Object The goal of this study was to assess the operative outcomes of adult patients with scoliosis who were treated surgically with minimally invasive correction and fusion. Methods This was a retrospective study of 28 consecutive patients who underwent minimally invasive correction and fusion over 3 or more levels for adult scoliosis. Hospital and office charts were reviewed for clinical data. Functional outcome data were collected at each visit and at the last follow-up through self-administered questionnaires. All radiological measurements were obtained using standardized computer measuring tools. Results The mean age of the patients in the study was 67.7 years (range 22–81 years), with a mean follow-up time of 22 months (range 13–37 months). Estimated blood loss for anterior procedures (transpsoas discectomy and interbody fusions) was 241 ml (range 20–2000 ml). Estimated blood loss for posterior procedures, including L5–S1 transsacral interbody fusion (and in some cases L4–5 and L5–S1 transsacral interbody fusion) and percutaneous screw fixation, was 231 ml (range 50–400 ml). The mean operating time, which was recorded from incision time to closure, was 232 minutes (range 104–448 minutes) for the anterior procedures, and for posterior procedures it was 248 minutes (range 141–370 minutes). The mean length of hospital stay was 10 days (range 3–20 days). The preoperative Cobb angle was 22° (range 15–62°), which corrected to 7° (range 0–22°). All patients maintained correction of their deformity and were noted to have solid arthrodesis on plain radiographs. This was further confirmed on CT scans in 21 patients. The mean preoperative visual analog scale and treatment intensity scale scores were 7.05 and 53.5; postoperatively these were 3.03 and 25.88, respectively. The mean preoperative 36-Item Short Form Health Survey and Oswestry Disability Index scores were 55.73 and 39.13; postoperatively they were 61.50 and 7, respectively. In terms of major complications, 2 patients had quadriceps palsies from which they recovered within 6 months, 1 sustained a retrocapsular renal hematoma, and 1 patient had an unrelated cerebellar hemorrhage. Conclusions Minimally invasive surgical correction of adult scoliosis results in mid- to long-term outcomes similar to traditional surgical approaches. Whereas operating times are comparable to those achieved with open approaches, blood loss and morbidity appear to be significantly lower in patients undergoing minimally invasive deformity correction. This approach may be particularly useful in the elderly.

Nanotechnology is the design and assembly of submicroscopic devices called nanoparticles, which are 1–100 nm in diameter. Nanomedicine is the application of nanotechnology for the diagnosis and treatment of human disease. Disease-specific receptors on the surface of cells provide useful targets for nanoparticles. Because nanoparticles can be engineered from components that (1) recognize disease at the cellular level, (2) are visible on imaging studies, and (3) deliver therapeutic compounds, nanotechnology is well suited for the diagnosis and treatment of a variety of diseases. Nanotechnology will enable earlier detection and treatment of diseases that are best treated in their initial stages, such as cancer. Advances in nanotechnology will also spur the discovery of new methods for delivery of therapeutic compounds, including genes and proteins, to diseased tissue. A myriad of nanostructured drugs with effective site-targeting can be developed by combining a diverse selection of targeting, diagnostic, and therapeutic components. Incorporating immune target specificity with nanostructures introduces a new type of treatment modality, nano-immunochemotherapy, for patients with cancer. In this review, we will discuss the development and potential applications of nanoscale platforms in medical diagnosis and treatment. To impact the care of patients with neurological diseases, advances in nanotechnology will require accelerated translation to the fields of brain mapping, CNS imaging, and nanoneurosurgery. Advances in nanoplatform, nano-imaging, and nano-drug delivery will drive the future development of nanomedicine, personalized medicine, and targeted therapy. We believe that the formation of a science, technology, medicine law–healthcare policy (STML) hub/center, which encourages collaboration among universities, medical centers, US government, industry, patient advocacy groups, charitable foundations, and philanthropists, could significantly facilitate such advancements and contribute to the translation of nanotechnology across medical disciplines.

Exposure of particulate air pollution is linked to increased incidences of cardiovascular diseases. Ambient ultra fine particles (UFP) from diesel vehicle engines have been shown to be pro-atherogenic in apoE knockout mice and may constitute a major cardiovascular risk in humans. We posited that circulating nano-sized particles from traffic pollution sources induced vascular oxidative stress via JNK activation in endothelial cells. Diesel UFP were collected from a 1998 Kenworth truck. Intra-cellular superoxide assay revealed that these UFP dose-dependently induced superoxide (O2·-) production in human aortic endothelial cells (HAEC). Flow cytometry (FACS) showed that UFP increased MitoSOX Red intensity specific for mitochondrial superoxide. Protein carbonyl content is increased by UFP as an indication of vascular oxidative stress. UFP also up-regulated hemeoxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pre-treatment with antioxidant, N-acetyl cysteine (NAC), significantly decreased their expression. Furthermore, UFP transiently activated JNK in HAEC. Treatment with JNK inhibitor SP600125 and silencing of both JNK1 and JNK2 with siRNA inhibited UFP stimulated O2·- production and mRNA expression of HO-1 and TF. Our findings suggest that JNK activation play an important role in UFP-induced oxidative stress and stress response gene expression.

Fluid shear stress is intimately linked with vascular oxidative stress and atherosclerosis. We posited that atherogenic oscillatory shear stress (OSS) induced mitochondrial superoxide (mtO 2 À ) production via NADPH oxidase and c-Jun NH 2 -terminal kinase ( JNK-1 and JNK-2) signaling. In bovine aortic endothelial cells, OSS (AE3 dyn=cm 2 ) induced JNK activation, which peaked at 1 h, accompanied by an increase in fluorescein isothiocyanate-conjugated JNK fluorescent and MitoSOX Red (specific for mtO 2 À production) intensities. Pretreatment with apocynin (NADPH oxidase inhibitor) or N-acetyl cysteine (antioxidant) significantly attenuated OSS-induced JNK activation. Apocynin further reduced OSS-mediated dihydroethidium and MitoSOX Red intensities specific for cytosolic O 2 À and mtO 2 À production, respectively. As a corollary, transfecting bovine aortic endothelial cells with JNK siRNA (siJNK) and pretreating with SP600125 ( JNK inhibitor) significantly attenuated OSS-mediated mtO 2 À production. Immunohistochemistry on explants of human coronary arteries further revealed prominent phosphorylated JNK staining in OSS-exposed regions. These findings indicate that OSS induces mtO 2 À production via NADPH oxidase and JNK activation relevant for vascular oxidative stress. Antioxid. Redox Signal. 15, 1379-1388.

Our 10-year experience supports current algorithms in the management of PPH. Key considerations include the recognition of the sentinel bleed, the presence of a pancreatic fistula, and the initial operative role of a long gastroduodenal artery stump with radiopaque marker for safe and effective embolization should PPH occur.