Alessandro De Luca

Bio: Alessandro De Luca is an academic researcher from Casa Sollievo della Sofferenza. The author has contributed to research in topics: Robot & Noonan syndrome. The author has an hindex of 50, co-authored 246 publications receiving 9464 citations. Previous affiliations of Alessandro De Luca include University of Rome Tor Vergata & Coventry University.

Robot Collisions: A Survey on Detection, Isolation, and Identification

Abstract: Robot assistants and professional coworkers are becoming a commodity in domestic and industrial settings. In order to enable robots to share their workspace with humans and physically interact with them, fast and reliable handling of possible collisions on the entire robot structure is needed, along with control strategies for safe robot reaction. The primary motivation is the prevention or limitation of possible human injury due to physical contacts. In this survey paper, based on our early work on the subject, we review, extend, compare, and evaluate experimentally model-based algorithms for real-time collision detection, isolation, and identification that use only proprioceptive sensors. This covers the context-independent phases of the collision event pipeline for robots interacting with the environment, as in physical human–robot interaction or manipulation tasks. The problem is addressed for rigid robots first and then extended to the presence of joint/transmission flexibility. The basic physically motivated solution has already been applied to numerous robotic systems worldwide, ranging from manipulators and humanoids to flying robots, and even to commercial products.

A landscape effect in tenosynovial giant-cell tumor from activation of CSF1 expression by a translocation in a minority of tumor cells.

Abstract: Tenosynovial giant-cell tumor (TGCT) and pigmented villonodular synovitis (PVNS) are related conditions with features of both reactive inflammatory disorders and clonal neoplastic proliferations. Chromosomal translocations involving chromosome 1p13 have been reported in both TGCT and PVNS. We confirm that translocations involving 1p13 are present in a majority of cases of TGCT and PVNS and show that CSF1 is the gene at the chromosome 1p13 breakpoint. In some cases of both TGCT and PVNS, CSF1 is fused to COL6A3 (2q35). The CSF1 translocations result in overexpression of CSF1. In cases of TGCT and PVNS carrying this translocation, it is present in a minority of the intratumoral cells, leading to CSF1 expression only in these cells, whereas the majority of cells express CSF1R but not CSF1, suggesting a tumor-landscaping effect with aberrant CSF1 expression in the neoplastic cells, leading to the abnormal accumulation of nonneoplastic cells that form a tumorous mass.

Founder and Recurrent CDH1 Mutations in Families With Hereditary Diffuse Gastric Cancer

Abstract: ContextHereditary diffuse gastric cancer is caused by germline mutations in the epithelial cadherin (CDH1) gene and is characterized by an increased risk for diffuse gastric cancer and lobular breast cancer.ObjectiveTo determine whether recurring germline CDH1 mutations occurred due to independent mutational events or common ancestry.Design, Setting, and PatientsThirty-eight families diagnosed clinically with hereditary diffuse gastric cancer were accrued between November 2004 and January 2006 and were analyzed for CDH1 mutations as part of an ongoing study at the British Columbia Cancer Agency. Twenty-six families had at least 2 gastric cancer cases with 1 case of diffuse gastric cancer in a person younger than 50 years; 12 families had either a single case of diffuse gastric cancer diagnosed in a person younger than 35 years or multiple cases of diffuse gastric cancer diagnosed in persons older than 50 years.Main Outcome MeasuresClassification of family members as carriers or noncarriers of CDH1 mutations. Haplotype analysis to assess recurring mutations for common ancestry was performed on 7 families from this study and 7 previously reported families with the same mutations.ResultsThirteen mutations (6 novel) were identified in 15 of the 38 families (40% detection rate). The 1137G>A splicing mutation and the 1901C>T (A634V) missense/splicing mutation occurred on common haplotypes in 2 families but on different haplotypes in a third family. The 2195G>A (R732Q) missense/splicing mutation occurred in 2 families on different haplotypes. The 2064-2065delTG mutation occurred on a common haplotype in 2 families. Two families from this study plus 2 additional families carrying the novel 2398delC mutation shared a common haplotype, suggesting a founder effect. All 4 families originate from the southeast coast of Newfoundland. Due to concentrations of lobular breast cancer cases, 2 branches of this family had been diagnosed as having hereditary breast cancer and were tested for BRCA mutations. Within these 4 families, the cumulative risk by age 75 years in mutation carriers for clinically detected gastric cancer was 40% (95% confidence interval [CI], 12%-91%) for males and 63% (95% CI, 19%-99%) for females and the risk for breast cancer in female mutation carriers was 52% (95% CI, 29%-94%).ConclusionsRecurrent CDH1 mutations in families with hereditary diffuse gastric cancer are due to both independent mutational events and common ancestry. The presence of a founder mutation from Newfoundland is strongly supported.Published online June 3, 2007 (doi:10.1001/jama.297.21.2360).

A depth space approach to human-robot collision avoidance

Abstract: In this paper a real-time collision avoidance approach is presented for safe human-robot coexistence. The main contribution is a fast method to evaluate distances between the robot and possibly moving obstacles (including humans), based on the concept of depth space. The distances are used to generate repulsive vectors that are used to control the robot while executing a generic motion task. The repulsive vectors can also take advantage of an estimation of the obstacle velocity. In order to preserve the execution of a Cartesian task with a redundant manipulator, a simple collision avoidance algorithm has been implemented where different reaction behaviors are set up for the end-effector and for other control points along the robot structure. The complete collision avoidance framework, from perception of the environment to joint-level robot control, is presented for a 7-dof KUKA Light-Weight-Robot IV using the Microsoft Kinect sensor. Experimental results are reported for dynamic environments with obstacles and a human.

Inhibition of Poly(ADP-Ribose) Polymerase in Tumors from BRCA Mutation Carriers

Abstract: Background The inhibition of poly(adenosine diphosphate [ADP]–ribose) polymerase (PARP) is a potential synthetic lethal therapeutic strategy for the treatment of cancers with specific DNA-repair defects, including those arising in carriers of a BRCA1 or BRCA2 mutation. We conducted a clinical evaluation in humans of olaparib (AZD2281), a novel, potent, orally active PARP inhibitor. Methods This was a phase 1 trial that included the analysis of pharmacokinetic and pharmacodynamic characteristics of olaparib. Selection was aimed at having a study population enriched in carriers of a BRCA1 or BRCA2 mutation. Results We enrolled and treated 60 patients; 22 were carriers of a BRCA1 or BRCA2 mutation and 1 had a strong family history of BRCA-associated cancer but declined to undergo mutational testing. The olaparib dose and schedule were increased from 10 mg daily for 2 of every 3 weeks to 600 mg twice daily continuously. Reversible dose-limiting toxicity was seen in one of eight patients receiving 400 mg twice...

Linear systems

Abstract: Most of the signal processing that we will study in this course involves local operations on a signal, namely transforming the signal by applying linear combinations of values in the neighborhood of each sample point. You are familiar with such operations from Calculus, namely, taking derivatives and you are also familiar with this from optics namely blurring a signal. We will be looking at sampled signals only. Let's start with a few basic examples. Local difference Suppose we have a 1D image and we take the local difference of intensities, DI(x) = 1 2 (I(x + 1) − I(x − 1)) which give a discrete approximation to a partial derivative. (We compute this for each x in the image.) What is the effect of such a transformation? One key idea is that such a derivative would be useful for marking positions where the intensity changes. Such a change is called an edge. It is important to detect edges in images because they often mark locations at which object properties change. These can include changes in illumination along a surface due to a shadow boundary, or a material (pigment) change, or a change in depth as when one object ends and another begins. The computational problem of finding intensity edges in images is called edge detection. We could look for positions at which DI(x) has a large negative or positive value. Large positive values indicate an edge that goes from low to high intensity, and large negative values indicate an edge that goes from high to low intensity. Example Suppose the image consists of a single (slightly sloped) edge:

Olaparib maintenance therapy in platinum-sensitive relapsed ovarian cancer.

Abstract: randomization on completion of chemotherapy; hazard ratio for progression or death, 0.35; 95% confidence interval [CI], 0.25 to 0.49; P<0.001). Subgroup analyses of progression-free survival showed that, regardless of subgroup, patients in the olaparib group had a lower risk of progression. Adverse events more commonly reported in the olaparib group than in the placebo group (by more than 10% of patients) were nausea (68% vs. 35%), fatigue (49% vs. 38%), vomiting (32% vs. 14%), and anemia (17% vs. 5%); the majority of adverse events were grade 1 or 2. An interim analysis of overall survival (38% maturity, meaning that 38% of the patients had died) showed no significant difference between groups (hazard ratio with olaparib, 0.94; 95% CI, 0.63 to 1.39; P = 0.75). CONCLUSIONS Olaparib as maintenance treatment significantly improved progression-free survival among patients with platinum-sensitive, relapsed, high-grade serous ovarian cancer. Interim analysis showed no overall survival benefit. The toxicity profile of olaparib in this population was consistent with that in previous studies. (Funded by AstraZeneca; ClinicalTrials.gov number, NCT00753545.)