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Biology subjects

Kavanaugh, M.

Publications and source records attributed to Kavanaugh, M..

3 recordsLinked to original sources

Hyperspectral Remote Sensing for Harmful Algal Bloom Detection: Pseudo-nitzschia in the Northeast Pacific

1Diatoms are microscopic marine algae that are critical for global primary production, carbon sequestration, and fisheries productivity. However, select diatoms may form harmful algal blooms, which threaten marine ecosystems and the fisheries they sustain. Rapidly identifying harmful blooms is necessary to effectively manage marine resources, yet current identification methods are limited by expensive and labor-intensive in situ point sampling. Hyperspectral remote sensing enables scalable monitoring, but its ability to resolve taxonomic shifts within phytoplankton groups (e.g. diatoms) is largely unknown. To investigate this uncertainty, we cultured four dominant diatom genera from the California Current upwelling system, including this systems most abundant harmful algae, Pseudo-nitzschia. The hyperspectral absorption and backscatter of these taxa were measured and used to model spectral reflectances that remote sensing platforms (satellites/drones) might detect. Differences between fingerprints of these taxa were quantified using vector-based and statistical analyses. Mean spectral differences of 48% were observed between the most dominant diatom, Thalassiosira, and the most toxic diatom, Pseudo-nitzschia. Differences of approximately 30% were found between Pseudo-nitzschia and the second and third most abundant diatoms, Chaetoceros and Asterionellopsis. Successful identification of Pseudo-nitzschias reflectance fingerprint was driven by the presence of a unique feature around 560 nm. The distinct spectral fingerprint of Pseudo-nitzschia indicates that it can be distinguished from benign diatom blooms using hyperspectral remote sensing platforms.

ecology↗

Genomic variations drive phenotypic heterogeneity in pancreatic cancer cells

ObjectivesTo evaluate the suitability of the MIA PaCa-2 cell line for studying pancreatic cancer intratumor heterogeneity, we aim to further characterize the nature of MIA PaCa-2 cells phenotypic, genomic, and transcriptomic heterogeneity. MethodsMIA PaCa-2 single-cell clones were established through flow cytometry. For the phenotypic study, we quantified the cellular morphology, proliferation rate, migration potential, and drug sensitivity of the clones. The chromosome copy number and transcriptomic profiles were quantified using SNPa and RNA-seq, respectively. ResultsFour MIA PaCa-2 clones showed distinctive phenotypes, with differences in cellular morphology, proliferation rate, migration potential, and drug sensitivity. We also observed a degree of genomic variations between these clones in form of chromosome copy number alterations and single nucleotide variations, suggesting the genomic heterogeneity of the population, and the intrinsic genomic instability of MIA PaCa-2 cells. Lastly, transcriptomic analysis of the clones also revealed gene expression profile differences between the clones, including the uniquely regulated ITGAV, which dictates the morphology of MIA PaCa-2 clones. ConclusionsMIA PaCa-2 is comprised of cells with distinctive phenotypes, heterogeneous genomes, and differential transcriptomic profiles, suggesting its suitability as a model to study the underlying mechanisms behind pancreatic cancer heterogeneity.

cancer biology↗

IFT-A deficiency in juvenile mice impairs biliary development and exacerbates ADPKD liver disease

Polycystic liver disease (PLD) is characterized by the growth of numerous biliary cysts and presents in patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD), causing significant morbidity. Interestingly, deletion of intraflagellar transport-B (IFT-B) genes in adult mouse models of ADPKD attenuates severity of PKD and PLD. Here we examine the role of deletion of IFT-A gene, Thm1, in PLD of juvenile and adult Pkd2 conditional knock-out mice. Perinatal deletion of Thm1 results in disorganized and expanded biliary regions, biliary fibrosis, shortened primary cilia on CK19+ biliary epithelial cells, and reduced Notch signaling. In contrast, perinatal deletion of Pkd2 causes PLD, with multiple CK19+ biliary epithelial cell-lined cysts, fibrosis, lengthened primary cilia, and increased Notch and ERK signaling. Perinatal deletion of Thm1 in Pkd2 conditional knock-out mice increased hepatomegaly and liver necrosis, indicating enhanced liver disease severity. In contrast to effects in the developing liver, deletion of Thm1 in adult mice, alone and together with Pkd2, did not cause a biliary phenotype nor affect Pkd2-mutant PLD, respectively. However, similar to juvenile PLD, Notch and ERK signaling were increased in adult Pkd2-mutant cyst-lining cholangiocytes. Taken together, Thm1 is required for biliary tract development, likely by enabling Notch signaling, and proper biliary development restricts PLD severity. Unlike IFT-B genes, Thm1 does not affect hepatic cystogenesis, suggesting divergent regulation of signaling and cystogenic processes in the liver by IFT-B and -A. Notably, increased Notch signaling in cyst-lining cholangiocytes may indicate that aberrant activation of this pathway promotes hepatic cystogenesis, presenting as a novel potential therapeutic target.

genetics↗