5,265 research outputs found

    Nanotechnology in dentistry: prevention, diagnosis, and therapy

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    Ensanya Ali Abou Neel,1–3 Laurent Bozec,3 Roman A Perez,4,5 Hae-Won Kim,4–6 Jonathan C Knowles3,5 1Division of Biomaterials, Operative Dentistry Department, Faculty of Dentistry, King Abdulaziz University, Jeddah, Saudi Arabia; 2Biomaterials Department, Faculty of Dentistry, Tanta University, Tanta, Egypt; 3UCL Eastman Dental Institute, Biomaterials and Tissue Engineering, London, UK; 4Institute of Tissue Regenerative Engineering (ITREN), 5Department of Nanobiomedical Science and BK21 Plus NBM Global Research Center for Regenerative Medicine, 6Department of Biomaterials Science, College of Dentistry, Dankook University, Cheonan, Republic of Korea Abstract: Nanotechnology has rapidly expanded into all areas of science; it offers significant alternative ways to solve scientific and medical questions and problems. In dentistry, nanotechnology has been exploited in the development of restorative materials with some significant success. This review discusses nanointerfaces that could compromise the longevity of dental restorations, and how nanotechnolgy has been employed to modify them for providing long-term successful restorations. It also focuses on some challenging areas in dentistry, eg, oral biofilm and cancers, and how nanotechnology overcomes these challenges. The recent advances in nanodentistry and innovations in oral health-related diagnostic, preventive, and therapeutic methods required to maintain and obtain perfect oral health, have been discussed. The recent advances in nanotechnology could hold promise in bringing a paradigm shift in dental field. Although there are numerous complex therapies being developed to treat many diseases, their clinical use requires careful consideration of the expense of synthesis and implementation. Keywords: nanotechnology, nanointerfaces, biofilm-related oral diseases, tissue engineering, drug delivery, toxicit

    Process intensification through staggered herringbone micro-channels: Mass transfer enhancement to a reactive wall

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    In the present study, the flow behaviour through different micro-herringbone channels configurations (1-peak, 2-peak, 1–2 alternated peak herringbone channel and a flow inversion geometry) have been numerically analysed as a mean of intensifying mass transfer to a reactive boundary. Results showed that the mass transfer coefficients were higher for the 1–2 alternated herringbone structure than those with, either, 1-peak or 2-peak structures. Moreover, the flow inversion structure mass transfer coefficients were double those obtained for the staggered herringbone channel. The alternated herringbone channel combines a different set of herringbone structures that are efficient at removing the boundary layer at different parts of the channel. The combination of these structures provide an enhanced mass transfer performance as compared to a standard herringbone channel. The obtained results showed that a 2D simplified model which uses hydrodynamic data from CFD simulations is a reasonable substitute for full 3D particle tracking simulations in terms of the mass transfer behavior of the 1PSHC with a 97.5 % of accuracy related to the asymptotic Sherwood number. The mixing capacity of the herringbones was accounted for by an apparent effective diffusion coefficient. The agreement between the 3D and 2D simulation was reasonable

    Phase III Open-Label Randomized Study of Eribulin Mesylate Versus Capecitabine in Patients With Locally Advanced or Metastatic Breast Cancer Previously Treated With an Anthracycline and a Taxane

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    Purpose: This phase III randomized trial (ClinicalTrials.gov identifier: NCT00337103) compared eribulin with capecitabine in patients with locally advanced or metastatic breast cancer (MBC). Patients and Methods: Women with MBC who had received prior anthracycline- and taxane-based therapy were randomly assigned to receive eribulin or capecitabine as their first-, second-, or third-line chemotherapy for advanced/metastatic disease. Stratification factors were human epidermal growth factor receptor-2 (HER2) status and geographic region. Coprimary end points were overall survival (OS) and progression-free survival (PFS). Results: Median OS times for eribulin (n = 554) and capecitabine (n = 548) were 15.9 and 14.5 months, respectively (hazard ratio [HR], 0.88; 95% CI, 0.77 to 1.00; P = .056). Median PFS times for eribulin and capecitabine were 4.1 and 4.2 months, respectively (HR, 1.08; 95% CI, 0.93 to 1.25; P = .30). Objective response rates were 11.0% for eribulin and 11.5% for capecitabine. Global health status and overall quality-of-life scores over time were similar in the treatment arms. Both treatments had manageable safety profiles consistent with their known adverse effects; most adverse events were grade 1 or 2. Conclusion: In this phase III study, eribulin was not shown to be superior to capecitabine with regard to OS or PFS

    AdS/BCFT Correspondence for Higher Curvature Gravity: An Example

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    We consider the effects of higher curvature terms on a holographic dual description of boundary conformal field theory. Specifically, we consider three-dimensional gravity with a specific combination of Ricci tensor square and curvature scalar square, so called, new massive gravity. We show that a boundary entropy and an entanglement entropy are given by similar expression with those of the Einstein gravity case when we introduce an {\it effective} Newton's constant and an {\it effective} cosmological constant. We also show that the holographic g-theorem still holds in this extension, and we give some comments about the central charge dependence of boundary entropy in the holographic construction. In the same way, we consider new type black holes and comment on the boundary profile. Moreover, we reproduce these results through auxiliary field formalism in this specific higher curvature gravity.Comment: 27pages, minor corrections, accepted in JHE

    Biopsy confirmation of metastatic sites in breast cancer patients:clinical impact and future perspectives

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    Determination of hormone receptor (estrogen receptor and progesterone receptor) and human epidermal growth factor receptor 2 status in the primary tumor is clinically relevant to define breast cancer subtypes, clinical outcome,and the choice of therapy. Retrospective and prospective studies suggest that there is substantial discordance in receptor status between primary and recurrent breast cancer. Despite this evidence and current recommendations,the acquisition of tissue from metastatic deposits is not routine practice. As a consequence, therapeutic decisions for treatment in the metastatic setting are based on the features of the primary tumor. Reasons for this attitude include the invasiveness of the procedure and the unreliable outcome of biopsy, in particular for biopsies of lesions at complex visceral sites. Improvements in interventional radiology techniques mean that most metastatic sites are now accessible by minimally invasive methods, including surgery. In our opinion, since biopsies are diagnostic and changes in biological features between the primary and secondary tumors can occur, the routine biopsy of metastatic disease needs to be performed. In this review, we discuss the rationale for biopsy of suspected breast cancer metastases, review issues and caveats surrounding discordance of biomarker status between primary and metastatic tumors, and provide insights for deciding when to perform biopsy of suspected metastases and which one (s) to biopsy. We also speculate on the future translational implications for biopsy of suspected metastatic lesions in the context of clinical trials and the establishment of bio-banks of biopsy material taken from metastatic sites. We believe that such bio-banks will be important for exploring mechanisms of metastasis. In the future,advances in targeted therapy will depend on the availability of metastatic tissue

    Grain Boundary Chemistry Before and After Ion Implantation in ODS Steels

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    Obstructive jaundice secondary to pancreatic head adenocarcinoma in a young teenage boy: a case report

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    <p>Abstract</p> <p>Introduction</p> <p>Pancreatic adenocarcinoma is extremely rare in childhood. We report a case of metastatic pancreatic adenocarcinoma in a 13-year-old boy, revealed by jaundice.</p> <p>Case presentation</p> <p>A 13-year-old Moroccan boy was admitted with obstructive jaundice to the children's Hospital of Rabat, Department of Pediatric Oncology. Laboratory study results showed a high level of total and conjugated bilirubin. Computerized tomography of the abdomen showed a dilatation of the intra-hepatic and extra-hepatic bile ducts with a tissular heterogeneous tumor of the head of the pancreas and five hepatic lesions. Biopsy of a liver lesion was performed, and a histopathological examination of the sample confirmed the diagnosis of metastatic ductal adenocarcinoma of the pancreas. Our patient underwent a palliative biliary derivation. After that, chemotherapy was administered (5-fluorouracil and epirubicin), however no significant response to treatment was noted and our patient died six months after diagnosis.</p> <p>Conclusion</p> <p>Malignant pancreatic tumors, especially ductal carcinomas, are exceedingly rare in the pediatric age group and their clinical features and treatment usually go unappreciated by most pediatric oncologists and surgeons.</p

    Synthetic Lethality of Chk1 Inhibition Combined with p53 and/or p21 Loss During a DNA Damage Response in Normal and Tumor Cells

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    Cell cycle checkpoints ensure genome integrity and are frequently compromised in human cancers. A therapeutic strategy being explored takes advantage of checkpoint defects in p53-deficient tumors in order to sensitize them to DNA-damaging agents by eliminating Chk1-mediated checkpoint responses. Using mouse models, we demonstrated that p21 is a key determinant of how cells respond to the combination of DNA damage and Chk1 inhibition (combination therapy) in normal cells as well as in tumors. Loss of p21 sensitized normal cells to the combination therapy much more than did p53 loss and the enhanced lethality was partially blocked by CDK inhibition. In addition, basal pools of p21 (p53 independent) provided p53 null cells with protection from the combination therapy. Our results uncover a novel p53-independent function for p21 in protecting cells from the lethal effects of DNA damage followed by Chk1 inhibition. As p21 levels are low in a significant fraction of colorectal tumors, they are predicted to be particularly sensitive to the combination therapy. Results reported in this study support this prediction
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