Percorrer por autor "Baptista, Pedro V."
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- Genetic predisposition for aggressive behaviour related with dopamine and serotonin pathways : an overviewPublication . Paulino, Cathy; Fernandes, Alexandra R.; Baptista, Pedro V.; Soeiro, Cristina; Grosso, Ana Rita; Quintas, Alexandre
- Shared inflammatory genetic susceptibility underlying spontaneous preterm birth and periodontitis : a case–control studyPublication . Couceiro, Joana; Família, Carlos; Brito, José; Mendes, José João; Baptista, Pedro V.; Fernandes, Alexandra R.; Quintas, AlexandreBackground: Preterm birth (PTB) remains the leading cause of neonatal morbidity and mortality worldwide, with approximately two-thirds of cases occurring spontaneously (SPTB), but the etiology is still poorly understood. Chronic inflammatory diseases, such as periodontitis (PD), have been considered SPTB risk factors. However, we hypothesized that SPTB may instead represent a clinical manifestation of a broader genetic predisposition to dysregulated inflammation. Using PD as a model of chronic inflammation, we examined shared genetic susceptibility. Methods: In a case–control study (N = 126 Portuguese postpartum women), we screened 56 SNPs in 36 inflammation-related genes. Four functionally plausible variants (IL1RN rs4251961, TLR1 rs5743618, IL6 rs2069827, and IL6R rs4845617) were selected for detailed regression, adjusting for gestational age, floss usage, and an SPTBxPD interaction term. Results: IL1RN rs4251961 was recessively associated with SPTB risk, consistent with reduced IL-1RA expression linked to this variant. IL6R rs4845617 showed a modest protective effect. TLR1 rs5743618 exhibited the strongest association with the composite “inflammation” phenotype under multiple models, with CC homozygotes showing four-fold increased odds, independent of SPTB/PD co-occurrence. Conclusions: This study provides original evidence that shared genetic variants in inflammatory pathways—particularly TLR1 rs5743618—may underlie susceptibility to SPTB and PD. Our findings suggest a paradigm shift, viewing SPTB as a possible outcome of systemic inflammatory dysregulation rather than merely a consequence of comorbid inflammatory conditions. Future studies should validate this marker in larger cohorts.
- Specific antiproliferative properties of proteinaceous toxin secretions from the marine annelid Eulalia sp. onto ovarian cancer cellsPublication . Rodrigo, Ana P.; Mendes, Vera M.; Manadas, Bruno; Grosso, Ana R.; Matos, António P. Alves de; Baptista, Pedro V.; Costa, Pero M.; Fernandes, Alexandra R.As Yondelis joins the ranks of approved anti-cancer drugs, the benefit from exploring the oceans’ biodiversity becomes clear. From marine toxins, relevant bioproducts can be obtained due to their potential to interfere with specific pathways. We explored the cytotoxicity of toxin-bearing secretions of the polychaete Eulalia onto a battery of normal and cancer human cell lines and discovered that the cocktail of proteins is more toxic towards an ovarian cancer cell line (A2780). The secretions’ main proteins were identified by proteomics and transcriptomics: 14-3-3 protein, Hsp70, Rab3, Arylsulfatase B and serine protease, the latter two being known toxins. This mixture of toxins induces cell-cycle arrest at G2/M phase after 3h exposure in A2780 cells and extrinsic programmed cell death. These findings indicate that partial re-activation of the G2/M checkpoint, which is inactivated in many cancer cells, can be partly reversed by the toxic mixture. Protein–protein interaction networks partake in two cytotoxic effects: cell-cycle arrest with a link to RAB3C and RAF1; and lytic activity of arylsulfatases. The discovery of both mechanisms indicates that venomous mixtures may affect proliferating cells in a specific manner, highlighting the cocktails’ potential in the fine-tuning of anti-cancer therapeutics targeting cell cycle and protein homeostasis.
- The genetic susceptibility linking preterm birth and periodontal disease : a reviewPublication . Couceiro, Joana; Grosso, Ana Rita; Baptista, Pedro V.; Mendes, José João; Fernandes, Alexandra R.; Quintas, Alexandre