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Spiny lobsters (Decapoda: Palinuridae) in the genus Panulirus are targets of lucrative fisheries globally and have relevant ecological functions in tropical and subtropical environments. Only a few, but increasing, number of genetic and genomic resources exist for them. Nuclear and mitochondrial genome assemblies can provide insights into their phylogenetic relationships and support fishery management strategies in species that are heavily exploited. Herein, using Illumina short reads whole genome sequencing, we assembled the nuclear and mitochondrial genomes of a total of 14 species. Genomic DNA was extracted from specimens deposited at Clemson University Crustacean Collection and sequenced in a HiSeq X Ten system. The number of paired-end (PE) reads generated for the different studied species varied between 219,917,346 in P. argus and 70,215,423 in P. cygnus. Nuclear and mitochondrial genomes were ‘de novo’ assembled. Nuclear genomes ranged between 1,624,400,357 bp in P. guttatus and 935,571,898 bp in P. cygnus with scaffold numbers varying between 466,583 in P. versicolor and 852,228 in P. longipes. Mitochondrial genomes varied between 15,613 bp and 15,768 bp in P. pascuensis and P. versicolor, respectively. The totality of the short reads, nuclear, and mitochondrial genome assemblies are available at NCBI's GenBank.

Abstract Nearly half of cancer patients who receive standard-of-care treatments fail to respond to their first-line chemotherapy, demonstrating the pressing need for improved methods to select personalized cancer therapies. Low-coherence digital holography has the potential to fill this need by performing dynamic contrast OCT on living cancer biopsies treated ex vivo with anti-cancer therapeutics. Fluctuation spectroscopy of dynamic light scattering under conditions of holographic phase stability captures ultra-low Doppler frequency shifts down to 10 mHz caused by light scattering from intracellular motions. In the comparative preclinical/clinical trials presented here, a two-species (human and canine) and two-cancer (esophageal carcinoma and B-cell lymphoma) analysis of spectral phenotypes identifies a set of drug response characteristics that span species and cancer type. Spatial heterogeneity across a centimeter-scale patient biopsy sample is assessed by measuring multiple millimeter-scale sub-samples. Improved predictive performance is achieved for chemoresistance profiling by identifying red-shifted sub-samples that may indicate impaired metabolism and removing them from the prediction analysis. These results show potential for using biodynamic imaging for personalized selection of cancer therapy.

Throughout the Caribbean, coral reefs are transitioning from rugose, coral-dominated communities to flat, soft coral-dominated habitats, triggering declines in biodiversity. To help mitigate these losses, artificial structures have been used to re-create substrate complexity and support reef inhabitants. This study used natural and artificial structures to investigate the factors influencing the use of habitat by reef fish. During 2018 and 2019, divers added artificial structures and monitored the fish assemblages associating with both the artificial structures and naturally occurring corals. Overall, there were more fish on natural structures than on artificial structures. While structure shape did not influence fish use, there was a non-significant trend for increased use of larger structures. Fish observations did not differ across a gradient of shallow, complex reefs to deeper, flatter reefs; however, analyses of feeding guilds revealed clearer patterns: herbivores and omnivores were positively associated with low rugosity reefs where macroalgal abundance was higher, whereas invertivores preferred more rugose reefs. These results suggest that as reefs lose structural complexity, fish communities may become dominated by herbivores and omnivores. It also appears that the addition of artificial structures of the type used here may not mitigate the effects of structure loss on reef fish assemblages.

Marine diseases have caused large scale decreases in coral cover across the Caribbean and are unfortunately projected to increase as sea surface temperatures rise. Identifying the main drivers of disease transmission is essential for our understanding and response to diseases in the future. This study investigates the effects of direct-contact, waterborne, Symbiodiniaceae composition, and butterflyfish foraging on the transmission rates of stony coral tissue loss disease (SCTLD) across Montastraea cavernosa (MCAV) coral fragments. M. cavernosa fragments were placed in direct contact with diseased Orbicella and Montastraea colonies with the purpose of creating disease MCAV fragments for experimental trials with butterflyfish. Three treatments were used to investigate waterborne transmission (control), mechanically injury to a healthy coral (limited), and direct contact feeding across a diseased and healthy coral (unlimited). After the experimental trials, the composition of Symbiodiniaceae was analyzed for every MCAV fragment. Direct contact transmission took on average 3.9 days in 2019 and 11.9 days in 2020 with significantly quicker rates of transmission between donor diseased Orbicella and Montastraea than Montastraea to Montastraea. The composition of Symbiodiniaceae differed significantly between the fragments used in 2019 (dominated by Durusdinium) than in 2020 (dominated by Cladocopium spp.). The limited treatment had the quickest time to transmission compared to the unlimited and control treatments. Symbiodiniaceae differences between 2019 and 2020 might explain differences in transmission rates and overall susceptibility between the years. The species of Symbiodiniaceae may play a role in the susceptibility of corals to the transmission of SCTLD. Additionally, we also have some suggestive evidence that butterflyfish do not directly increase infection rates, but instead might be increasing infection recovery.

We previously described a population of lymphoid progenitor cells (LPCs) in canine B-cell lymphoma defined by retention of the early progenitor markers CD34 and CD117 and “slow proliferation” molecular signatures that persist in the xenotransplantation setting. We examined whether valspodar, a selective inhibitor of the ATP binding cassette B1 transporter (ABCB1, a.k.a., p-glycoprotein/multidrug resistance protein-1) used in the neoadjuvant setting would sensitize LPCs to doxorubicin and extend the length of remission in dogs with therapy naïve large B-cell lymphoma. Twenty dogs were enrolled into a double-blinded, placebo controlled study where experimental and control groups received oral valspodar (7.5 mg/kg) or placebo, respectively, twice daily for five days followed by five treatments with doxorubicin 21 days apart with a reduction in the first dose to mitigate the potential side effects of ABCB1 inhibition. Lymph node and blood LPCs were quantified at diagnosis, on the fourth day of neoadjuvant period, and 1-week after the first chemotherapy dose. Valspodar therapy was well tolerated. There were no differences between groups in total LPCs in lymph nodes or peripheral blood, nor in event-free survival or overall survival. Overall, we conclude that valspodar can be administered safely in the neoadjuvant setting for canine B-cell lymphoma; however, its use to attenuate ABCB1+ cells does not alter the composition of lymph node or blood LPCs, and it does not appear to be sufficient to prolong doxorubicin-dependent remissions in this setting.

We previously described a population of lymphoid progenitor cells (LPCs) in canine B-cell lymphoma defined by retention of the early progenitor markers CD34 and CD117 and “slow proliferation” molecular signatures that persist in the xenotransplantation setting. We examined whether valspodar, a selective inhibitor of the ATP binding cassette B1 transporter (ABCB1, a.k.a., p-glycoprotein/multidrug resistance protein-1) used in the neoadjuvant setting would sensitize LPCs to doxorubicin and extend the length of remission in dogs with therapy naïve large B-cell lymphoma. Twenty dogs were enrolled into a double-blinded, placebo controlled study where experimental and control groups received oral valspodar (7.5 mg/kg) or placebo, respectively, twice daily for five days followed by five treatments with doxorubicin 21 days apart with a reduction in the first dose to mitigate the potential side effects of ABCB1 inhibition. Lymph node and blood LPCs were quantified at diagnosis, on the fourth day of neoadjuvant period, and 1-week after the first chemotherapy dose. Valspodar therapy was well tolerated. There were no differences between groups in total LPCs in lymph nodes or peripheral blood, nor in event-free survival or overall survival. Overall, we conclude that valspodar can be administered safely in the neoadjuvant setting for canine B-cell lymphoma; however, its use to attenuate ABCB1+ cells does not alter the composition of lymph node or blood LPCs, and it does not appear to be sufficient to prolong doxorubicin-dependent remissions in this setting.

We previously described a population of lymphoid progenitor cells (LPCs) in canine B-cell lymphoma defined by retention of the early progenitor markers CD34 and CD117 and “slow proliferation” molecular signatures that persist in the xenotransplantation setting. We examined whether valspodar, a selective inhibitor of the ATP binding cassette B1 transporter (ABCB1, a.k.a., p-glycoprotein/multidrug resistance protein-1) used in the neoadjuvant setting would sensitize LPCs to doxorubicin and extend the length of remission in dogs with therapy naïve large B-cell lymphoma. Twenty dogs were enrolled into a double-blinded, placebo controlled study where experimental and control groups received oral valspodar (7.5 mg/kg) or placebo, respectively, twice daily for five days followed by five treatments with doxorubicin 21 days apart with a reduction in the first dose to mitigate the potential side effects of ABCB1 inhibition. Lymph node and blood LPCs were quantified at diagnosis, on the fourth day of neoadjuvant period, and 1-week after the first chemotherapy dose. Valspodar therapy was well tolerated. There were no differences between groups in total LPCs in lymph nodes or peripheral blood, nor in event-free survival or overall survival. Overall, we conclude that valspodar can be administered safely in the neoadjuvant setting for canine B-cell lymphoma; however, its use to attenuate ABCB1 + cells does not alter the composition of lymph node or blood LPCs, and it does not appear to be sufficient to prolong doxorubicin-dependent remissions in this setting.

We previously described a population of lymphoid progenitor cells (LPCs) in canine B-cell lymphoma defined by retention of the early progenitor markers CD34 and CD117 and “slow proliferation” molecular signatures that persist in the xenotransplantation setting. We examined whether valspodar, a selective inhibitor of the ATP binding cassette B1 transporter (ABCB1, a.k.a., p-glycoprotein/multidrug resistance protein-1) used in the neoadjuvant setting would sensitize LPCs to doxorubicin and extend the length of remission in dogs with therapy naïve large B-cell lymphoma. Twenty dogs were enrolled into a double-blinded, placebo controlled study where experimental and control groups received oral valspodar (7.5 mg/kg) or placebo, respectively, twice daily for five days followed by five treatments with doxorubicin 21 days apart with a reduction in the first dose to mitigate the potential side effects of ABCB1 inhibition. Lymph node and blood LPCs were quantified at diagnosis, on the fourth day of neoadjuvant period, and 1-week after the first chemotherapy dose. Valspodar therapy was well tolerated. There were no differences between groups in total LPCs in lymph nodes or peripheral blood, nor in event-free survival or overall survival. Overall, we conclude that valspodar can be administered safely in the neoadjuvant setting for canine B-cell lymphoma; however, its use to attenuate ABCB1 + cells does not alter the composition of lymph node or blood LPCs, and it does not appear to be sufficient to prolong doxorubicin-dependent remissions in this setting.

We previously described a population of lymphoid progenitor cells (LPCs) in canine B-cell lymphoma defined by retention of the early progenitor markers CD34 and CD117 and “slow proliferation” molecular signatures that persist in the xenotransplantation setting. We examined whether valspodar, a selective inhibitor of the ATP binding cassette B1 transporter (ABCB1, a.k.a., p-glycoprotein/multidrug resistance protein-1) used in the neoadjuvant setting would sensitize LPCs to doxorubicin and extend the length of remission in dogs with therapy naïve large B-cell lymphoma. Twenty dogs were enrolled into a double-blinded, placebo controlled study where experimental and control groups received oral valspodar (7.5 mg/kg) or placebo, respectively, twice daily for five days followed by five treatments with doxorubicin 21 days apart with a reduction in the first dose to mitigate the potential side effects of ABCB1 inhibition. Lymph node and blood LPCs were quantified at diagnosis, on the fourth day of neoadjuvant period, and 1-week after the first chemotherapy dose. Valspodar therapy was well tolerated. There were no differences between groups in total LPCs in lymph nodes or peripheral blood, nor in event-free survival or overall survival. Overall, we conclude that valspodar can be administered safely in the neoadjuvant setting for canine B-cell lymphoma; however, its use to attenuate ABCB1 + cells does not alter the composition of lymph node or blood LPCs, and it does not appear to be sufficient to prolong doxorubicin-dependent remissions in this setting.