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About

Daniel Vasconcelos is an Intellectual Property manager at INESC TEC’s Technology Licensing Office, scouting emerging technologies generated in the institute’s R&D activities. He teams up with researchers to evaluate strategies of IP valorisation, namely through patents. Currently, he is in charge for a patent portfolio of 23 active and internationalized patent families on ICT and medical technology fields. Daniel has been doing several workshops on technology transfer and intellectual property rights in prestigious entities such as ASTP-Proton (NL), EPO (NL and DE), and CEIPI (FR), being a member of I3PM (International Institute for IP Management). He is invited professor at Faculdade de Engenharia da Universidade do Porto for medical technology development (Biodesign) and Economics and Management courses.

Prior to this position at INESC TEC, Daniel was a researcher at i3S / INEB (U Porto) for 9 years, studying the immune response induced by implantable orthopaedic biomaterials. He has published 9 scientific papers, all in Q1 journals and 2 of them in journals with an IF>8 as first author, and a book chapter on medical devices regulation and standards. 

Daniel holds a PhD in Biomedical Sciences (ICBAS, U Porto + Universitats Klinikum Heidelberg), a MSc in Bioengineering (FEUP-ICBAS, U Porto + Université Paris 13), and a MSc in Innovation Economics and Management (FEP, U Porto).

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Publications

2018

The use of chitosan porous 3D scaffolds embedded with resolvin D1 to improve in vivo bone healing

Authors
Vasconcelos, DP; Costa, M; Neves, N; Teixeira, JH; Vasconcelos, DM; Santos, SG; Aguas, AP; Barbosa, MA; Barbosa, JN;

Publication
Journal of Biomedical Materials Research Part A

Abstract

2018

Profiling the circulating miRnome reveals a temporal regulation of the bone injury response

Authors
Silva, AM; Almeida, MI; Teixeira, JH; Ivan, C; Oliveira, J; Vasconcelos, D; Neves, N; Ribeiro Machado, C; Cunha, C; Barbosa, MA; Calin, GA; Santos, SG;

Publication
THERANOSTICS

Abstract
Bone injury healing is an orchestrated process that starts with an inflammatory phase followed by repair and remodelling of the bone defect. The initial inflammation is characterized by local changes in immune cell populations and molecular mediators, including microRNAs (miRNAs). However, the systemic response to bone injury remains largely uncharacterized. Thus, this study aimed to profile the changes in the plasma miRnome after bone injury and determine its biological implications. Methods: A rat model of femoral bone defect was used, and animals were evaluated at days 3 and 14 after injury. Non-operated (NO) and sham operated animals were used as controls. Blood and spleen were collected and peripheral blood mononuclear cells (PBMC) and plasma were separated. Plasma miRnome was determined by RT-qPCR array and bioinformatics Ingenuity pathway analysis (IPA) was performed. Proliferation of bone marrow mesenchymal stem/stromal cells (MSC) was evaluated by Ki67 staining and high-throughput cell imaging. Candidate miRNAs were evaluated in splenocytes by RT-qPCR, and proteins found in the IPA analysis were analysed in splenocytes and PBMC by Western blot. Results: Bone injury resulted in timely controlled changes to the miRNA expression profile in plasma. At day 3 there was a major down-regulation of miRNA levels, which was partially recovered by day 14 post-injury. Interestingly, bone injury led to a significant up-regulation of let-7a, let-7d and miR-21 in plasma and splenocytes at day 14 relative to day 3 after bone injury, but not in sham operated animals. IPA predicted that most miRNAs temporally affected were involved in cellular development, proliferation and movement. MSC proliferation was analysed and found significantly increased in response to plasma of animals days 3 and 14 post-injury, but not from NO animals. Moreover, IPA predicted that miRNA processing proteins Ago2 and Dicer were specifically inhibited at day 3 post-injury, with Ago2 becoming activated at day 14. Protein levels of Ago2 and Dicer in splenocytes were increased at day 14 relative to day 3 post-bone injury and NO animals, while in PBMC, levels were reduced at day 3 (albeit Dicer was not significant) and remained low at day 14. Ephrin receptor B6 followed the same tendency as Ago2 and Dicer, while Smad2/3 was significantly decreased in splenocytes from day 14 relative to NO and day 3 post-bone injury animals. Conclusion: Results show a systemic miRNA response to bone injury that is regulated in time and is related to inflammation resolution and the start of bone repair/regeneration, unravelling candidate miRNAs to be used as biomarkers in the monitoring of healthy bone healing and as therapeutic targets for the development of improved bone regeneration therapies.

2018

Interplay between sympathetic nervous system and inflammation in aseptic loosening of hip joint replacement

Authors
Ribeiro-da-Silva, M; Vasconcelos, DM; Alencastre, IS; Oliveira, MJ; Linhares, D; Neves, N; Costa, G; Henrique, R; Lamghari, M; Alves, CJ;

Publication
Scientific Reports

Abstract

2018

Interplay between sympathetic nervous system and inflammation in aseptic loosening of hip joint replacement

Authors
Ribeiro da Silva, M; Vasconcelos, DM; Alencastre, IS; Oliveira, MJ; Linhares, D; Neves, N; Costa, G; Henrique, R; Lamghari, M; Alves, CJ;

Publication
SCIENTIFIC REPORTS

Abstract
Inflammation is a common symptom in joint disorders such as rheumatoid arthritis, osteoarthritis (OA) and implant aseptic loosening (AL). The sympathetic nervous system is well known to play a critical role in regulating inflammatory conditions, and imbalanced sympathetic activity has been observed in rheumatoid arthritis. In AL it is not clear whether the sympathetic nervous system is altered. In this study we evaluated the systemic and local profile of neuroimmune molecules involved in the interplay between the sympathetic nervous system and the periprosthetic inflammation in hip AL. Our results showed that periprosthetic inflammation does not trigger a systemic response of the sympathetic nervous system, but is mirrored rather by the impairment of the sympathetic activity locally in the hip joint. Moreover, macrophages were identified as key players in the local regulation of inflammation by the sympathetic nervous system in a process that is implant debris-dependent and entails the reduction of both adrenergic and Neuropetide Y (NPY)-ergic activity. Additionally, our results showed a downregulation of semaphorin 3A (SEMA3A) that may be part of the mechanism sustaining the periprosthetic inflammation. Overall, the local sympathetic nervous system emerges as a putative target to mitigate the inflammatory response to debris release and extending the lifespan of orthopedic implants.

2017

Neuroimmune expression in hip osteoarthritis: a systematic review

Authors
da Silva, MR; Linhares, D; Vasconcelos, DM; Alves, CJ; Neves, N; Costa, G; Lamghari, M;

Publication
BMC MUSCULOSKELETAL DISORDERS

Abstract
Background: Neuroimmune axis is central in the physiopathology of hip osteoarthritis (OA), but its specific pathways are still unclear. This systematic review aims to assess the nervous and immune system profile of patients with hip osteoarthritis (OA) when compared to healthy controls. Methods: A systematic review followed PRISMA guidelines was conducted. A two-step selection process was completed, and from 609 references 17 were included. The inclusion criteria were: original articles on adult patients with hip OA, with assessment of neuroimmune expression. Articles with other interventions prior to analysis and those without a control group were excluded. Results: Thirty-nine relevant neuroimmune markers were identified, with assessments in bone, cartilage, synovial membrane, synovial fluid, whole blood, serum and/or immune cells. GM-CSF, IFN-gamma, IL-1 alpha, IL-6, IL-8, IL-1 and TNF-alpha presented variable expression among tissues studied when compared between hip OA and controls. VEGFs and TGF-beta isoforms showed similar tendencies among tissues and studies. On nervous expression, CGRP, Tuj-1 and SP were increased in synovial membrane. Overall, patients with hip OA presented a higher number of overexpressed markers. Conclusions: For the first time a systematic review on neuroimmune expression in patients with hip OA found an upregulation of neuroimmune markers, with deregulated balance between pro and anti-inflammatory cytokines. However, no clear systematic pattern was found, and few information is available on nervous expression. This highlights the importance of future research with clear methodologies to guide the management of these patients.