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Biology subjects

Moreira, A. d. S.

Publications and source records attributed to Moreira, A. d. S..

2 recordsLinked to original sources

Harnessing Interpretable Deep Learning to Predict Meropenem Resistance in Klebsiella pneumoniae

Antimicrobial resistance constitutes an escalating global health threat, complicating therapeutic management and increasing morbidity and mortality. Deep learning approaches have emerged as promising tools for bacterial profiling based on omics data, particularly for predicting antimicrobial susceptibility from genomic information. This task relies on identifying genomic signatures associated with resistance mechanisms. Here, DeepMDC is introduced as a deep learning architecture designed for bacterial profiling using whole-genome data. Given that precise annotation at the gene or mutation level is often costly and ambiguous, phenotypic classification is formulated as a Multiple Instance Learning (MIL) problem, in which each genome is represented as a bag of instances with a single associated label. The core of DeepMDC is a Modern Hopfield Network that processes all open reading frames (ORFs), including small ones, derived from genomic data. A key feature of the architecture is its interpretability, enabled by attention mechanisms that facilitate biological insight and hypothesis generation. The model was evaluated against Klebsiella pneumoniae and four clinically relevant antibiotics (meropenem, cefepime, ceftazidime, and gentamicin), achieving strong performance in several metrics. Notably, genes associated with resistance consistently received high attention scores during inference, which validates the architecture and eventually may generate new hypotheses.

systems biology↗

Oral Lisinopril Raises Tissue Levels of ACE2, the SARS-CoV-2 Receptor, in Healthy Male and Female Mice

Angiotensin-converting enzyme 2 (ACE2) is the established cellular receptor for SARS-CoV-2. However, it is unclear whether ACE1 inhibitors (e.g., lisinopril) or angiotensin receptor blockers (e.g., losartan) alter tissue ACE2 expression. This study sought to determine whether lisinopril or losartan, as monotherapies or in combination, change tissue levels of ACE2 in healthy male and female mice. Mice received lisinopril (10 mg/kg/day), losartan (10 mg/kg/day), or both for 21 days via drinking water. A control group received water without drug. ACE2 protein index (ACE2 protein / total protein) was determined on small intestine, lung, kidney, and brain. Oral lisinopril increased ACE2 protein index across all tissues (p < 0.0001 vs control). In contrast, the combination of lisinopril plus losartan did not increase ACE2 levels in any tissue (p = 0.89 vs control) and even decreased tissue expression of the Ace2 gene (p < 0.001 vs control). Tissue ACE2 remained elevated in mice 21 days after cessation of lisinopril (p = 0.02). Across both cohorts, plasma ACE2 did not correlate with ACE2 protein index in any tissue. A sex difference was observed: kidney ACE2 levels were higher in males than females (p < 0.0001). Oral lisinopril increases ACE2, the cellular receptor for SARS-CoV-2, in tissues that are relevant to the transmission and pathogenesis of COVID-19. Remarkably, the addition of losartan prevented lisinopril-induced increases in ACE2 across tissues. These results suggest that ACE inhibitors and angiotensin receptor blockers interact to determine tissue levels of ACE2.

pharmacology and toxicology↗