Long-term quality of life after en-bloc vertebrectomy: 25 patients followed up for 9 years

AbstractObjectiveAssess quality-of-life results in patients who have undergone extensive curative surgery for spinal tumor and compare them to the general population in France.IntroductionLife expectancy is not the only criterion to assess the outcomes after massive tumor resections. Residual quality of life is also crucial. An indication for major surgery for spinal tumor should take the patient's long-term functional status into account, but the literature is limited on this question.Materials and methodsTwenty-five living patients from a group of 120 operated were assessed, all of whom were operated on by the same surgeon between 1984 and 2007. The mean follow-up was 9 years (range, 3–25 years). The mean age at surgery was 49 years. The patients completed different functional and quality-of-life questionnaires: the Oswestry Disability Index version 2 (ODI), the PROLO, the Karnofsky Index of performance status (KI), the Eastern Cooperative Oncology Group performance status (ECOG), the Short Form-36 Health Survey (SF-36), and the EuroQol-5 Dimensions (EQ5D). In addition, each patient was clinically and radiographically evaluated. Subgroups were identified considering the number of levels resected and histology. Their results on the SF-36 were compared with the results from the general population in France.ResultsThe mean PCS (physical component summary of the SF-36) was 52.4, the MCS (mental component summary, the psychological component of the SF-36) was 47.7, the ODI was 18.2, the PROLO was 7, the ECOG was 1, and the KI was 80%. The resections at three levels were associated with worse results in terms of quality of life, but overall, the results were similar to the French general population data for all categories of the SF-36.ConclusionAppropriate indications for massive spinal resection give good oncological and functional results. Although the expected life expectancy justifies this aggressive surgery, postoperative quality of life shows that it can also be successful on a functional level.Level of evidenceLevel IV; retrospective clinical study

Emergence of the arterial worm Elaeophora schneideri in moose (Alces alces) and tabanid fly vectors in northeastern Minnesota, USA

Background Moose (Alces alces) are a culturally and economically valued species in Minnesota. However, the moose population has experienced a sudden, marked decline in their range, including extirpation in the northwest and a 66% decline in the last decade in the northeast portions of the state. Although the exact cause of this decline is unclear, parasitic metastrongylid and filarioid nematode infections are known causes of morbidity and mortality in moose across North America. Methods To determine if these parasitic nematodes could be contributing to the Minnesota moose population decline, we molecularly examined banked tissues obtained from moose that died of known and unknown causes for the presence of nematode DNA. Extracted brain DNA of 34 individual moose was amplified utilizing primers targeting the 18S rRNA gene and internal transcribed spacer regions of nematodes. Results DNA sequencing revealed that PCR products obtained from 15 (44.1%) of the moose were 99% identical to Parelaphostrongylus tenuis, a metastrongylid known to cause neurological disease and death. Additionally, brain tissue from 20 (58.8%) individuals yielded sequences that most closely aligned with Elaeophora schneideri, a parasite associated with neurological impairment but previously unreported in Minnesota. Setaria yehi, a common filarioid parasite of deer, was also detected in the brain tissue of 5 (14.7%) moose. Molecular screening of 618 captured tabanid flies from four trapping sites revealed E. schneideri was present (6%) in the Minnesota environment and transmission could occur locally. Prevalence rates among the flies ranged between 0–100% per trapping site, with Chrysops spp. and Hybomitra spp. implicated as the vectors. Conclusions Ultimately, these data confirm that P. tenuis is widespread in the Minnesota moose population and raises the question of the significance of E. schneideri as a contributing factor to morbidity and mortality in moose

Pretreatment minimal staging for non-small cell lung cancer: an updated consensus report

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31247/1/0000153.pd

Cisplatin-based adjuvant chemotherapy in patients with completely resected non-small-cell lung cancer

BACKGROUND

Heme Drives Susceptibility of Glomerular Endothelium to Complement Overactivation Due to Inefficient Upregulation of Heme Oxygenase-1

Atypical hemolytic uremic syndrome (aHUS) is a severe disease characterized by microvascular endothelial cell (EC) lesions leading to thrombi formation, mechanical hemolysis and organ failure, predominantly renal. Complement system overactivation is a hallmark of aHUS. To investigate this selective susceptibility of the microvascular renal endothelium to complement attack and thrombotic microangiopathic lesions, we compared complement and cyto-protection markers on EC, from different vascular beds, in in vitro and in vivo models as well as in patients. No difference was observed for complement deposits or expression of complement and coagulation regulators between macrovascular and microvascular EC, either at resting state or after inflammatory challenge. After prolonged exposure to hemolysis-derived heme, higher C3 deposits were found on glomerular EC, in vitro and in vivo, compared with other EC in culture and in mice organs (liver, skin, brain, lungs and heart). This could be explained by a reduced complement regulation capacity due to weaker binding of Factor H and inefficient upregulation of thrombomodulin (TM). Microvascular EC also failed to upregulate the cytoprotective heme-degrading enzyme heme-oxygenase 1 (HO-1), normally induced by hemolysis products. Only HUVEC (Human Umbilical Vein EC) developed adaptation to heme, which was lost after inhibition of HO-1 activity. Interestingly, the expression of KLF2 and KLF4—known transcription factors of TM, also described as possible transcription modulators of HO-1- was weaker in micro than macrovascular EC under hemolytic conditions. Our results show that the microvascular EC, and especially glomerular EC, fail to adapt to the stress imposed by hemolysis and acquire a pro-coagulant and complement-activating phenotype. Together, these findings indicate that the vulnerability of glomerular EC to hemolysis is a key factor in aHUS, amplifying complement overactivation and thrombotic microangiopathic lesions

Concomitant and alternating radiation therapy (RT) and chemotherapy (CT) for inoperable, M0, non-small cell lung cancers (NSCLC): a consensus report

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/31248/1/0000154.pd

LICSTER -- A Low-cost ICS Security Testbed for Education and Research

Unnoticed by most people, Industrial Control Systems (ICSs) control entire productions and critical infrastructures such as water distribution, smart grid and automotive manufacturing. Due to the ongoing digitalization, these systems are becoming more and more connected in order to enable remote control and monitoring. However, this shift bears significant risks, namely a larger attack surface, which can be exploited by attackers. In order to make these systems more secure, it takes research, which is, however, difficult to conduct on productive systems, since these often have to operate twenty-four-seven. Testbeds are mostly very expensive or based on simulation with no real-world physical process. In this paper, we introduce LICSTER, an open-source low-cost ICS testbed, which enables researchers and students to get hands-on experience with industrial security for about 500 Euro. We provide all necessary material to quickly start ICS hacking, with the focus on low-cost and open-source for education and research

Plasminogen Controls Inflammation and Pathogenesis of Influenza Virus Infections via Fibrinolysis

Detrimental inflammation of the lungs is a hallmark of severe influenza virus infections. Endothelial cells are the source of cytokine amplification, although mechanisms underlying this process are unknown. Here, using combined pharmacological and gene-deletion approaches, we show that plasminogen controls lung inflammation and pathogenesis of infections with influenza A/PR/8/34, highly pathogenic H5N1 and 2009 pandemic H1N1 viruses. Reduction of virus replication was not responsible