Fos and Ids, and also exerts anti-bone erosion effects.