281 research outputs found

    Perfect tag identification protocol in RFID networks

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    Radio Frequency IDentification (RFID) systems are becoming more and more popular in the field of ubiquitous computing, in particular for objects identification. An RFID system is composed by one or more readers and a number of tags. One of the main issues in an RFID network is the fast and reliable identification of all tags in the reader range. The reader issues some queries, and tags properly answer. Then, the reader must identify the tags from such answers. This is crucial for most applications. Since the transmission medium is shared, the typical problem to be faced is a MAC-like one, i.e. to avoid or limit the number of tags transmission collisions. We propose a protocol which, under some assumptions about transmission techniques, always achieves a 100% perfomance. It is based on a proper recursive splitting of the concurrent tags sets, until all tags have been identified. The other approaches present in literature have performances of about 42% in the average at most. The counterpart is a more sophisticated hardware to be deployed in the manufacture of low cost tags.Comment: 12 pages, 1 figur

    Transcending Towards Personal Freedom: Exploring the Lived Experiences of Professional Working Mothers

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    “What are the lived experiences of professional working mothers?” An integrated theoretical model provided an historical context and framework for discovering distinctions between social discourse and individual lifestyles. Professional working mothers participated in phenomenological research with an introductory telephone call and two in-person interviews. Through language and story, participants depicted what it means to be a professional working mother in contemporary, American society. Demographic characteristics included five female participants, who held a professional or executive level position. All participants earned a college degree and ranged in age from 30-65 with children living at home (ages ranged from 3-20). Additionally, four of the participants were married. Thematically, participants described their world in terms of employer and employee job expectations, an intertwining commitment to work and family, and living in alignment with one’s personal values when it comes to work-life balance. Mirroring the findings of similar studies, social conditioning, work culture, and technology heavily influenced their lived experiences as professional working mothers. Often prolonged work-life imbalances led to personal crises and fatigue; inspired to transcend old work-life paradigms, most women consciously created an integrated lifestyle, blending work and family to complement one another. Aligned with a global trend towards the integration of spiritual, social, and scientific/technological evolution, more research is required to (a) discern how self-identity and society co-create the lived experiences of professional working mothers; (b) research organizational development structures to support integrated lifestyles and, (c) evaluate the impact of ongoing work-life balance issues for future generations

    Micro-evaporators for kinetic exploration of phase diagrams

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    We use pervaporation-based microfluidic devices to concentrate species in aqueous solutions with spatial and temporal control of the process. Using experiments and modelling, we quantitatively describe the advection-diffusion behavior of the concentration field of various solutions (electrolytes, colloids, etc) and demonstrate the potential of these devices as universal tools for the kinetic exploration of the phases and textures that form upon concentration

    Therapeutic targeting of CK2 in acute and chronic leukemias

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    CK2 is a ubiquitously expressed, constitutively active Ser/Thr protein kinase, which is considered the most pleiotropic protein kinase in the human kinome. Such a pleiotropy explains the involvement of CK2 in many cellular events. However, its predominant roles are stimulation of cell growth and prevention of apoptosis. High levels of CK2 messenger RNA and protein are associated with CK2 pathological functions in human cancers. Over the last decade, basic and translational studies have provided evidence of CK2 as a pivotal molecule driving the growth of different blood malignancies. CK2 overexpression has been demonstrated in nearly all the types of hematological cancers, including acute and chronic leukemias, where CK2 is a key regulator of signaling networks critical for cell proliferation, survival and drug resistance. The findings that emerged from these studies suggest that CK2 could be a valuable therapeutic target in leukemias and supported the initiation of clinical trials using CK2 antagonists. In this review, we summarize the recent advances on the understanding of the signaling pathways involved in CK2 inhibition-mediated effects with a particular emphasis on the combinatorial use of CK2 inhibitors as novel therapeutic strategies for treating both acute and chronic leukemia patients

    Improving nelarabine efficacy in T cell acute lymphoblastic leukemia by targeting aberrant PI3K/AKT/mTOR signaling pathway

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    Background: Although in recent years, the introduction of novel chemotherapy protocols has improved the outcome of T cell acute lymphoblastic leukemia (T-ALL) patients, refractory and/or relapsing disease remains a foremost concern. In this context, a major contribution was provided by the introduction of the nucleoside analog nelarabine, approved for salvage treatment of T-ALL patients with refractory/relapsed disease. However, nelarabine could induce a life-threatening, dose-dependent neurotoxicity. To improve nelarabine efficacy, we have analyzed its molecular targets, testing selective inhibitors of such targets in combination with nelarabine. Methods: The effectiveness of nelarabine as single agent or in combination with PI3K, Bcl2, and MEK inhibitors was evaluated on human T-ALL cell lines and primary T-ALL refractory/relapsed lymphoblasts. The efficacy of signal modulators in terms of cytotoxicity, induction of apoptosis, and changes in gene and protein expression was assessed by flow cytometry, western blotting, and quantitative real-time PCR in T-ALL settings. Results: Treatment with nelarabine as a single agent identified two groups of T-ALL cell lines, one sensitive and one resistant to the drug. Whereas sensitive T-ALL cells showed a significant increase of apoptosis and a strong down-modulation of PI3K signaling, resistant T-ALL cells showed a hyperactivation of AKT and MEK/ERK1/2 signaling pathways, not caused by differences in the expression of nelarabine transporters or metabolic activators. We then studied the combination of nelarabine with the PI3K inhibitors (both pan and dual γ/δ inhibitors), with the Bcl2 specific inhibitor ABT199, and with the MEK inhibitor trametinib on both T-ALL cell lines and patient samples at relapse, which displayed constitutive activation of PI3K signaling and resistance to nelarabine alone. The combination with the pan PI3K inhibitor ZSTK-474 was the most effective in inhibiting the growth of T-ALL cells and was synergistic in decreasing cell survival and inducing apoptosis in nelarabine-resistant T-ALL cells. The drug combination caused AKT dephosphorylation and a downregulation of Bcl2, while nelarabine alone induced an increase in p-AKT and Bcl2 signaling in the resistant T-ALL cells and relapsed patient samples. Conclusions: These findings indicate that nelarabine in combination with PI3K inhibitors may be a promising therapeutic strategy for the treatment of T-ALL relapsed patients

    Therapeutic potential of targeting sphingosine kinases and sphingosine 1-phosphate in hematological malignancies

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    Sphingolipids, such as ceramide, sphingosine and sphingosine 1-phosphate (S1P) are bioactive molecules that have important functions in a variety of cellular processes, which include proliferation, survival, differentiation and cellular responses to stress. Sphingolipids have a major impact on the determination of cell fate by contributing to either cell survival or death. Although ceramide and sphingosine are usually considered to induce cell death, S1P promotes survival of cells. Sphingosine kinases (SPHKs) are the enzymes that catalyze the conversion of sphingosine to S1P. There are two isoforms, SPHK1 and SPHK2, which are encoded by different genes. SPHK1 has recently been implicated in contributing to cell transformation, tumor angiogenesis and metastatic spread, as well as cancer cell multidrug-resistance. More recent findings suggest that SPHK2 also has a role in cancer progression. This review is an overview of our understanding of the role of SPHKs and S1P in hematopoietic malignancies and provides information on the current status of SPHK inhibitors with respect to their therapeutic potential in the treatment of haematological cancers

    Synergistic cytotoxic effects of bortezomib and CK2 inhibitor CX-4945 in acute lymphoblastic leukemia: turning offthe prosurvival ER chaperone BIP/Grp78 and turning on the proapoptotic NF-ÎşB

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    The proteasome inhibitor bortezomib is a new targeted treatment option for refractory or relapsed acute lymphoblastic leukemia (ALL) patients. However, a limited efficacy of bortezomib alone has been reported. A terminal pro-apoptotic endoplasmic reticulum (ER) stress/unfolded protein response (UPR) is one of the several mechanisms of bortezomib-induced apoptosis. Recently, it has been documented that UPR disruption could be considered a selective anti-leukemia therapy. CX- 4945, a potent casein kinase (CK) 2 inhibitor, has been found to induce apoptotic cell death in T-ALL preclinical models, via perturbation of ER/UPR pathway. In this study, we analyzed in T- and B-ALL preclinical settings, the molecular mechanisms of synergistic apoptotic effects observed after bortezomib/CX-4945 combined treatment. We demonstrated that, adding CX-4945 after bortezomib treatment, prevented leukemic cells from engaging a functional UPR in order to buffer the bortezomibmediated proteotoxic stress in ER lumen. We documented that the combined treatment decreased pro-survival ER chaperon BIP/Grp78 expression, via reduction of chaperoning activity of Hsp90. Bortezomib/CX-4945 treatment inhibited NF-ÎşB signaling in T-ALL cell lines and primary cells from T-ALL patients, but, intriguingly, in B-ALL cells the drug combination activated NF-ÎşB p65 pro-apoptotic functions. In fact in B-cells, the combined treatment induced p65-HDAC1 association with consequent repression of the anti-apoptotic target genes, Bcl-xL and XIAP. Exposure to NEMO (IKKÎł)-binding domain inhibitor peptide reduced the cytotoxic effects of bortezomib/CX-4945 treatment. Overall, our findings demonstrated that CK2 inhibition could be useful in combination with bortezomib as a novel therapeutic strategy in both T- and B-ALL
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