Browsing by Issue Date, starting with "2021-04-21"
Now showing 1 - 4 of 4
Results Per Page
Sort Options
- Metabolomics and transcriptomics to decipher molecular mechanisms underlying ectomycorrhizal root colonization of an oak treePublication . Sebastiana, M.; Gargallo-Garriga, A.; Sardans, J.; Pérez-Trujillo, M.; Monteiro, Filipa; Figueiredo, A.; Maia, M.; Nascimento, R.; Silva, M. Sousa; Ferreira, A. N.; Cordeiro, C.; Marques, A. P.; Sousa, L.; Malhó, R.; Peñuelas, J.Mycorrhizas are known to have a positive impact on plant growth and ability to resist major biotic and abiotic stresses. However, the metabolic alterations underlying mycorrhizal symbiosis are still understudied. By using metabolomics and transcriptomics approaches, cork oak roots colonized by the ectomycorrhizal fungus Pisolithus tinctorius were compared with non-colonized roots. Results show that compounds putatively corresponding to carbohydrates, organic acids, tannins, long-chain fatty acids and monoacylglycerols, were depleted in ectomycorrhizal cork oak colonized roots. Conversely, non-proteogenic amino acids, such as gamma-aminobutyric acid (GABA), and several putative defense-related compounds, including oxylipin-family compounds, terpenoids and B6 vitamers were induced in mycorrhizal roots. Transcriptomic analysis suggests the involvement of GABA in ectomycorrhizal symbiosis through increased synthesis and inhibition of degradation in mycorrhizal roots. Results from this global metabolomics analysis suggest decreases in root metabolites which are common components of exudates, and in compounds related to root external protective layers which could facilitate plant-fungal contact and enhance symbiosis. Root metabolic pathways involved in defense against stress were induced in ectomycorrhizal roots that could be involved in a plant mechanism to avoid uncontrolled growth of the fungal symbiont in the root apoplast. Several of the identified symbiosis-specific metabolites, such as GABA, may help to understand how ectomycorrhizal fungi such as P. tinctorius benefit their host plants.
- Identificação do risco nutricional em crianças com paralisia cerebralPublication . Mendes, Inês Curvelo; Ferreira, Joana Alves Dias Martins de SousaA Paralisia Cerebral (PC) é a principal causa de incapacidade na infância. A malnutrição afeta o desenvolvimento físico e cognitivo destas crianças. A identificação de risco nutricional (IRN) com recurso a ferramentas validadas e práticas é fundamental para o rastreio das crianças que necessitarão de uma avaliação nutricional completa e intervenção nutricional subsequentes. O objetivo deste estudo consistiu em comparar os resultados obtidos com a aplicação de diferentes ferramentas de IRN em crianças com PC. A amostra, recolhida entre fevereiro e dezembro de 2020, incluiu um total de 30 participantes observados no Hospital Divino Espírito Santo, EPER e na Associação de Paralisia Cerebral de São Miguel. Para cada participante foram recolhidos os dados clínicos e sociodemográficos, avaliação antropométrica, avaliação da ingestão alimentar e hídrica, e a aplicação indireta de cinco ferramentas de IRN (STRONGkids, Bell et al. (2019), CP-MST, Bushell (2014) e Malnutrition Risk Score) e dois instrumentos de classificação do estado nutricional (Organização Mundial de Saúde e Subjective Global Nutrition Assessment). O Malnutrition Risk Score mostrou elevada sensibilidade (>87%) e especificidade (>71%), assim como os valores preditivos positivo e negativo mais elevados (77,8% e >83%, respetivamente) e um Kappa superior a 0,59, em comparação com as restantes ferramentas e independentemente do método de avaliação do estado nutricional. Para além disso, este estudo também revelou que a gordura e a água são os macronutrientes que necessitam de otimização na terapêutica nutricional das crianças com PC. Em suma, o Malnutrition Risk Score demonstrou ser o instrumento mais eficiente para a IRN em crianças com PC.
- HER2-Targeted immunotherapy and combined protocols showed promising antiproliferative effects in feline mammary carcinoma cell-based modelsPublication . Gameiro, Andreia; Nascimento, Catarina; Correia, Jorge Manuel de Jesus; Ferreira, FernandoABSTRACT - Feline mammary carcinoma (FMC) is a highly prevalent tumor, showing aggressive clinicopathological features, with HER2-positive being the most frequent subtype. While, in human breast cancer, the use of anti-HER2 monoclonal antibodies (mAbs) is common, acting by blocking the extracellular domain (ECD) of the HER2 protein and by inducing cell apoptosis, scarce information is available on use these immunoagents in FMC. Thus, the antiproliferative effects of two mAbs (trastuzumab and pertuzumab), of an antibody–drug conjugate compound (T-DM1) and of combined treatments with a tyrosine kinase inhibitor (lapatinib) were evaluated on three FMC cell lines (CATMT, FMCm and FMCp). In parallel, the DNA sequence of the her2 ECD (subdomains II and IV) was analyzed in 40 clinical samples of FMC, in order to identify mutations, which can lead to antibody resistance or be used as prognostic biomarkers. Results obtained revealed a strong antiproliferative effect in all feline cell lines, and a synergistic response was observed when combined therapies were performed. Additionally, the mutations found were not described as inducing resistance to therapy in breast cancer patients. Altogether, our results suggested that anti-HER2 mAbs could become useful in the treatment of FMC, particularly, if combined with lapatinib, since drug-resistance seems to be rare.
- PINK1 : a bridge between mitochondria and Parkinson's diseasePublication . Gonçalves, Filipa; Morais, Vanessa A.Mitochondria are known as highly dynamic organelles essential for energy production. Intriguingly, in the recent years, mitochondria have revealed the ability to maintain cell homeostasis and ultimately regulate cell fate. This regulation is achieved by evoking mitochondrial quality control pathways that are capable of sensing the overall status of the cellular environment. In a first instance, actions to maintain a robust pool of mitochondria take place; however, if unsuccessful, measures that lead to overall cell death occur. One of the central key players of these mitochondrial quality control pathways is PINK1 (PTEN-induce putative kinase), a mitochondrial targeted kinase. PINK1 is known to interact with several substrates to regulate mitochondrial functions, and not only is responsible for triggering mitochondrial clearance via mitophagy, but also participates in maintenance of mitochondrial functions and homeostasis, under healthy conditions. Moreover, PINK1 has been associated with the familial form of Parkinson’s disease (PD). Growing evidence has strongly linked mitochondrial homeostasis to the central nervous system (CNS), a system that is replenished with high energy demanding long-lasting neuronal cells. Moreover, sporadic cases of PD have also revealed mitochondrial impairments. Thus, one could speculate that mitochondrial homeostasis is the common denominator in these two forms of the disease, and PINK1 may play a central role in maintaining mitochondrial homeostasis. In this review, we will discuss the role of PINK1 in the mitochondrial physiology and scrutinize its role in the cascade of PD pathology.