Percorrer por autor "Couceiro, Joana"
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- Assessing the content of a package of SGT-151 sold onlinePublication . Luzio, Ana; Couceiro, Joana; Ferreira, Carla; Quintas, Alexandre
- A biophysical perspective on the unexplored mechanisms driving Parkinson’s disease by amphetamine-like stimulantsPublication . Ferreira, Carla; Couceiro, Joana; Tenreiro, Sandra; Quintas, Alexandre
- Evaluation of toxic impact of the synthetic cannabinoids JWH-018 and its N-(3-hydroxypentyl) metabolite on human cell linesPublication . Couceiro, Joana; Sultan, Haider; Duranovic, Smilja; Bell, Suzanne; Quintas, Alexandre
- Methamphetamine use as a developmental factor in Parkinson's DiseasePublication . Martins, Ana; Leça, Diogo; Couceiro, Joana; Bernardes, Catarina
- SENTINEL : tackling dangerous nitazene opioidsPublication . Maria, Marisa H.; Pereira, Joana R. P.; Ferreira, Daniela R.; Barra, Bárbara F. C.; Antunes, Alexandra M. M.; Família, Carlos; Oliveira-Torres, Edite; Justino, Gonçalo C.; Gaspar, Helena; Couceiro, Joana; Caldeira, Maria; Serra, Patrícia A.; Almeida, Rui M.; Fonseca, Suzana; Silva, Zoé E. Vaz da; Quintas, Alexandre; Neng, Nuno R.Poster apresentado nas VI Jornadas Científicas Universitárias e Politécnicas Egas Moniz. Monte de Caparica, 24 a 28 de novembro 2025
- 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.
- 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
- Toxicity of synthetic cannabinoids is increasing along with the regulatory measures taken for their controlPublication . Couceiro, Joana; Luzio, Ana; Ferreira, Carla; Quintas, Alexandre
- Toxicological impact of JWH-018 and its phase I metabolite N-(3-hydroxypentyl) on human cell linesPublication . Couceiro, Joana; Bandarra, Susana; Sultan, Haider; Bell, Suzanne; Constantino, Susana; Quintas, Alexandre"The emergence and abuse of synthetic cannabinoids has been increasing as an alternative to cannabis, mainly among youth. As their appearance on the drug market has been recent, the pharmacological and toxicological profiles of these psychoactive substances are poorly understood. Current studies suggest that they have stronger effects compared to their natural alternatives and their metabolites retain affinity towards CB1 receptors in CNS. Since studies on its toxicological properties are scarce, the effects of the drug in human derived cell lines were investigated. The present study was designed to explore the toxicological impact of parent drug versus phase I metabolites of synthetic cannabinoids on human cells with and without CB1 receptor. The human cell line of neuroblastoma SH-SY5Y and human kidney cell line HEK-293T were exposed to JWH-018 and to its N-(3-hydroxypentyl) metabolite. Cell toxicity was evaluated using the MTT and LDH assay. Additionally, a dual staining methodology with fluorescent Annexin V-FITC and propidium iodide was performed to address the question of whether JWH-018 N-(3-hydroxypentyl) metabolite is inducing cell death through apoptosis or necrosis, in HEK293T and SH-SY5Y cell lines. The obtained results show that JWH-018 does not cause a statistically significant decrease in cell viability, in contrast to its N-(3-hydroxypentyl) metabolite, which at ≥25μM causes a significant decrease in cell viability. Both cell lines are affected by JWH-018 metabolite. Our results point to higher toxicity of JWH-018 metabolite when compared to its parent drug, suggesting a non-CB1 receptor mediated toxicological mechanism. Comparing the results from Annexin V/PI with MTT and LDH assays of SH-SY5Y and HEK293T in the presence of the synthetic cannabinoid metabolite, emerges the picture that cellular viability decreases and associated death is occurring through necrosis."