A low-power wireless video sensor node for distributed object detection

In this paper we propose MicrelEye, a wireless video node for cooperative distributed video processing applications that involve image classification. The node is equipped with a low-cost VGA CMOS image sensor, a reconfigurable processing engine (FPGA, Microcontroller, SRAM) and a Bluetooth 100-m transceiver. It has a size of few cubic centimeters and its typical power consumption is approximately ten times less than that of typical commercial DSP-based solutions. As regards classification, a highly optimized hardware-oriented support vector machine-like (SVM-like) algorithm called ERSVM is proposed and implemented. We describe our hardware and software architecture, its performance and power characteristics. The case study considered in this paper is people detection. The obtained results suggest that the present technology allows for the design of simple intelligent video nodes capable of performing classification tasks locally.

A theoretical analysis of the influence of fixational instability on the development of thalamocortical connectivity

Under natural viewing conditions, the physiological instability of visual fixation keeps the projection of the stimulus on the retina in constant motion. After eye opening, chronic exposure to a constantly moving retinal image might influence the experience-dependent refinement of cell response characteristics. The results of previous modeling studies have suggested a contribution of fixational instability to the Hebbian maturation of the receptive fields of V1 simple cells (Rucci, Edelman, & Wray, 2000; Rucci & Casile, 2004). This letter examines the origins of such a contribution. Using quasilinear models of lateral geniculate nucleus units and V1 simple cells, we derive analytical expressions for the second-order statistics of thalamocortical activity before and after eye opening. We show that in the presence of natural stimulation, fixational instability introduces a spatially uncorrelated signal in the retinal input, which strongly influences the structure of correlated activity in the model. This input signal produces a regime of thalamocortical activity similar to that present before eye opening and compatible with the Hebbian maturation of cortical receptive fields.     

Using fold-in and fold-out in the architecture recovery of software systems

In this paper we present an approach to automate the architecture recovery process of software systems. The approach is built on information retrieval and clustering techniques, and, in particular, uses Latent Semantic Indexing (LSI) to get similarities among software entities (e.g., programs or classes) and the k-means clustering algorithm to form groups of software entities that implement similar functionality. In order to improve computational time in the context of the software evolution and then reduce energy waste, the architecture recovery process can be also applied by using fold-in and fold-out mechanisms that, respectively, add and remove software entities to the LSI representation of the understudy software system. The approach has been implemented in a prototype of a supporting software system as an Eclipse plug-in. Finally, to assess the approach and the plug-in, we have conducted an empirical investigation on five open source software systems implemented using the programming languages Java and C/C++. In the investigation special emphasis has been also given to the effect of using the fold-in and fold-out mechanisms.     

The Serotonergic Agonists Quipazine, CGS-12066A, and α-Methylserotonin Alter Motor Activity and Induce Hindlimb Stepping in the Intact and Spinal Rat Fetus.

The effects of serotonergic agonists were examined in intact and spinal fetuses, using an in vivo fetal rat preparation. On Gestational Day 20, fetuses were prepared with a midthoracic or sham spinal transection. Dose-response curves were obtained for quipazine (nonselective 5-hydroxytryptamine [5-HT] agonist; 1.0-10.0 mg/kg), CGS-12066A (5-HT1B agonist; 1.0-30.0 mg/kg), and α-methylserotonin (α-Me-5-HT; 5-HT? agonist; 0.2-15.0 mg/kg). During a 10-min test, each of the agonists (delivered via intraperitoneal injection) influenced fetal behavior: They increased the occurrence of head movements, mouthing, and hindlimb stepping. Quipazine and α-Me-5-HT also promoted hindlimb activity in spinal fetuses. Thus, stimulation of the fetal 5-HT system modulates motor activity at multiple levels of the developing central nervous system. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Identification of a Maturation Plasma Cell Index through a Highly Sensitive Droplet Digital PCR Assay Gene Expression Signature Validation in Newly Diagnosed Multiple Myeloma Patients

DNA microarrays and RNA-based sequencing approaches are considered important discovery tools in clinical medicine. However, cross-platform reproducibility studies undertaken so far have highlighted that microarrays are not able to accurately measure gene expression, particularly when they are expressed at low levels. Here, we consider the employment of a digital PCR assay (ddPCR) to validate a gene signature previously identified by gene expression profile. This signature included ten Hedgehog (HH) pathways’ genes able to stratify multiple myeloma (MM) patients according to their self-renewal status. Results show that the designed assay is able to validate gene expression data, both in a retrospective as well as in a prospective cohort. In addition, the plasma cells’ differentiation status determined by ddPCR was further confirmed by other techniques, such as flow cytometry, allowing the identification of patients with immature plasma cells’ phenotype (i.e., expressing CD19+/CD81+ markers) upregulating HH genes, as compared to others, whose plasma cells lose the expression of these markers and were more differentiated. To our knowledge, this is the first technical report of gene expression data validation by ddPCR instead of classical qPCR. This approach permitted the identification of a Maturation Index through the integration of molecular and phenotypic data, able to possibly define upfront the differentiation status of MM patients that would be clinically relevant in the future.     

The Proteoglycan Glypican-1 as a Possible Candidate for Innovative Targeted Therapeutic Strategies for Pancreatic Ductal Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) accounts for 90% of all pancreatic cancers, with a 5-year survival rate of 7% and 80% of patients diagnosed with advanced or metastatic malignancies. Despite recent advances in diagnostic testing, surgical techniques, and systemic therapies, there remain limited options for the effective treatment of PDAC. There is an urgent need to develop targeted therapies that are able to differentiate between cancerous and non-cancerous cells to reduce side effects and better inhibit tumor growth. Antibody-targeted strategies are a potentially effective option for introducing innovative therapies. Antibody-based immunotherapies and antibody-conjugated nanoparticle-based targeted therapies with antibodies targeting specific tumor-associated antigens (TAA) can be proposed. In this context, glypican-1 (GPC1), which is highly expressed in PDAC and not expressed or expressed at very low levels in non-malignant lesions and healthy pancreatic tissues, is a useful TAA that can be achieved by a specific antibody-based immunotherapy and antibody-conjugated nanoparticle-based targeted therapy. In this review, we describe the main clinical features of PDAC. We propose the proteoglycan GPC1 as a useful TAA for PDAC-targeted therapies. We also provide a digression on the main developed approaches of antibody-based immunotherapy and antibody-conjugated nanoparticle-based targeted therapy, which can be used to target GPC1.     

Modeling Lung Carcinoids with Zebrafish Tumor Xenograft

Lung carcinoids are neuroendocrine tumors that comprise well-differentiated typical (TCs) and atypical carcinoids (ACs). Preclinical models are indispensable for cancer drug screening since current therapies for advanced carcinoids are not curative. We aimed to develop a novel in vivo model of lung carcinoids based on the xenograft of lung TC (NCI-H835, UMC-11, and NCI-H727) and AC (NCI-H720) cell lines and patient-derived cell cultures in Tg(fli1a:EGFP)^y1 zebrafish embryos. We exploited this platform to test the anti-tumor activity of sulfatinib. The tumorigenic potential of TC and AC implanted cells was evaluated by the quantification of tumor-induced angiogenesis and tumor cell migration as early as 24 h post-injection (hpi). The characterization of tumor-induced angiogenesis was performed in vivo and in real time, coupling the tumor xenograft with selective plane illumination microscopy on implanted zebrafish embryos. TC-implanted cells displayed a higher pro-angiogenic potential compared to AC cells, which inversely showed a relevant migratory behavior within 48 hpi. Sulfatinib inhibited tumor-induced angiogenesis, without affecting tumor cell spread in both TC and AC implanted embryos. In conclusion, zebrafish embryos implanted with TC and AC cells faithfully recapitulate the tumor behavior of human lung carcinoids and appear to be a promising platform for drug screening.     

Characterisation of Progressive Skeletal Muscle Fibrosis in the Mdx Mouse Model of Duchenne Muscular Dystrophy: An In Vivo and In Vitro Study

Duchenne muscular dystrophy (DMD) is a rare genetic disease leading to progressive muscle wasting, respiratory failure, and cardiomyopathy. Although muscle fibrosis represents a DMD hallmark, the organisation of the extracellular matrix and the molecular changes in its turnover are still not fully understood. To define the architectural changes over time in muscle fibrosis, we used an mdx mouse model of DMD and analysed collagen and glycosaminoglycans/proteoglycans content in skeletal muscle sections at different time points during disease progression and in comparison with age-matched controls. Collagen significantly increased particularly in the diaphragm, quadriceps, and gastrocnemius in adult mdx, with fibrosis significantly correlating with muscle degeneration. We also analysed collagen turnover pathways underlying fibrosis development in cultured primary quadriceps-derived fibroblasts. Collagen secretion and matrix metalloproteinases (MMPs) remained unaffected in both young and adult mdx compared to wt fibroblasts, whereas collagen cross-linking and tissue inhibitors of MMP (TIMP) expression significantly increased. We conclude that, in the DMD model we used, fibrosis mostly affects diaphragm and quadriceps with a higher collagen cross-linking and inhibition of MMPs that contribute differently to progressive collagen accumulation during fibrotic remodelling. This study offers a comprehensive histological and molecular characterisation of DMD-associated muscle fibrosis; it may thus provide new targets for tailored therapeutic interventions.