Charge Management for Gravitational Wave Observatories using UV LEDs

Accumulation of electrical charge on the end mirrors of gravitational wave observatories, such as the space-based LISA mission and ground-based LIGO detectors, can become a source of noise limiting the sensitivity of such detectors through electronic couplings to nearby surfaces. Torsion balances provide an ideal means for testing gravitational wave technologies due to their high sensitivity to small forces. Our torsion pendulum apparatus consists of a movable Au-coated Cu plate brought near a Au-coated Si plate pendulum suspended from a non-conducting quartz fiber. A UV LED located near the pendulum photoejects electrons from the surface, and a UV LED driven electron gun directs photoelectrons towards the pendulum surface. We have demonstrated both charging and discharging of the pendulum with equivalent charging rates of $\sim$$10^5 e/\mathrm{s}$, as well as spectral measurements of the pendulum charge resulting in a white noise level equivalent to $3\times10^5 e/\sqrt{Hz}$.Comment: 5 pages, submitted to PR

Scattering into Cones and Flux across Surfaces in Quantum Mechanics: a Pathwise Probabilistic Approach

We show how the scattering-into-cones and flux-across-surfaces theorems in Quantum Mechanics have very intuitive pathwise probabilistic versions based on some results by Carlen about large time behaviour of paths of Nelson diffusions. The quantum mechanical results can be then recovered by taking expectations in our pathwise statements.Comment: To appear in Journal of Mathematical Physic

The Neoadjuvant Net: A patient- and surgeon-friendly device to facilitate safe breast-conserving surgery in patients who underwent neoadjuvant treatment

The primary goal of the study was to describe an innovative and helpful tool in defining the minimal surgical margins necessary during breast-conserving surgery (BCS) after neoadjuvant treatment: the Neoadjuvant Net (NN). The secondary endpoint was to assess its usefulness in achieving postoperative disease-free margins and reducing Ipsilateral Breast Tumor Recurrences (IBRTs). The breast-conserving surgical technique together with the use of the Neoadjuvant Net is herein reported. Age, stage at diagnosis, clinical and pathological response, lymph node status, type of surgery, margin status, and incidence of local and distant recurrence were retrospectively analyzed. Seventy-five patients underwent BCS following medical treatment from 2000 to 2011. The majority of the patients had significant size reduction (63/75, 84%). Twenty-two had a complete clinical response but only 11 (11/75, 14.7%) showed a complete pathological response. Two patients (2/75, 2.67%) had infiltrated surgical margins. After a mean follow-up of seventy months, 3 patients (3/75, 4%) had IBRTs and 4 women had distant metastases (4/75, 5.34%). The NN is an easy-to-use, non-invasive instrument designed with the purpose of facilitating the surgeon's task of reducing infiltrated margins and IBTRs

Polymorphonuclear myeloid-derived suppressor cells limit antigen crosspresentation by dendritic cells in cancer

DCs are a critical component of immune responses in cancer primarily due to their ability to cross-present tumor-associated antigens. Cross-presentation by DCs in cancer is impaired, which may represent one of the obstacles for the success of cancer immunotherapies. Here, we report that polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) blocked crosspresentation by DCs without affecting direct presentation of antigens by these cells. This effect did not require direct cell-cell contact and was associated with transfer of lipids. Neutrophils (PMN) and PMN-MDSC transferred lipid to DCs equally well; however, PMN did not affect DC cross-presentation. PMN-MDSC generate oxidatively truncated lipids previously shown to be involved in impaired cross-presentation by DCs. Accumulation of oxidized lipids in PMN-MDSC was dependent on myeloperoxidase (MPO). MPO-deficient PMN-MDSC did not affect cross-presentation by DCs. Cross-presentation of tumor-associated antigens in vivo by DCs was improved in MDSC-depleted or tumor-bearing MPO-KO mice. Pharmacological inhibition of MPO in combination with checkpoint blockade reduced tumor progression in different tumor models. These data suggest MPO-driven lipid peroxidation in PMN-MDSC as a possible non–cell autonomous mechanism of inhibition of antigen cross-presentation by DCs and propose MPO as potential therapeutic target to enhance the efficacy of current immunotherapies for patients with cancer

Kidney transplantation from living donor with monolateral renal artery fibromuscular dysplasia using a cryopreserved iliac graft for arterial reconstruction: a case report and review of the literature

Background Aging and mortality of patients on waiting lists for kidney transplantation have increased, as a result of the shortage of organs available all over the world. Living donor grafts represent a significant source to maintain the donor pool, and resorting successfully to allografts with arterial disease has become a necessity. The incidence of renal artery fibromuscular dysplasia (FMD) in potential living renal donors is reported to be 2-6%, and up to 4% of them present concurrent extra-renal involvement. Case presentation We present a case of renal transplantation using a kidney from a living donor with monolateral FMD. Resection of the affected arterial segment and its subsequent replacement with a cryopreserved iliac artery graft from a deceased donor were performed. No intraoperative nor post-operative complications were reported. The allograft function promptly resumed, with satisfying creatinine clearance, and adequate patency of the vascular anastomoses was detected by Doppler ultrasounds. Conclusion Literature lacks clear guidelines on the eligibility of potential living renal donors with asymptomatic FMD. Preliminary assessment of the FMD living donor should always rule out any extra-renal involvement. Whenever possible, resection and reconstruction of the affected arterial segment should be taken into consideration as this condition may progress after implantation

Complement activation in the plasma and placentas of women with different subsets of antiphospholipid syndrome

Problem: As antiphospholipid antibody\u2010positive women with adverse pregnancy outcomes have higher plasma complement activation product levels, and the placentas of women with antiphospholipid syndrome (APS) exhibit C4d complement component deposition, complement activation involvement has been hypothesized in APS pregnancy complications. Method of study: Plasma levels of C5a and C5b\u20109 complement components of 43 APS non\u2010pregnant patients and 17 pregnant APS women were measured using enzyme\u2010 linked immunosorbent assay. The results were compared with those of 16 healthy non\u2010pregnant women and eight healthy pregnant women, respectively. Placenta samples of five APS patients at high risk of pregnancy complications and of five healthy controls were subjected to immunoblotting analysis with specific antibodies to C5b\u20109 and CD46, CD55, CD59 complement regulators. Results: The mean plasma C5a and C5b\u20109 levels were significantly higher in the nonpregnant APS patients with previous thrombosis \ub1 pregnancy morbidity (P = .0001 and P = .0034, respectively) and in the pregnant APS women with adverse outcomes (P = .0093 for both). Similarly, C5b\u20109 amounts were significantly higher in the adverse pregnancy outcome placenta (P = .0115) than in those associated to a favorable outcome. The mean CD46, CD55 and CD59 amounts were, instead, lower, although not always significantly, in the placentas of all the high\u2010risk APS women with respect to the control placentas. Conclusion: Data analysis demonstrated that there was significant complement activation in the more severe subset of APS patients and in only the adverse pregnancy outcome APS women. Further studies will clarify whether the lower CD46, CD55, and CD59 expressions in the APS placentas are limited to only high\u2010risk APS patients

Suited for Success? : Suits, Status, and Hybrid Masculinity

This document is the Accepted Manuscript version. The final, definitive version of this paper has been published in Men and Masculinities, March 2017, doi: https://doi.org/10.1177/1097184X17696193, published by SAGE Publishing, All rights reserved.This article analyzes the sartorial biographies of four Canadian men to explore how the suit is understood and embodied in everyday life. Each of these men varied in their subject positions—body shape, ethnicity, age, and gender identity—which allowed us to look at the influence of men’s intersectional identities on their relationship with their suits. The men in our research all understood the suit according to its most common representation in popular culture: a symbol of hegemonic masculinity. While they wore the suit to embody hegemonic masculine configurations of practice—power, status, and rationality—most of these men were simultaneously marginalized by the gender hierarchy. We explain this disjuncture by using the concept of hybrid masculinity and illustrate that changes in the style of hegemonic masculinity leave its substance intact. Our findings expand thinking about hybrid masculinity by revealing the ways subordinated masculinities appropriate and reinforce hegemonic masculinity.Peer reviewe

Tumors carrying BRAF-mutations over-express NAMPT that is genetically amplified and possesses oncogenic properties

Background: Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in nicotinamide adenine dinucleotide (NAD) biosynthesis, is up-regulated in several cancers, including metastatic melanoma (MM). The BRAF oncogene is mutated in different cancer types, among which MM and thyroid carcinoma (THCA) are prominent. Drugs targeting mutant BRAF are effective, especially in MM patients, even though resistance rapidly develops. Previous data have linked NAMPT over-expression to the acquisition of BRAF resistance, paving the way for therapeutic strategies targeting the two pathways. Methods: Exploiting the TCGA database and a collection of MM and THCA tissue microarrays we studied the association between BRAF mutations and NAMPT expression. BRAF wild-type (wt) cell lines were genetically engineered to over-express the BRAF V600E construct to demonstrate a direct relationship between over-activation of the BRAF pathway and NAMPT expression. Responses of different cell line models to NAMPT (i)nhibitors were studied using dose–response proliferation assays. Analysis of NAMPT copy number variation was performed in the TCGA dataset. Lastly, growth and colony forming assays were used to study the tumorigenic functions of NAMPT itself. Results: The first finding of this work is that tumor samples carrying BRAF-mutations over-express NAMPT, as demonstrated by analyzing the TCGA dataset, and MM and THC tissue microarrays. Importantly, BRAF wt MM and THCA cell lines modified to over-express the BRAF V600E construct up-regulated NAMPT, confirming a transcriptional regulation of NAMPT following BRAF oncogenic signaling activation. Treatment of BRAF-mutated cell lines with two different NAMPTi was followed by significant reduction of tumor growth, indicating NAMPT addiction in these cells. Lastly, we found that several tumors over-expressing the enzyme, display NAMPT gene amplification. Over-expression of NAMPT in BRAF wt MM cell line and in fibroblasts resulted in increased growth capacity, arguing in favor of oncogenic properties of NAMPT. Conclusions: Overall, the association between BRAF mutations and NAMPT expression identifies a subset of tumors more sensitive to NAMPT inhibition opening the way for novel combination therapies including NAMPTi with BRAFi/MEKi, to postpone and/or overcome drug resistance. Lastly, the over-expression of NAMPT in several tumors could be a key and broad event in tumorigenesis, substantiated by the finding of NAMPT gene amplification

THE CROSSTALK BETWEEN THE COMPLEMENT SYSTEM AND THE COAGULATION CASCADE IN THE ANTIPHOSPHOLIPID SYNDROME. PRELIMINARY DATA FROM BASIC RESEARCH.

The association between antiphospholipid antibodies (aPL) and thrombophilic state in antiphospholipid syndrome (APS) is well recognized, but the underlying pathophysiology remains incompletely elucidated. Several findings suggest the role of complement system (CS) in the pathogenesis of antiphospholipid syndrome (APS). The importance of CS in APS is understandable since complement-derived inflammatory mediators increase vascular permeability, activate platelets and promote release of cytokines from monocytesthat favor systemic inflammation and coagulation. It has been demonstrated in a mouse model of aPL-induced pregnancy loss that complement activation can amplify the fetal injury. CS activation has been also documented in patients with APS, but there are far fewer clinical data