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Sobre

Daniel Vasconcelos é gestor de Propriedade Intelectual (PI) no Serviço de Apoio ao Licenciamento do INESC TEC, procurando por tecnologias emergentes geradas nas actividades de I&D do instituto. Unindo esforços com os investigadores, o Daniel avalia estratégias de valorização de PI, nomedamente através de patentes. Atualmente é responsável pela gestão de um portfólio de 23 famílias de patentes ativas nas áreas das TIC e de tecnologia médica. A nível internacional tem realizado várias formações sobre transferência de tecnologia e direitos de propriedade intelectual em organizações de prestígio como a ASTP-Proton (NL), o EPO (NL e DE) e o CEIPI (FR), sendo membro do I3PM (International Institute for IP Management). É ainda Professor convidado na Faculdade de Engenharia da Universidade do Porto para unidades curriculares de desenvolvimento de tecnologia médica (Inovação em Biodesign) e de Economia e Gestão.

Antes do seu cargo no INESC TEC, o Daniel foi investigador no i3S / INEB durante 9 anos, estudando a resposta imune induzida por biomaterais ortopédicos implantáveis. Publicou 9 artigos científicos, todos em revistas Q1 e dois dos quais em revistas com IF>8 como primeiro autor, assim como um capítulo de livro sobre standards e regulamentação de dispositivos médicos.

O Daniel tem o grau de Doutor em Ciências Biomédicas (ICBAS, U Porto + Universitats Klinikum Heidelberg), é Mestre em Bioengenharia (FEUP-ICBAS, U Porto + Université Paris 13) e Mestre em Economia e Gestão da Inovação (FEP, U Porto).

Tópicos
de interesse
Detalhes

Detalhes

009
Publicações

2019

Osteoclasts degrade fibrinogen scaffolds and induce mesenchymal stem/stromal osteogenic differentiation

Autores
Almeida, AR; Bessa Gonçalves, M; Vasconcelos, DM; Barbosa, MA; Santos, SG;

Publicação
Journal of Biomedical Materials Research Part A

Abstract

2018

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

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

Publicação
Journal of Biomedical Materials Research Part A

Abstract

2018

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

Autores
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;

Publicação
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

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

Publicação
Scientific Reports

Abstract

2018

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

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

Publicação
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.