Publications by authors named "Jennifer Cabral"

Generally, medicinal plants are harvested with high amount of water, so it is essential to subject the product to drying as soon as possible to prevent degradation before application. Most compounds from medicinal plants are sensitive to drying processes, so it is important to adjust the drying conditions. The objective of this study was to describe the drying of Rue (Ruta chalepensis L.

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The addition of anti-disialoganglioside-2 (GD2) monoclonal antibodies (mAbs) such as dinutuximab and naxitamab to standard therapies for high-risk (HR) neuroblastoma has significantly improved outcomes for children with this devastating disease. The care for these young patients receiving treatment for HR neuroblastoma is complex, with need for the involvement of a multidisciplinary team. Clinical implementation of anti-GD2 mAb treatment requires the same harmonized team approach.

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Objective: To build and validate an educational technology in the form of a booklet, aimed at the family members of people with venous ulcers to assist them in their care.

Methods: A methodological study, which went through the stages of bibliographic survey and situational diagnosis for the construction of the booklet and validation of content, appearance, and adequacy with judges and the target audience. The Content Validity Index, the Suitability Assessment of Materials, and the Concordance Index were used.

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We report high-quality closed reference genomes for 1 bovine strain and 10 human Shiga toxin (Stx)-producing (STEC) strains from serogroups O26, O45, O91, O103, O104, O111, O113, O121, O145, and O157. We also report draft assemblies, with standardized metadata, for 360 STEC strains isolated from watersheds, animals, farms, food, and human infections.

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The recent widespread application of whole-genome sequencing (WGS) for microbial disease investigations has spurred the development of new bioinformatics tools, including a notable proliferation of phylogenomics pipelines designed for infectious disease surveillance and outbreak investigation. Transitioning the use of WGS data out of the research laboratory and into the front lines of surveillance and outbreak response requires user-friendly, reproducible and scalable pipelines that have been well validated. Single Nucleotide Variant Phylogenomics (SNVPhyl) is a bioinformatics pipeline for identifying high-quality single-nucleotide variants (SNVs) and constructing a whole-genome phylogeny from a collection of WGS reads and a reference genome.

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Activin and TGFβ share SMAD signaling and colon cancers can inactivate either pathway alone or simultaneously. The differential effects of activin and TGFβ signaling in colon cancer have not been previously dissected. A key downstream target of TGFβ signaling is the cdk2 inhibitor p21 (p21(cip1/waf1)).

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Background: Activin receptor 2 (ACVR2) is commonly mutated in microsatellite unstable (MSI) colon cancers, leading to protein loss, signaling disruption, and larger tumors. Here, we examined activin signaling disruption in microsatellite stable (MSS) colon cancers.

Methods: Fifty-one population-based MSS colon cancers were assessed for ACVR1, ACVR2 and pSMAD2 protein.

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Signaling pathways enabling transforming growth factor-beta (TGFbeta)'s conversion from a tumor suppressor to a tumor promoter are not well characterized. TGFbeta utilizes intracellular SMADs to mediate growth suppression; however, TGFbeta-induced proliferative pathways may become more apparent when SMAD signaling is abrogated. Here, we determined regulation of the tumor suppressor PTEN by TGFbeta utilizing SMAD4-null colon cancer cells.

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Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is rarely mutated in pancreatic cancers, but its regulation by transforming growth factor (TGF)-beta might mediate growth suppression and other oncogenic actions. Here, we examined the role of TGFbeta and the effects of oncogenic K-RAS/ERK upon PTEN expression in the absence of SMAD4. We utilized two SMAD4-null pancreatic cell lines, CAPAN-1 (K-RAS mutant) and BxPc-3 (WT-K-RAS), both of which express TGFbeta surface receptors.

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Background & Aims: Colon cancers with high-frequency microsatellite instability (MSI-H) develop frameshift mutations in tumor suppressors as part of their pathogenesis. ACVR2 is mutated at its exon 10 polyadenine tract in >80% of MSI-H colon cancers, coinciding with loss of protein. ACVR2 transmits the growth effects of activin via phosphorylation of SMAD proteins to affect gene transcription.

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