Publications by authors named "D R Orlando"

Periodontal disease (PD) leads to the destruction of supportive tissues through an inflammatory response induced by biofilm accumulation. This low-grade systemic inflammation from PD increases the risk of comorbidities. Among potential therapeutic agents for PD, humic acids (HAs) are notable for their anti-inflammatory and immunomodulatory properties.

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Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest solid cancers; thus, identifying more effective therapies is a major unmet need. In this study, we characterized the super enhancer (SE) landscape of human PDAC to identify drivers of the disease that might be targetable. This analysis revealed MICAL2 as a super enhancer-associated gene in human PDAC, which encodes the flavin monooxygenase MICAL2 that induces actin depolymerization and indirectly promotes SRF transcription by modulating the availability of serum response factor coactivators myocardin-related transcription factors (MRTF-A and MRTF-B).

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Background And Purpose: The COVID-19 pandemic exacerbated pain and joint mobility outcomes in patients with temporomandibular disorders (TMD), being that effective treatments are of clinical interest. We aimed to evaluate the effects of manual therapy (MT) and dry needling (DN), compared to cognitive-behavioral therapy/control (CO), on pain, articular mobility, and fear of COVID-19 in patients with TMD.

Materials And Methods: Sixty participants with myofascial TMD were randomly assigned to three groups: MT, DN, and CO.

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Introduction: Excessive smartphone use has been linked to mental health impairments and may potentially alter human behavior. These effects are particularly pronounced among young individuals, with university students being especially susceptible to the negative influences of smartphone use.

Methods: This observational, cross-sectional study was conducted in a sample of 781 Brazilian university students.

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DNA polymerase eta (Pol η) is a Y-family translesion polymerase responsible for synthesizing new DNA across UV-damaged templates. It is recruited to replication forks following mono-ubiquitination of the PCNA DNA clamp. This interaction is mediated by PCNA-interacting protein (PIP) motifs within Pol η, as well as by its C-terminal ubiquitin-binding zinc finger (UBZ) domain.

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