43 research outputs found
Fluidic haptic interface for mechano-tactile feedback
Notable advancements have been achieved in providing amputees with sensation through invasive and non-invasive
haptic feedback systems such as mechano-, vibro-, electrotactile and hybrid systems. Purely mechanical-driven feedback
approaches, however, have been little explored. In this paper,
we now created a haptic feedback system that does not require
any external power source (such as batteries) or other electronic
components. The system is low-cost, lightweight, adaptable and
robust against external impact (such as water). Hence, it will be
sustainable in many aspects. We have made use of latest multimaterial 3D printing technology (Stratasys Objet500 Connex3)
being able to fabricate a soft sensor and a mechano-tactile
feedback actuator made of a rubber (TangoBlack Plus) and
plastic (VeroClear) material. When forces are applied to the
fingertip sensor, fluidic pressure inside the system acts on the
membrane of the feedback actuator resulting in mechano-tactile
sensation. We present the design, fabrication and validation of the
proposed haptic feedback system. Our ∅7 mm feedback actuator
is able to transmit a force range between 0.2 N (the median touch
threshold) and 2.1 N (the maximum force transmitted by the
feedback actuator at a 3 mm indentation) corresponding to force
range exerted to the fingertip sensor of 1.2 − 18.49 N
Gene expression profiling of liver metastases from colorectal cancer as potential basis for treatment choice
At present no reports on gene expression profiling of liver metastases from colorectal cancer are available. We identified two different signatures using Affymetrix platform: epidermal growth factor receptor pathway was upregulated in metachronous lesions, whereas the pathway mainly related to angiogenesis was in synchronous lesions. Synchronous or metachronous liver metastases could be treated differently on the basis of different molecular pathways
Rationale for the treatment of children with CCSK in the UMBRELLA SIOP-RTSG 2016 protocol
The International Society of Paediatric Oncology-Renal Tumour Study Group (SIOP-RTSG) has developed a new protocol for the diagnosis, treatment, and follow-up monitoring of childhood renal tumours-the UMBRELLA SIOP-RTSG 2016 protocol (the UMBRELLA protocol). This protocol has been designed to continue international collaboration in the treatment of childhood renal tumours and will be implemented in over 50 different countries. Clear cell sarcoma of the kidney, which is a rare paediatric renal tumour that most commonly occurs in childre
Effects of increased paternal age on sperm quality, reproductive outcome and associated epigenetic risks to offspring
The use of biodiversity as source of new chemical entities against defined molecular targets for treatment of malaria, tuberculosis, and T-cell mediated diseases: a review
Genetic polymorphisms in the MMP-1 and MMP-3 gene may contribute to chronic periodontitis in a Brazilian population
Objectives: Matrix metalloproteinase-1 and -3 (MMP-1, MMP-3) represent proteinases that degrade macromolecules of the extracellular matrix. These enzymes play a fundamental role during destruction of periodontal tissues. Genetic polymorphisms were characterized in the promoter region of the MMP-1 and MMP-3 genes. The aim of this study was to investigate the relationship between these genetic variations with chronic periodontitis in a Brazilian population. Material and Methods: Non-smoking subjects (n=114) exhibiting sites >= 5 mm clinical attachment loss were recruited for study. Control subjects (n=109) should not exhibit clinical signals of periodontitis. MMP-1 (-1607 1G/2G, -519 A/G) and MMP-3 (-1612 5A/6A) gene promoter polymorphisms were genotyped using PCR-RFLP methods. Results: Analysis of polymorphisms showed no differences in distribution of the -1607 1G/2G and -519 A/G variants in the MMP-1 gene between the healthy and periodontitis group (p > 0.05). However, the distribution of genotype frequencies of the -1612 5A/6A polymorphism in the MMP-3 gene showed that the 5A/5A genotype was significantly more frequent in the periodontitis group (p=0.008). The same was not observed in the 5A/6A genotype once only one 5A allele is carried. We also observed a trend to increase the frequency of the MMP-1/MMP-3 haplotype (2G/5A) in the periodontitis group (p=0.08). Conclusion: On the basis of the results, no significant association is found for the MMP-1 polymorphisms with susceptibility of periodontitis, while the MMP-3 gene polymorphism may contribute to periodontal tissue destruction during periodontitis in Brazilian subjects.331069970
The molecular mechanisms responsible for resistance to ET-743 (Trabectidin; Yondelis) in the Ewing's sarcoma cell line, TC-71
Identification of new active agents against sarcoma is considered an important challenge in medical oncology. ET-743 (Trabectidin; Yondelis) has recently emerged as the first active drag developed against sarcoma in the last two decades, with promising results especially against soft-tissue sarcoma and Ewing's sarcoma (ES). In this study, we analyzed the molecular mechanisms responsible for resistance to ET-743 in ES cells. Three resistant cell variants (TC/ET 3 nM, TC/ET 6 nM and TC/ET 12 nM) were obtained, showing 28-, 47- and 102-fold increase in ET-743 resistance. Cross-resistance to other drugs was analyzed. Comparative genomic hybridization and cDNA microarray technology were employed to characterize and compare the gene expression profile of two TC/ET variants with the parental cell line. TC/ET cells show a conventional multidrug resistance phenotype and Pglycoprotein over-expression was found to significantly contribute to ET-743 resistance. However, functional studies with the cyclosporine analogue, PSC-833, indicate that other mechanisms are involved in resistance to ET-743. The gene expression profile of TC/ET cells indicated, among up-regulated genes, an increase in expression of insulin-like growth factor receptor-I (IGF-IR) and one of its major intracellular mediators, insulin receptor substrate-1. Functional studies using a neutralizing antibody anti-IGF-IR confirmed involvement of this signaling pathway in resistance to ET-743. Simultaneous blockage of both P-glycoprotein and IGF-IR completely restored sensitivity to ET-743 in ES cells. Overall, these findings provide impetus for future studies testing the therapeutic value of new specific inhibitors of P-glycoprotein and IGF-IR, which could represent a concrete therapeutic option for ES patients refractory to conventional agents