Radiation arteritis is a rare cause of lower extremity peripheral arterial occlusive disease, and has been traditionally treated with open interventions. There have been only a few reported cases of endovascular interventions for this disease. Previous reports described endovascular treatment in the iliac and common femoral regions, but intervention in the superficial femoral artery have not been described. Described here is a case of acute lower extremity ischemia caused by remote radiation arteritis of the superficial femoral artery, which was successfully treated by percutaneous endovascular technique.

No description available.

Cardiac dysfunction is a major consequence of sepsis/septic shock and contributes to the high mortality of sepsis. Innate and inflammatory responses mediated by TLRs play a critical role in sepsis-induced cardiac dysfunction. MicroRNA-146 (miR-146) was first identified as a negative regulator in innate immune and inflammatory responses induced by LPS. This study examined whether miR-146a will have a protective effect on sepsis-induced cardiac dysfunction. Lentivirus-expressing miR-146a (LmiR-146a) or lentivirusexpressing scrambled miR (LmiR-control) was delivered into the myocardium via the right carotid artery. Seven days after transfection, mice were subjected to cecal ligation and puncture (CLP). Untransfected mice were also subjected to CLP-induced sepsis. Cardiac function was examined by echocardiography before and 6 h after CLP. In vitro studies showed that increased miR-146a levels suppress LPS-induced IkBa phosphorylation and inflammatory cytokine production in both H9C2 cardiomyocytes and J774 macrophages. In vivo transfection of LmiR-146a attenuated sepsis-induced cardiac dysfunction. The values for percent ejection fraction and percent fractional shortening in LmiR-146a-transfected CLP mice were significantly greater than in untransfected CLP control. LmiR-146a transfection prevented sepsis-induced NF-κB activity, suppressed IRAK and TRAF6 expression in the myocardium, and attenuated sepsis-induced inflammatory cytokine production in both plasma and peritoneal fluid. In addition, LmiR-146a transfection decreased sepsis-induced infiltration of neutrophils and macrophages into the myocardium. LmiR-146a can also transfect macrophages in the periphery. We conclude that miR-146a attenuates sepsis-induced cardiac dysfunction by preventing NF-kB activation, inflammatory cell infiltration, and inflammatory cytokine production via targeting of IRAK and TRAF6 in both cardiomyocytes and inflammatory monocytic cells.

This case report describes an immune-competent patient with acute upper extremity ischemia caused by thromboembolism from an Aspergillus-infected ascending aortic pseudoaneurysm. Efforts to identify the source of an acute arterial thromboembolic occlusion should be made, and a high index of suspicion for mycotic infection should be maintained in patients with an atypical presentation, such as fevers of unknown origin. Additional measures, such as pathologic examination of thromboembolic debris, blood cultures, and positron emission tomography, should be performed to identify the etiology in these unexplained situations.

Background: The current study examined the role(s) of autophagy in myotoxicity induced by bupivacaine in mouse myoblast C2c12 cells. Methods: C2c12 cells were treated with bupivacaine. Myotoxicity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (n = 3 to 30), live/dead assay (n = 3 to 4), and morphological alterations (n = 3). Autophagosome formation was reflected by microtubule-associated protein light chain 3 conversion (n = 4 to 12) and light chain 3 punctation (n = 4 to 5). Autophagosome clearance was evaluated by p62 protein level (n = 4) and autolysosomes generation (n = 3). Results: Bupivacaine induced significant cell damage. Notably, there was a significant increase in autophagosome generation as evidenced by light chain 3 puncta formation (72.7 ± 6.9 vs. 2.1 ± 1.2) and light chain 3 conversion (2.16 ± 0.15 vs. 0.33 ± 0.04) in bupivacaine-treated cells. Bupivacaine inactivated the protein kinase B/mammalian target of rapamycin/p70 ribosomal protein S6 kinase signaling. However, cellular levels of p62 protein were significantly increased upon bupivacaine treatment (1.29 ± 0.15 vs. 1.00 ± 0.15), suggesting that the drug impaired autophagosome clearance. Further examination revealed that bupivacaine interrupted autophagosome-lysosome fusion (10.87% ± 1.48% vs. 32.94% ± 4.22%). Administration of rapamycin increased autophagosome clearance and, most importantly, improved the survival in bupivacaine-treated cells. However, knockdown of autophagy-related protein 5 (atg5) exacerbated bupivacaine-induced impairment of autophagosome clearance and myotoxicity. Conclusions: The data suggest that autophagosome formation was induced as a stress response mechanism after bupivacaine challenge; however, autophagosome clearance was impaired due to inadequate autophagosome-lysosome fusion. Therefore, impairment of autophagosome clearance appears to be a novel mechanism underlying bupivacaine-induced myotoxicity.

Objective Abdominal aortic aneurysms (AAAs) may rupture at smaller diameters in women than in men, and women may be at higher risk and have poorer outcomes in elective and emergent interventions because of age and comorbidities. Practice guidelines recommending elective AAA repair at >5.5 cm are gender neutral and may not adequately reflect increased risks in women or the potential advantages of elective lower risk endovascular procedures. Methods Patients with a diagnosis of AAA discharged from a single referral hospital during a 14-year period were identified for retrospective analysis. Results A total of 2121 patients with AAAs were studied, 499 women (23.5%) and 1622 men (76.5%). Women were older and had a greater incidence of hypertension, smoking, chronic obstructive pulmonary disease, dyslipidemia, and renal insufficiency. Intact AAAs in 467 women had a mean diameter of 4.4 ± 1.3 cm compared with 1538 men at 5.0 ± 1.4 cm (P <.01). The ruptured AAAs in 32 women (6.4%) had a mean diameter of 6.1 ± 1.5 cm compared with 84 men (5.2%) at 7.7 ± 1.9 cm (P <.01). Women had a twofold increased frequency of AAA rupture than men at all size intervals (P <.01). The frequency of ruptured AAAs <5.5 cm among 10 of 32 women with ruptured AAAs was 31.3%; among 7 of 84 men with ruptured AAAs, it was 8.3% (P <.01). The frequency of ruptured AAAs <5.5 cm in all 383 women with AAAs <5.5 cm was 2.6%; in 1042 men, it was 0.6% (P <.01). Of the 1211 AAA repairs, 574 (47.4%) were open aneurysm repair (OAR) and 637 (52.6%) were endovascular aneurysm repair (EVAR). Mortality after elective OAR in 475 patients of both sexes was 5.1%; for EVAR in 676 patients, mortality was 1.6% (P <.01). No differences in mortality with respect to OAR or EVAR were found between the female and male cohorts in either intact or ruptured AAAs. Conclusions Women with AAAs are older and have a higher frequency of cardiovascular risk factors than men. Women rupture AAAs with a greater frequency than men at all size intervals and have a fourfold increased frequency of rupture at <5.5 cm. No differences in surgical mortality between women and men were found. Current practice guidelines for elective AAA operative intervention should be reconsidered and stratified by gender.

Objective Junctional component separation producing type IIIa endoleak after endovascular abdominal aortic aneurysm repair (EVAR) is an uncommon but serious complication requiring unanticipated reinterventions. This retrospective study analyzed main-body EVAR component uncoupling and type IIIa endoleaks encountered with Powerlink and AFX (Endologix Inc, Irvine, Calif) endografts during an 8-year period. Methods Type IIIa endoleaks were identified from a database of secondary interventions and clinical surveillance. Operative reports, medical records, and computed tomography studies were reviewed. Clinical and imaging characteristics were analyzed over time, and differences were compared at appropriate follow-up intervals. Results Since 2006, 701 patients underwent primary EVAR using Endologix Powerlink (352 patients, 2006-2011) or AFX (349 patients, 2011-2014) endografts. Endoleaks required 32 secondary interventions (4.6%), including type Ia in 4 patients (1 proximal extension and 3 explants); type Ib in 8 patients (all distal extensions for enlarging iliac aneurysms); type II in 1 patient (explant); type IIIa in 17 patients (2.4%), who were the subject of this report; and type IIIb in 2 patients (both EVAR relining). The 17 patients with type IIIa endoleak were an average age of 71 years, and 14 (82%) were men. The mean preoperative abdominal aortic aneurysm (AAA) diameter was 70 ± 18 mm. The repair was elective in 16 patients and an emergency in one. Ten cases were performed with Powerlink and seven with AFX. Analysis of serial computed tomography scans found significant changes in AAA diameter; renal-to-bifurcation straight-line, centerline, and greater curvature lengths; EVAR angulation; and loss of EVAR component overlap. The average time from EVAR to reintervention was 32 months. Three patients returned with a ruptured AAA and three with AAA thrombosis, and three of these patients (18%) died ≤30 days of the emergency reintervention. Secondary procedures included EVAR relining with additional bridging components in 14 patients (82%), explant in 2, and axillobifemoral bypass in 1. No new cases of endograft uncoupling have been identified in patients treated with AFX since December 2012 after adoption of revised instructions for use. Conclusions Although a small number of secondary interventions were needed after EVAR with the Endologix Powerlink or AFX endografts, most were undertaken for late main-body component uncoupling and type IIIa endoleak, which can occur after sideways displacement of the endograft in large and angulated AAAs. Patients treated before 2013 under the old instructions for use should be evaluated for signs of impending component separation and monitored annually, noting that expected indicators of endograft failure, such as increasing AAA diameter and endoleak, may be absent.

Background: Acellular dermal matrix has proven to be a useful adjunct in tissue expander or direct-to-implant breast reconstruction. Although versatile, acellular dermal matrix adds considerable cost. Vicryl (polyglactin) mesh has an established track record in many fields of surgery, and is considerably less costly than acellular dermal matrix. This study examines the use and long-term follow-up of Vicryl mesh in breast reconstruction. Methods: Vicryl mesh was used in 46 breast reconstructions (38 patients; 35 immediate and three delayed). The mesh was used along the inframammary fold to maintain position of the inferior pectoral edge, and/or along the lateral border to maintain expander position and prevent lateral migration. Eight breasts received adjuvant radiation therapy. Results: Mean follow-up at the time of review was 43 months. In the nonirradiated group (38 breasts), there was one postoperative infection (2.6 percent), which required expander removal. In the irradiated group, there were three complications requiring expander removal (37.5 percent): two infections and one device exposure after irradiation. Significant malposition was not observed in any breast where Vicryl mesh was used, and no visible mesh remained at the time of implant placement. The incidence of symptomatic capsular contracture in nonirradiated breasts was 3.2 percent. At latest follow-up, nonirradiated breasts had an average Baker capsule grade of 1.1, compared with 1.5 in the irradiated group. Conclusions: Vicryl mesh is an effective alternative to acellular dermal matrix in nonirradiated breast reconstruction and is available at approximately onetwentieth the cost. Acellular dermal matrix or full muscle coverage may be preferable in irradiated reconstructions.

Glucans are natural product carbohydrates that stimulate immunity. Glucans are internalized by the pattern recognition receptor, Dectin-1. Glucans were thought to be trafficked to phagolysosomes, but this is unproven. We examined the internalization and trafficking of soluble glucans in macrophages. Incubation of macrophages with glucan resulted in internalization of Dectin-1 and glucan. Inhibition of clathrin blocked internalization of the Dectin-1/glucan complex. Lipid raft depletion resulted in decreased Dectin levels and glucan uptake. Once internalized, glucans colocalized with early endosomes at 0 to 15 min, with the Golgi apparatus at 15 min to 24 h, and with Dectin-1 immediately (0 h) and again later (15 min-24 h). Glucans did not colocalize with lysosomes at any time interval examined. We conclude that the internalization of Dectin-1/glucan complexes in macrophages is mediated by clathrin and negatively regulated by lipid rafts and/or caveolin-1. Upon internalization, soluble glucans are trafficked via endosomes to the Golgi apparatus, not lysosomes.

In the last decade, stem cell research has gained significant attention in China with exponential increase in support during the last few years. Although both embryonic and adult stem cells can be used for cellular cardiomyoplasty, only clinical studies using adult stem cells are summarized in this chapter with our results described in detail. We harvested stem cells from skeletal muscle (satellite cells) or bone marrow from different patients and utilized for cellular cardiomyoplasty. Eighteen male patients suffering acute myocardial infarction were evenly assigned to coronary artery bypass graft and autologous satellite cell implantation or percutaneous coronary intervention and autologous bone marrow cell intra-coronary infusion. Cardiac functions were assessed before and at six month after the treatment. All patients survived the procedures without obvious arrhythmia, had an uneventful recovery, and were discharged from the hospital. Significant improvement in NYHA classification and left ventricular ejection fraction were observed to a similar degree for both treatments at six month later. Comparable improvements in local contractility, blood perfusion, tissue viability, and wall thickness at the infarct area for all patients receiving either type of autologous stem cells were also found. A longer follow-up time and large scale randomized controlled trail will be needed.