Towards Inferring Mechanical Lock Combinations using Wrist-Wearables as a Side-Channel

Wrist-wearables such as smartwatches and fitness bands are equipped with a variety of high-precision sensors that support novel contextual and activity-based applications. The presence of a diverse set of on-board sensors, however, also expose an additional attack surface which, if not adequately protected, could be potentially exploited to leak private user information. In this paper, we investigate the feasibility of a new attack that takes advantage of a wrist-wearable's motion sensors to infer input on mechanical devices typically used to secure physical access, for example, combination locks. We outline an inference framework that attempts to infer a lock's unlock combination from the wrist motion captured by a smartwatch's gyroscope sensor, and uses a probabilistic model to produce a ranked list of likely unlock combinations. We conduct a thorough empirical evaluation of the proposed framework by employing unlocking-related motion data collected from human subject participants in a variety of controlled and realistic settings. Evaluation results from these experiments demonstrate that motion data from wrist-wearables can be effectively employed as a side-channel to significantly reduce the unlock combination search-space of commonly found combination locks, thus compromising the physical security provided by these locks

Gene expression analysis in calcific tendinopathy of the rotator cuff

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A Meta-Analysis of Genome-Wide Association Scans Identifies IL18RAP, PTPN2, TAGAP, and PUS10 As Shared Risk Loci for Crohn's Disease and Celiac Disease

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Intravesical prostaglandin e2 effectiveness in the prevention of urinary retention after transvaginal reconstruction of the pubo-cervical fascia and short arm sling according to Lahodny: a prospective randomized clinical trial

Intravesical prostaglandin E2 is effective in the recovery of spontaneous voiding after transvaginal reconstruction of the pubocervical fascia and short arm sling according to Lahodny. The aim of the study was to compare the effects of intravesical prostaglandin E2 in the prevention of urinary retention after transvaginal reconstruction of the pubocervical fascia and short arm sling according to Lahodny. STUDY DESIGN: From November 1996 to June 1999 fifty women underwent the Lahodny procedure for moderate/severe cystocele and stress urinary incontinence. Women were randomly assigned to 1 of the 2 study groups: intravesical prostaglandin E2 versus controls. Data obtained were analyzed with the Student t test and the Fisher exact test. RESULTS: Two patients of the treatment group had to be excluded from the study, one because of the wrong measurement of the post-voidal residual volume and another due to a fastidious burning sensation which appeared immediately after prostaglandin instillation and required the suspension of the treatment. No other side effects such as nausea, vomiting, diarrhea or hyperthermia were observed. Patients who underwent the prostaglandin E2 treatment showed a recovery of spontaneous voiding after 7.9±6.7 days, whereas this interval was significantly longer in the control group, being 12.9±9.7 days (p=0.04, Two tailed Unpaired Student's T test). CONCLUSION: The effectiveness and the low associated morbidity mark the treatment with intravesical prostaglandin E2 useful in the recovery of normal voiding after transvaginal pubocervical fascia reconstruction and short arm sling with the procedure according to Lahodny

Generation of induced Pluripotent Stem Cells (UNIBSi008-A, UNIBSi008-B, UNIBSi008-C) from an Ataxia-Telangiectasia (AT) patient carrying a novel homozygous deletion in ATM gene.

Abstract Using a Sendai Virus based vector delivering Yamanaka Factors, we generated induced Pluripotent Stem Cells (iPSCs) from peripheral blood mononuclear cells of a patient affected by Ataxia Telangiectasia (AT), caused by a novel homozygous deletion in ATM, spanning exons 5 to 7. Three clones were fully characterized for pluripotency and capability to differentiate. These clones preserved the causative mutation of parental cells and genomic stability over time (>100 passages). Furthermore, in AT derived iPSCs we confirmed the impaired DNA damage response after ionizing radiation. All these data underline potential usefulness of our clones as in vitro AT disease model

Increased p21 expression in chondrocytes of achondroplasic children independently from the presence of the G380R FGFR3 mutation

Background. Achondroplasia (ACH) represents the major cause of dwarfi sm and is due to mutations in the fi broblast growth factor receptor 3 (FGFR3) gene. The cellular mechanisms involved in the reduced growth have been mainly described for in vitro or in vivo models, but few data have been obtained for humans. Methods. Thirteen children with ACH were enrolled in the study; the presence of FGFR3 mutations was determined by restriction fragment length polymorphism analysis and sequencing, whereas protein expression in cartilage biopsy was assessed by immunohistochemistry. Results. Chondrocytes in cartilage biopsies of ACH children were characterized by the presence of growth arrest mediated by STAT activation (both STAT1 and STAT5) and increased expression of p21 and cyclin D1, whereas no expression of either p53 or cyclin D3 could be detected. This mechanism was present in ACH children carrying the G380R mutation but also in a patient in whom no mutation could be detected in the entire coding region of the FGFR3 gene. Conclusions. These data thus demonstrate the presence of a common fi nal mechanism involving p21 and possibly leading to a block in chondrocyte proliferation

Usefulness of the organ culture system in the in vitro diagnosis of coeliac disease: A multicentre study

Objective. Diagnosis of coeliac disease is based on the presence of villous atrophy which recovers following a gluten-free diet. The presence of circulating antiendomysial antibodies as well as their disappearance after a gluten-free diet supports the diagnosis. It has also been demonstrated that antiendomysial antibodies are detectable in supernatants of cultured intestinal biopsies from patients with coeliac disease. The objective of this study was to compare the histology and antiendomysial antibodies in culture supernatants of intestinal biopsies to validate the in vitro organ culture system as a future diagnostic tool for coeliac disease. Material and methods. Seventy-five antiendomysial serum-positive patients on a gluten-containing diet were evaluated. Patients underwent endoscopy with 5 biopsy fragments: 3 for histology, 1 cultured with and the other without gliadin-peptide activator. Antiendomysial antibodies were evaluated in all culture supernatants. Results. Sixty-eight patients had evidence of villous atrophy, while 73 out of 75 were positive to the organ culture system. The agreement rate between organ culture and histology results was 94%. Conclusions. As all the centres participating in the study obtained good agreement between organ culture and histology results, the new system could be considered a reliable tool for the diagnosis of coeliac disease. Nevertheless, it is possible to highlight cases with an organ culture-positive and -negative histology. This feature could be of considerable interest because, as the sensitivity of organ culture seems to be greater than the initial histology, the new system might be useful in uncertain cases where the risk of missing the diagnosis of coeliac disease is high

Adalimumab in Patients with Active Noninfectious Uveitis

BACKGROUND: Patients with noninfectious uveitis are at risk for long-term complications of uncontrolled inflammation, as well as for the adverse effects of long-term glucocorticoid therapy. We conducted a trial to assess the efficacy and safety of adalimumab as a glucocorticoid-sparing agent for the treatment of noninfectious uveitis. METHODS: This multinational phase 3 trial involved adults who had active noninfectious intermediate uveitis, posterior uveitis, or panuveitis despite having received prednisone treatment for 2 or more weeks. Investigators and patients were unaware of the study-group assignments. Patients were randomly assigned in a 1:1 ratio to receive adalimumab (a loading dose of 80 mg followed by a dose of 40 mg every 2 weeks) or matched placebo. All patients received a mandatory prednisone burst followed by tapering of prednisone over the course of 15 weeks. The primary efficacy end point was the time to treatment failure occurring at or after week 6. Treatment failure was a multicomponent outcome that was based on assessment of new inflammatory lesions, best corrected visual acuity, anterior chamber cell grade, and vitreous haze grade. Nine ranked secondary efficacy end points were assessed, and adverse events were reported. RESULTS: The median time to treatment failure was 24 weeks in the adalimumab group and 13 weeks in the placebo group. Among the 217 patients in the intention-to-treat population, those receiving adalimumab were less likely than those in the placebo group to have treatment failure (hazard ratio, 0.50; 95% confidence interval, 0.36 to 0.70; P<0.001). Outcomes with regard to three secondary end points (change in anterior chamber cell grade, change in vitreous haze grade, and change in best corrected visual acuity) were significantly better in the adalimumab group than in the placebo group. Adverse events and serious adverse events were reported more frequently among patients who received adalimumab (1052.4 vs. 971.7 adverse events and 28.8 vs. 13.6 serious adverse events per 100 person-years). CONCLUSIONS: In our trial, adalimumab was found to be associated with a lower risk of uveitic flare or visual impairment and with more adverse events and serious adverse events than was placebo

Coeliac disease-associated risk variants in TNFAIP3 and REL implicate altered NF-kappaB signalling

Objective: Our previous coeliac disease genome-wide association study (GWAS) implicated risk variants in the human leucocyte antigen (HLA) region and eight novel risk regions. To identify more coeliac disease loci, we selected 458 single nucleotide polymorphisms (SNPs) that showed more modest association in the GWAS for genotyping and analysis in four independent cohorts. Design: 458 SNPs were assayed in 1682 cases and 3258 controls from three populations (UK, Irish and Dutch). We combined the results with the original GWAS cohort (767 UK cases and 1422 controls); six SNPs showed association with p Results: We identified two novel coeliac disease risk regions: 6q23.3 (OLIG3-TNFAIP3) and 2p16.1 (REL), both of which reached genome-wide significance in the combined analysis of all 2987 cases and 5273 controls (rs2327832 p= 1.3x10(-08), and rs842647 p= 5.26x10(-07)). We investigated the expression of these genes in the RNA isolated from biopsies and from whole blood RNA. We did not observe any changes in gene expression, nor in the correlation of genotype with gene expression. Conclusions: Both TNFAIP3 (A20, at the protein level) and REL are key mediators in the nuclear factor kappa B (NF-kappa B) inflammatory signalling pathway. For the first time, a role for primary heritable variation in this important biological pathway predisposing to coeliac disease has been identified. Currently, the HLA risk factors and the 10 established non-HLA risk factors explain similar to 40% of the heritability of coeliac disease