<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/">
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3703">
    <dcterms:title><![CDATA[<p class="c-article-title">Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na<sup>+</sup><span> </span>channel</p>]]></dcterms:title>
    <dcterms:subject><![CDATA[Physiology<br />
Cardiovascular biology<br />
Kidney<br />
Neurophysiology<br />
Membrane trafficking<br />
Ion channels<br />
Sodium channels<br />
Kinases<br />
Cellular neuroscience]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Activity of the Epithelial Na+ Channel (ENaC) in the distal nephron fine-tunes renal sodium excretion. Appropriate sodium excretion is a key factor in the regulation of blood pressure. Consequently, abnormalities in ENaC function can cause hypertension. Casein Kinase II (CKII) phosphorylates ENaC. The CKII phosphorylation site in ENaC resides within a canonical “anchor” ankyrin binding motif. CKII-dependent phosphorylation of ENaC is necessary and sufficient to increase channel activity and is thought to influence channel trafficking in a manner that increases activity. We test here the hypothesis that phosphorylation of ENaC by CKII within an anchor motif is necessary for ankyrin-3 (Ank-3) regulation of the channel, which is required for normal channel locale and function, and the proper regulation of renal sodium excretion. This was addressed using a fluorescence imaging strategy combining total internal reflection fluorescence (TIRF) microscopy with fluorescence recovery after photobleaching (FRAP) to quantify ENaC expression in the plasma membrane in living cells; and electrophysiology to quantify ENaC activity in split-open collecting ducts from principal cell-specific Ank-3 knockout mice. Sodium excretion studies also were performed in parallel in this knockout mouse. In addition, we substituted a key serine residue in the consensus CKII site in β-ENaC with alanine to abrogate phosphorylation and disrupt the anchor motif. Findings show that disrupting CKII signaling decreases ENaC activity by decreasing expression in the plasma membrane. In the principal cell-specific Ank-3 KO mouse, ENaC activity and sodium excretion were significantly decreased and increased, respectively. These results are consistent with CKII phosphorylation of ENaC functioning as a “switch” that favors Ank-3 binding to increase channel activity.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Abd El-Aziz, T. M., Soares, A. G., Mironova, E., Boiko, N., Kaur, A., Archer, C. R., Stockand, J. D., &amp; Berman, J. M.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Scientific Reports</em>, Volume 11, Issue 1, July 2021, Article 14600]]></dcterms:source>
    <dcterms:publisher><![CDATA[Springer Science and Business Media LLC]]></dcterms:publisher>
    <dcterms:date><![CDATA[2021]]></dcterms:date>
    <dcterms:rights><![CDATA[Copyright © The Author(s) 2021 <br /><strong>Open Access</strong> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit <a href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</a>.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/3e3892ed56d7f3745aff88994ae5f4a0.pdf">https://repository.nyitlibrary.org/files/original/3e3892ed56d7f3745aff88994ae5f4a0.pdf</a>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.1038/s41598-021-94118-3">https://doi.org/10.1038/s41598-021-94118-3</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Abd El-Aziz, T. M., Soares, A. G., Mironova, E., Boiko, N., Kaur, A., Archer, C. R., Stockand, J. D., &amp; Berman, J. M. (2021). Mechanisms and consequences of casein kinase II and ankyrin-3 regulation of the epithelial Na+ channel. In Scientific Reports (Vol. 11, Issue 1). Springer Science and Business Media LLC. <a href="https://doi.org/10.1038/s41598-021-94118-3">https://doi.org/10.1038/s41598-021-94118-3</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3753">
    <dcterms:title><![CDATA[A comparative study of the effectiveness of an osteopathic primary care sports medicine led intervention on performance in men’s collegiate lacrosse players]]></dcterms:title>
    <dcterms:subject><![CDATA[Collegiate sports<br />
Family medicine<br />
Health; lacrosse<br />
Osteopathic medicine<br />
Performance<br />
Primary care<br />
Sports medicine]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<p><strong class="sub-title">Context:<span> </span></strong>Comprehensive sports medicine care goes beyond the treatment of injuries resulting from athletic activities. Ultimately, it is a competence that includes knowledge in physical therapy, training, nutrition, coaching, motivation, competition, mentoring, psychology, and spirituality that allows the physician and patient to collaborate on promoting the patient's health goals. The current literature demonstrates a lack of knowledge in the Osteopathic Primary Care Sports Medicine Model's effectiveness in performance.</p>
<p><strong class="sub-title">Objectives:<span> </span></strong>To determine whether a comprehensive osteopathic primary care sports medicine approach can improve performance and health outcomes in collegiate athletes.</p>
<p><strong class="sub-title">Methods:<span> </span></strong>A randomized controlled trial commenced just prior to the start of the lacrosse season and concluded at the end of the season. All the New York Institute of Technology (NYIT) collegiate lacrosse players were educated first in a 1-day seminar of the core competencies, and all participants had access to ask questions on their own volition. Then they were randomized into two groups, either the experimental group receiving the direct osteopathic primary care sports medicine intervention (n=18) or the control group not having active intervention (n=19). Also, the overall team winning percentage for that season was computed and compared to that for the previous years and the following year. Participants were assessed before and after the intervention with the Patient Health Questionnaire (PHQ-9), the 36-Item Short Form Survey (SF-36), custom Osteopathic Primary Care Sports Medicine questionnaire, and body fat composition, and their changes were compared between the experimental group and the control group. Collected data were analyzed using the repeated-measures analysis of variance.</p>
<p><strong class="sub-title">Results:<span> </span></strong>Thirty-seven participants were enrolled in the study. After 14 participants were excluded due to being lost to follow-up, 23 athlete records were analyzed. The winning percentage of the team was highest during the year of the study period time than in the 3 previous years and the following year. The test group did not have any statistically significant change in the PHQ-9, SF-36, custom Osteopathic Primary Care Sports Medicine questionnaire, as well as in body fat composition.</p>
<p><strong class="sub-title">Conclusions:<span> </span></strong>When used during a collegiate lacrosse season, this Osteopathic Primary Care Sports Medicine intervention did not significantly improve health outcomes. This preliminary study, despite its limitations in compliance and study population size, did demonstrate improvement in overall team performance when comparing the intervention sport season to other seasons but was not statistically significantly. Therefore, further studies are warranted to improve the understanding in this approach to athlete health outcomes and performance.</p>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Rao, N. C., Zwibel, H., Berezanskaya, J., Pena, P., &amp; Jung, M.-K.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Journal of Osteopathic Medicine</em>, Volume 122, Issue 2, November 2021, pages 71-77]]></dcterms:source>
    <dcterms:publisher><![CDATA[Walter de Gruyter GmbH]]></dcterms:publisher>
    <dcterms:date><![CDATA[2021]]></dcterms:date>
    <dcterms:rights><![CDATA[CC BY 4.0 DEED Attribution 4.0 International © 2021 Naresh C. Rao et al., published by De Gruyter, Berlin/Boston.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/5a126b18dce9e48bf5f1789d34af0825.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.1515/jom-2021-0083">https://doi.org/10.1515/jom-2021-0083</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Rao, N. C., Zwibel, H., Berezanskaya, J., Pena, P., &amp; Jung, M.-K. (2021). A comparative study of the effectiveness of an osteopathic primary care sports medicine led intervention on performance in men’s collegiate lacrosse players. In Journal of Osteopathic Medicine (Vol. 122, Issue 2, pp. 71–77). Walter de Gruyter GmbH. <a href="https://doi.org/10.1515/jom-2021-0083">https://doi.org/10.1515/jom-2021-0083</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><br />
<b>Warning</b>:  Undefined array key "path" in <b>/home/nyitlibr/repository.nyitlibrary.org/plugins/ClickableLinksPlus/ClickableLinksPlusPlugin.php</b> on line <b>207</b><br />
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3669">
    <dcterms:title><![CDATA[A Miocene cetacean vertebra showing a partially healed longitudinal shear-compression fracture, possibly the result of domoic acid toxicity or failed predation]]></dcterms:title>
    <dcterms:subject><![CDATA[Calvert Cliffs<br />
Cetacean vertebrae<br />
Failed predation<br />
Harmful algal bloom<br />
Miocene<br />
Otodus megalodon<br />
Seizure<br />
Shear-compression fracture<br />
Acid<br />
Algal bloom<br />
Cetacean<br />
Compression<br />
Fracture<br />
Miocene<br />
Pathology<br />
Predation<br />
Shark<br />
Shear<br />
Tooth<br />
Toxicity]]></dcterms:subject>
    <dcterms:abstract><![CDATA[CT-scans of a cetacean pathological vertebra from the Calvert Formation of the Miocene Chesapeake Group of Maryland, show features characteristic of a shear-compression fracture with comminution and significant periosteal reaction. The etiology of the injury suggests an intense hyperflexion of vertebrae in at least the lumbar region of the axial column. The trauma was sufficiently forceful to break much of the lower two-fifths of the centrum away from the anterior end of the body of the vertebra. However, the trauma was not immediately fatal as significant fusion of fragmented elements was well underway at the time of death. Much of the lateral and ventral surfaces of the centrum are covered with a thick layer of periosteal reactive bone. This reactive periosteal bone growth could be due to spondyloarthritis, infection, or from the traumatic event itself, if the direct muscle attachments on the vertebra were avulsed.<br />
<br />
A single megatoothed shark tooth from Otodus megalodon was found with the vertebra. It is not known if the tooth came to be there serendipitously, or if it was associated because it was lost as a result of the possible originating failed predation event, or during a final successful predation or subsequent scavenging event.<br />
<br />
The fractures are severe and unlikely to have had an endogenous origin like convulsions, seizures, or spasms. Seizures can cause vertebral fractures in humans, including elderly adults with poor bone health as well as physically fit younger individuals. Seizures causing injuries of this magnitude have not been observed in cetaceans, though domoic acid toxicity from harmful algal blooms are known to cause seizures in cetaceans, and are implicated in the deaths of neonatal skim-feeding mysticetes. It is unlikely, but possible, that a large mysticete would be affected by domoic acid toxicity to the point of a spinal fracture-causing seizure. Similarly, protozoal infections are known to cause seizures in cetaceans, though physical diagnosis of this is impossible in a fossil. Partly healed bone fractures of the face from possible collisions with the seafloor have been reported from fossil mysticetes of shallower regions of this fauna, but a spinal fracture this far back in the spinal column seems unlikely to be the result of a seafloor collision. Even though the cause of the vertebral hyperflexion and resulting trauma is unknown, a plausible cause was a crushing ambush delivered by a macropredatory shark or macroraptorial physeteroid. In spite of extant cetaceans being subjected to anthropogenically-induced trauma, which include vessel-strike blunt force injuries of many different kinds, shear-compression fractures and periosteal reactions like the ones detailed here have not yet been reported in extant cetaceans. Therefore, we consider the fracture as likely due to an impact from a predator, such as Otodus megalodon, or possibly from seizures due to a harmful algal bloom and resulting domoic acid toxicity. In either scenario, the cetacean survived.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Godfrey S.J. &amp; Beatty B.L.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Palaeontologia Electronica</em><span>, Article 25.3.a28, September 2022</span>]]></dcterms:source>
    <dcterms:publisher><![CDATA[Coquina Press]]></dcterms:publisher>
    <dcterms:date><![CDATA[2022]]></dcterms:date>
    <dcterms:rights><![CDATA[Copyright: September 2022 Society of Vertebrate Paleontology. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/625ed29d2da781f30e49559144d0beca.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<span class="linkify-target external-link">https://doi.org/10.26879/1171</span>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[Godfrey, S., &amp; Beatty, B. (2022). A Miocene cetacean vertebra showing a partially healed longitudinal shear-compression fracture, possibly the result of domoic acid toxicity or failed predation. In Palaeontologia Electronica. Coquina Press. https://doi.org/10.26879/1171]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3783">
    <dcterms:title><![CDATA[A Practical Guide to Sliding and Surface Semilandmarks in Morphometric Analyses]]></dcterms:title>
    <dcterms:subject><![CDATA[Amphibians / anatomy &amp; histology<br />
Anatomic Landmarks / anatomy &amp; histology<br />
Animals<br />
Biological Evolution<br />
Birds / anatomy &amp; histology<br />
Models, Anatomic<br />
Phenotype<br />
Reptiles<br />
Skull]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Advances in imaging technologies, such as computed tomography (CT) and surface scanning, have facilitated the rapid generation of large datasets of high-resolution three-dimensional (3D) specimen reconstructions in recent years. The wealth of phenotypic information available from these datasets has the potential to inform our understanding of morphological variation and evolution. However, the ever-increasing ease of compiling 3D datasets has created an urgent need for sophisticated methods of capturing high-density shape data that reflect the biological complexity in form. Landmarks often do not take full advantage of the rich shape information available from high-resolution 3D specimen reconstructions, as they are typically restricted to sutures or processes that can be reliably identified across specimens and exclude most of the surface morphology. The development of sliding and surface semilandmark techniques has greatly enhanced the quantification of shape, but their application to diverse datasets can be challenging, especially when dealing with the variable absence of some regions within a structure. Using comprehensive 3D datasets of crania that span the entire clades of birds, squamates and caecilians, we demonstrate methods for capturing morphology across incredibly diverse shapes. We detail many of the difficulties associated with applying semilandmarks to comparable regions across highly disparate structures, and provide solutions to some of these challenges, while considering the consequences of decisions one makes in applying these approaches. Finally, we analyze the benefits of high-density sliding semilandmark approaches over landmark-only studies for capturing shape across diverse organisms and discuss the promise of these approaches for the study of organismal form.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Bardua, C., Felice, R. N., Watanabe, A., Fabre, A.-C., &amp; Goswami, A.]]></dcterms:creator>
    <dcterms:source><![CDATA[<i>Integrative Organismal Biology</i>, Volume 1, Issue 1, July 2019]]></dcterms:source>
    <dcterms:publisher><![CDATA[Oxford University Press]]></dcterms:publisher>
    <dcterms:date><![CDATA[2019]]></dcterms:date>
    <dcterms:rights><![CDATA[<div class="copyright copyright-statement">© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Integrative and Comparative Biology.</div>
<div class="license">
<div class="license-p">This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<a class="link link-uri openInAnotherWindow" href="http://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noreferrer noopener">http://creativecommons.org/licenses/by/4.0/</a>), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.</div>
</div>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/0d49a32ca2112ca28ed0bda2ed7a8f85.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.1093/iob/obz016">https://doi.org/10.1093/iob/obz016</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Bardua, C., Felice, R. N., Watanabe, A., Fabre, A.-C., &amp; Goswami, A. (2019). A Practical Guide to Sliding and Surface Semilandmarks in Morphometric Analyses. In Integrative Organismal Biology (Vol. 1, Issue 1). Oxford University Press (OUP). <a href="https://doi.org/10.1093/iob/obz016">https://doi.org/10.1093/iob/obz016</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3686">
    <dcterms:title><![CDATA[A Systematic Review of the Giant Alligatoroid Deinosuchus From the Campanian of North America and Its Implications for the Relationships at the Root of Crocodylia]]></dcterms:title>
    <dcterms:abstract><![CDATA[Deinosuchus is a lineage of giant (≥10 m) Late Cretaceous crocodylians from North America. These were the largest semiaquatic predators in their environments and are known to have fed on large vertebrates, including contemporaneous terrestrial vertebrates such as dinosaurs. Fossils have been found in units of Campanian age from northern Mexico to Montana in the west and Mississippi to New Jersey in the east. Three species have been named, and recent consensus suggests that they represent a single, widely ranging species. The authors studied newly collected material from western Texas and increased sampling from throughout North America to review species-level systematics of Deinosuchus and help refine its phylogenetic placement among crocodylians. Deinosuchus from eastern and western North America can be consistently differentiated and represent different species. A phylogenetic study is conducted including new character states. This work reinforces the identity of the ‘terror crocodile’ as an alligatoroid. Reference to the holotypes indicates that the generic name holder, Deinosuchus hatcheri, is extremely incomplete. As a result, the three known species of Deinosuchus cannot be differentiated. To ensure nomenclatural stability, the type species for Deinosuchus should be transferred to Deinosuchus riograndensis, a species known from multiple mostly complete individuals. Additionally, Deinosuchus rugosus is based on a holotype that is not diagnostic, and a new species, Deinosuchus schwimmeri, is named to encompass some specimens formerly assigned to D. rugosus.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Cossette, A. P., &amp; Brochu, C. A.]]></dcterms:creator>
    <dcterms:source><![CDATA[<i>Journal of Vertebrate Paleontology</i><span>, vol. 40, no. 1, Jan. 2020, pp. 1–21</span>]]></dcterms:source>
    <dcterms:publisher><![CDATA[Taylor &amp; Francis]]></dcterms:publisher>
    <dcterms:date><![CDATA[2020]]></dcterms:date>
    <dcterms:rights><![CDATA[© 2020. Adam P. Cossette and Christopher A. Brochu. Published by Informa UK Limited, trading as Taylor &amp; Francis Group.<br />This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (<a href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http://creativecommons.org/licenses/by-nc-nd/4.0/</a>), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/f67eee8af23a2dc21eb45398705ca87e.pdf">https://repository.nyitlibrary.org/files/original/f67eee8af23a2dc21eb45398705ca87e.pdf</a><br /><br /><a href="https://doi.org/10.1080/02724634.2020.1767638">https://doi.org/10.1080/02724634.2020.1767638</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Cossette, A. P., &amp; Brochu, C. A. (2020). A systematic review of the giant alligatoroidDeinosuchusfrom the Campanian of North America and its implications for the relationships at the root of Crocodylia. In Journal of Vertebrate Paleontology (Vol. 40, Issue 1, p. e1767638). Informa UK Limited. <a href="https://doi.org/10.1080/02724634.2020.1767638">https://doi.org/10.1080/02724634.2020.1767638</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><br />
<b>Warning</b>:  Undefined array key "path" in <b>/home/nyitlibr/repository.nyitlibrary.org/plugins/ClickableLinksPlus/ClickableLinksPlusPlugin.php</b> on line <b>207</b><br />
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3771">
    <dcterms:title><![CDATA[Adaptations for Bipedal Walking: Musculoskeletal Structure and Three-Dimensional Joint Mechanics of Humans and Bipedal Chimpanzees (Pan troglodytes)]]></dcterms:title>
    <dcterms:subject><![CDATA[Bipedalism<br />
Elastic energy<br />
Force<br />
Locomotion<br />
Power<br />
Work]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Humans are unique among apes and other primates in the musculoskeletal design of their lower back, pelvis, and lower limbs. Here, we describe the three-dimensional ground reaction forces and lower/hindlimb joint mechanics of human and bipedal chimpanzees walking over a full stride and test whether: 1) the estimated limb joint work and power during the stance phase, especially the single-support period, is lower in humans than bipedal chimpanzees, 2) the limb joint work and power required for limb swing is lower in humans than in bipedal chimpanzees, and 3) the estimated total mechanical power during walking, accounting for the storage of passive elastic strain energy in humans, is lower in humans than in bipedal chimpanzees. Humans and bipedal chimpanzees were compared at matched dimensionless and dimensional velocities. Our results indicate that humans walk with significantly less work and power output in the first double-support period and the single-support period of stance, but markedly exceed chimpanzees in the second double-support period (i.e., push-off). Humans generate less work and power in limb swing, although the species difference in limb swing power was not statistically significant. We estimated that total mechanical positive &#039;muscle fiber&#039; work and power were 46.9% and 35.8% lower, respectively, in humans than in bipedal chimpanzees at matched dimensionless speeds. This is due in part to mechanisms for the storage and release of elastic energy at the ankle and hip in humans. Furthermore, these results indicate distinct &#039;heel strike&#039; and &#039;lateral balance&#039; mechanics in humans and bipedal chimpanzees and suggest a greater dissipation of mechanical energy through soft tissue deformations in humans. Together, our results document important differences between human and bipedal chimpanzee walking mechanics over a full stride, permitting a more comprehensive understanding of the mechanics and energetics of chimpanzee bipedalism and the evolution of hominin walking.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[O’Neill, M. C., Demes, B., Thompson, N. E., Larson, S. G., Stern, J. T., Jr., &amp; Umberger, B. R.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Journal of Human Evolution </em>Volune 168, July 2022, page 103195]]></dcterms:source>
    <dcterms:publisher><![CDATA[Elsevier BV]]></dcterms:publisher>
    <dcterms:date><![CDATA[2022]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>This article is available under the </span><a target="_blank" href="https://creativecommons.org/licenses/" rel="noreferrer noopener">Creative Commons CC-BY-NC-ND</a><span> license and permits non-commercial use of the work as published, without adaptation or alteration provided the work is fully attributed.</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/f7057fd6ee58739b43e0eb1fc5fe61b2.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<span class="linkify-target external-link">https://doi.org/10.1016/j.jhevol.2022.103195</span>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>O’Neill, M. C., Demes, B., Thompson, N. E., Larson, S. G., Stern, J. T., Jr., &amp; Umberger, B. R. (2022). Adaptations for bipedal walking: Musculoskeletal structure and three-dimensional joint mechanics of humans and bipedal chimpanzees (Pan troglodytes). In Journal of Human Evolution (Vol. 168, p. 103195). Elsevier BV. <a href="https://doi.org/10.1016/j.jhevol.2022.103195">https://doi.org/10.1016/j.jhevol.2022.103195</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3761">
    <dcterms:title><![CDATA[Addressing Discrepancies between Experimental and Computational Procedures]]></dcterms:title>
    <dcterms:subject><![CDATA[Chordae Tendineae<br />
Chordal Structure<br />
Comprehensive Computational Model<br />
Fluid-Structure Interaction<br />
Heart Valve<br />
Smooth Particle Hydrodynamics]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Imaging subject-specific heart valve, a crucial step to its design, has experimental variables that if unaccounted for, may lead to erroneous computational analysis and geometric errors of the resulting model. Preparation methods are developed to mitigate some sources of the geometric error. However, the resulting 3D geometry often does not retain the original dimensions before excision. Inverse fluid–structure interaction analysis is used to analyze the resulting geometry and to assess the valve’s closure. Based on the resulting closure, it is determined if the geometry used can yield realistic results. If full closure is not reached, the geometry is adjusted adequately until closure is observed.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Toma, M., Guru, S. K., Wu, W., Ali, M., &amp; Ong, C. W. ]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Biology</em>, Volume 10, Issue 6, June 2021, page 536]]></dcterms:source>
    <dcterms:publisher><![CDATA[MDPI AG]]></dcterms:publisher>
    <dcterms:date><![CDATA[2021]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>© 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (</span><a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noreferrer noopener">https://creativecommons.org/licenses/by/4.0/</a><span>).</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/5f4d0a05b468fb97ccfa623ce3e3a322.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3390/biology10060536">https://doi.org/10.3390/biology10060536</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Toma, M., Guru, S. K., Wu, W., Ali, M., &amp; Ong, C. W. (2021). Addressing Discrepancies between Experimental and Computational Procedures. In Biology (Vol. 10, Issue 6, p. 536). MDPI AG. <a href="https://doi.org/10.3390/biology10060536">https://doi.org/10.3390/biology10060536</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3736">
    <dcterms:title><![CDATA[Adverse transverse-tubule remodeling in a rat model of heart failure is attenuated with low-dose triiodothyronine treatment]]></dcterms:title>
    <dcterms:subject><![CDATA[Calcium transients<br />
Contractility<br />
Heart failure<br />
T-tubules<br />
Triiodothyronine]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<p>Pre-clinical animal studies have shown that triiodothyronine (T3) replacement therapy improves cardiac contractile function after myocardial infarction (MI). We hypothesized that T3 treatment could prevent adverse post-infarction cardiomyocyte remodeling by maintaining transverse-tubule (TT) structures, thus improving calcium dynamics and contractility.</p>
<h3 class="c-article__sub-heading">Methods</h3>
<p>Myocardial infarction (MI) or sham surgeries were performed on female Sprague-Dawley rats (aged 12 wks), followed by treatment with T3 (5μg/kg/d) or vehicle in drinking water for 16 wks (<i>n</i> = 10–11/group). After in vivo echocardiographic and hemodynamic analyses, left ventricular myocytes were isolated by collagenase digestion and simultaneous calcium and contractile transients in single cardiomyocytes were recorded using IonOptix imaging. Live cardiomyocytes were stained with AlexaFluor-488 conjugated wheat germ agglutinin (WGA-488) or di-8-ANEPPS, and multiple z-stack images per cell were captured by confocal microscopy for analysis of TT organization. RTqPCR and immunoblot approaches determined expression of TT proteins.</p>
<h3 class="c-article__sub-heading">Results</h3>
<p>Echocardiography and in vivo hemodynamic measurements showed significant improvements in systolic and diastolic function in T3- vs vehicle-treated MI rats. Isolated cardiomyocyte analysis showed significant dysfunction in measurements of myocyte relengthening in MI hearts, and improvements with T3 treatment: max relengthening velocity (Vmax, um/s), 2.984 ± 1.410 vs 1.593 ± 0.325,<span> </span><i>p</i> &lt; 0.05 and time to Vmax (sec), 0.233 ± 0.037 vs 0.314 ± 0.019,<span> </span><i>p</i> &lt; 0.001; MI + T3 vs MI + Veh, respectively. Time to peak contraction was shortened by T3 treatment (0.161 ± 0.021 vs 0.197 ± 0.011 s.,<span> </span><i>p</i> &lt; 0.01; MI + T3 vs MI + Veh, respectively). Analysis of TT periodicity of WGA- or ANEPPS-stained cardiomyocytes indicated significant TT disorganization in MI myocytes and improvement with T3 treatment (transverse-oriented tubules (TE%): 9.07 ± 0.39 sham, 6.94 ± 0.67 MI + Veh and 8.99 ± 0.38 MI + T3; sham vs MI + Veh,<span> </span><i>p</i> &lt; 0.001; MI + Veh vs MI + T3,<span> </span><i>p</i> &lt; 0.01). Quantitative RT-PCR showed that reduced expression of BIN1 (Bridging integrator-1), Jph2 (junctophilin-2), RyR2 (ryanodine receptor) and Ca<sub>v</sub>1.2 (L-type calcium channel) in the failing myocardium were increased by T3 and immunoblot analysis further supporting a potential T3 effect on the TT-associated proteins, BIN1 and Jph2.</p>
<p>In conclusion, low dose T3 treatment initiated immediately after myocardial infarction attenuated adverse TT remodeling, improved calcium dynamics and contractility, thus supporting the potential therapeutic utility of T3 treatment in heart failure.</p>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[An, S., Gilani, N., Huang, Y., Muncan, A., Zhang, Y., Tang, Y.-D., Gerdes, A. M., &amp; Ojamaa, K.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Molecular Medicine</em>, Volume 25, Issue 1, December 2019]]></dcterms:source>
    <dcterms:publisher><![CDATA[Springer Science and Business Media LLC]]></dcterms:publisher>
    <dcterms:date><![CDATA[2019]]></dcterms:date>
    <dcterms:rights><![CDATA[This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article unless otherwise stated.<br />
Reprints and Permissions.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/92cc176f4f16e234d4fcc18ed703933c.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.1186/s10020-019-0120-3">https://doi.org/10.1186/s10020-019-0120-3</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>An, S., Gilani, N., Huang, Y., Muncan, A., Zhang, Y., Tang, Y.-D., Gerdes, A. M., &amp; Ojamaa, K. (2019). Adverse transverse-tubule remodeling in a rat model of heart failure is attenuated with low-dose triiodothyronine treatment. In Molecular Medicine (Vol. 25, Issue 1). Springer Science and Business Media LLC. <a href="https://doi.org/10.1186/s10020-019-0120-3">https://doi.org/10.1186/s10020-019-0120-3</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3776">
    <dcterms:title><![CDATA[ALT Positivity in Human Cancers: Prevalence and Clinical Insights]]></dcterms:title>
    <dcterms:subject><![CDATA[Alternative lengthening of telomeres<br />
Cancers<br />
ALT biomarkers<br />
ATRX<br />
DAXX]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<span>Many exciting advances in cancer-related telomere biology have been made in the past decade. Of these recent advances, great progress has also been made with respect to the Alternative Lengthening of Telomeres (ALT) pathway. Along with a better understanding of the molecular mechanism of this unique telomere maintenance pathway, many studies have also evaluated ALT activity in various cancer subtypes. We first briefly review and assess a variety of commonly used ALT biomarkers. Then, we provide both an update on ALT-positive (ALT+) tumor prevalence as well as a systematic clinical assessment of the presently studied ALT+ malignancies. Additionally, we discuss the pathogenetic alterations in ALT+ cancers, for example, the mutation status of </span><span class="html-italic">ATRX</span><span> and </span><span class="html-italic">DAXX</span><span>, and their correlations with the activation of the ALT pathway. Finally, we highlight important ALT+ clinical associations within each cancer subtype and subdivisions within, as well as their prognoses. We hope this alternative perspective will allow scientists, clinicians, and drug developers to have greater insight into the ALT cancers so that together, we may develop more efficacious treatments and improved management strategies to meet the urgent needs of cancer patients.</span>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[MacKenzie, D., Jr., Watters, A. K., To, J. T., Young, M. W., Muratori, J., Wilkoff, M. H., Abraham, R. G., Plummer, M. M., &amp; Zhang, D.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Cancers</em>, Volume 13, Issue 10, May 2021, Page 2384]]></dcterms:source>
    <dcterms:publisher><![CDATA[MDPI AG]]></dcterms:publisher>
    <dcterms:date><![CDATA[2021]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>All articles published by MDPI are made immediately available worldwide under an open access license. No special permission is required to reuse all or part of the article published by MDPI, including figures and tables. For articles published under an open access Creative Common CC BY license, any part of the article may be reused without permission provided that the original article is clearly cited.</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/45fb0fa9261ac518b5a1a88b1977f092.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3390/cancers13102384">https://doi.org/10.3390/cancers13102384</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>MacKenzie, D., Jr., Watters, A. K., To, J. T., Young, M. W., Muratori, J., Wilkoff, M. H., Abraham, R. G., Plummer, M. M., &amp; Zhang, D. (2021). ALT Positivity in Human Cancers: Prevalence and Clinical Insights. In Cancers (Vol. 13, Issue 10, p. 2384). MDPI AG. <a href="https://doi.org/10.3390/cancers13102384">https://doi.org/10.3390/cancers13102384</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3754">
    <dcterms:title><![CDATA[AMPK promotes the survival of colorectal cancer stem cells]]></dcterms:title>
    <dcterms:subject><![CDATA[AMP‐activated protein kinase<br />
Cancer metabolism<br />
Colorectal cancer stem cells<br />
Patient‐derived xenograft]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Background<br />
Colorectal cancer (CRC) is the third most commonly diagnosed cancer in males and the second in females worldwide in 2012. In the past 20 years, strong evidence suggests that cancer stem cells are the main culprit of cancer metastasis, chemotherapy resistance, and relapse.<br />
<br />
Methods<br />
To further understand the unique biological properties of cancer stem cells and uncover novel molecular targets to eradicate them, we first established a panel of patient-derived xenograft (PDX) tumor models using tumors surgically removed from human colorectal cancer patients. We then isolated CRC cancer stem cells based on their ALDH activity using fluorescent-activated cell sorting (FACS) and characterized their metabolic properties.<br />
<br />
Results<br />
Interestingly, we found that the CRC cancer stem cells (ie, CRC cells with higher ALDH activity, or ALDH+) express higher level of antioxidant genes and have lower level of reactive oxygen species (ROS) than non-CRC cancer stem cells (ie, CRC cells with lower ALDH activity, or ALDH−). The CRC cancer stem cells also possess more mitochondria mass and show higher mitochondrial activity. More intriguingly, we observed higher AMP-activated protein kinase (AMPK) activities in these CRC cancer stem cells. Inhibition of the AMPK activity using 2 AMPK inhibitors, Compound C and Iodotubercidin, preferentially induces cell death in CRC cancer stem cells.<br />
<br />
Conclusion<br />
We propose that AMPK inhibitors may help to eradicate the CRC cancer stem cells and prevent the relapse of CRCs.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Guo, B., Han, X., Tkach, D., Huang, S., &amp; Zhang, D.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Animal Models and Experimental Medicine</em>, Volume 1, Issue 2, July 2018, pages 134-142]]></dcterms:source>
    <dcterms:publisher><![CDATA[Wiley]]></dcterms:publisher>
    <dcterms:date><![CDATA[2018]]></dcterms:date>
    <dcterms:rights><![CDATA[CC BY-NC 4.0 DEED Attribution-NonCommercial 4.0 International]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/5a126b18dce9e48bf5f1789d34af0825.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3390/biology10050374">https://doi.org/10.3390/biology10050374</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Guo, B., Han, X., Tkach, D., Huang, S., &amp; Zhang, D. (2018). AMPK promotes the survival of colorectal cancer stem cells. In Animal Models and Experimental Medicine (Vol. 1, Issue 2, pp. 134–142). Wiley. <a href="https://doi.org/10.1002/ame2.12016">https://doi.org/10.1002/ame2.12016</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3688">
    <dcterms:title><![CDATA[An Ethics Assessment Model for Teaching Global Health Program and Policy Implementation ]]></dcterms:title>
    <dcterms:subject><![CDATA[Ethics<br />
Global Health<br />
High-Income Countries (HIC)<br />
Low-to-Middle Income Countries (LMICs)<br />
Sustainable Development Goals (SDGs)<br />
Teaching &amp; Learning Methods]]></dcterms:subject>
    <dcterms:abstract><![CDATA[This mixed-method study surveyed and interviewed 60 High Income Country (HIC) US citizens/immigrants and Low-to-Middle-Income-Country (LMIC) citizens of African heritage on their perceptions of mental health services in African communities for implementation and research planning. In this study, ethics was a core emergent theme for global health initiatives and challenges, including political will for ethical change, community gatekeepers, level of government involvement, community-wide participation, public-private sector collaboration, health literacy and education, transparency, continuous monitoring, and consequences for ethical infractions. Based on our findings, we propose an active teaching and learning methodology of problem-based (PBL) and team-based learning (TBL) with multi-level HIC-LMIC citizen engagement for ethics in global health program productivity and sustainability. The intended result is to produce ethically trained and equipped health professionals, enhanced HIC and LMIC capacity building, cultural humility, and decolonization of health programs and policies.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Oji, V., Knight, C., Mahatara, R., &amp; Oladoyin, V.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Journal of Global Awareness</em>, vol. 3, no. 2, Dec. 2022, pp. 1–20]]></dcterms:source>
    <dcterms:publisher><![CDATA[St. John&#039;s Scholar]]></dcterms:publisher>
    <dcterms:date><![CDATA[2022]]></dcterms:date>
    <dcterms:rights><![CDATA[This Article is brought to you for free and open access by St. John's Scholar. It has been accepted for inclusion in Journal of Global Awareness by an authorized editor of St. John's Scholar. For more information, please contact <a href="mailto:karniks@stjohns.edu">karniks@stjohns.edu</a>, <a href="mailto:fuchsc@stjohns.edu">fuchsc@stjohns.edu</a>.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/7c7f0d85a98dd711898476adf47b3389.pdf">https://repository.nyitlibrary.org/files/original/7c7f0d85a98dd711898476adf47b3389.pdf</a><br /><br /><a href="https://doi.org/10.24073/jga/3/02/05">https://doi.org/10.24073/jga/3/02/05</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Oji, V., Knight, C., Mahatara, R., &amp; Oladoyin, V. (2022). An Ethics Assessment Model for Teaching Global Health Program and Policy Implementation. In Journal of Global Awareness (Vol. 3, Issue 2). St. John’s University. <a href="https://doi.org/10.24073/jga/3/02/05">https://doi.org/10.24073/jga/3/02/05</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3696">
    <dcterms:title><![CDATA[Antihyperalgesic Effects of Meteorin in the Rat Chronic Constriction Injury Model: A Replication Study]]></dcterms:title>
    <dcterms:subject><![CDATA[0<br />
Analgesics administration &amp; dosage therapeutic use<br />
Animals<br />
Disease Models, Animal<br />
Hyperalgesia drug therapy etiology<br />
Index Medicus<br />
Male<br />
Nerve Tissue Proteins administration &amp; dosage therapeutic use<br />
Neuralgia drug therapy etiology<br />
Pain Measurement<br />
Pain Threshold drug effects<br />
Peripheral Nerve Injuries complications<br />
Rats<br />
Rats, Sprague-Dawley<br />
Reproducibility of Results]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Data from preclinical research have been suggested to suffer from a lack of inherent reproducibility across laboratories. The goal of our study was to replicate findings from a previous report that demonstrated positive effects of Meteorin, a novel neurotrophic factor, in a rat model of neuropathic pain induced by chronic constriction injury (CCI). Notably, 5 to 6 intermittent subcutaneous (s.c.) injections of Meteorin had been reported to produce reversal of mechanical allodynia/thermal hyperalgesia after injury, wherein maximum efficacy of Meteorin was reached slowly and outlasted the elimination of the compound from the blood by several weeks. Here, we evaluated the efficacy of Meteorin in reversing hindpaw mechanical hyperalgesia and cold allodynia in male, Sprague-Dawley rats with CCI. Nociceptive behavior was monitored before and after CCI, and after drug treatment until day 42 after injury. Systemic administration of recombinant mouse Meteorin (0.5 and 1.8 mg/kg, s.c.) at days 10, 12, 14, 17, and 19 after CCI produced a prolonged reversal of neuropathic hypersensitivity with efficacy comparable with that obtained with gabapentin (100 mg/kg, orally). Despite some protocol deviations (eg, nociceptive endpoint, animal vendor, testing laboratory, investigator, etc.) being incurred, these did not affect study outcome. By paying careful attention to key facets of study design, using bioactive material, and confirming drug exposure, the current data have replicated the salient findings of the previous study, promoting confidence in further advancement of this novel molecule as a potential therapy for neuropathic pain.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Jennifer Y. Xie, Chaoling Qiu, Gordon Munro, Kenneth A. Peterson, Frank Porreca]]></dcterms:creator>
    <dcterms:source><![CDATA[Pain, vol. 160, no. 8, Aug. 2019, p. 1847]]></dcterms:source>
    <dcterms:publisher><![CDATA[Pain (Wolters Kluwer Health)]]></dcterms:publisher>
    <dcterms:date><![CDATA[2019]]></dcterms:date>
    <dcterms:rights><![CDATA[Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain. This is an open-access article distributed under the terms of the <a href="https://creativecommons.org/licenses/by-nc-nd/4.0/">Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND)</a>, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/7d1ea959754f0f1c17fafe5f99d1a2b7.pdf">https://repository.nyitlibrary.org/files/original/7d1ea959754f0f1c17fafe5f99d1a2b7.pdf</a><br /><br /><a href="https://doi.org/10.1097/j.pain.0000000000001569">https://doi.org/10.1097/j.pain.0000000000001569</a>]]></dcterms:identifier>
</rdf:Description><br />
<b>Warning</b>:  Undefined array key "path" in <b>/home/nyitlibr/repository.nyitlibrary.org/plugins/ClickableLinksPlus/ClickableLinksPlusPlugin.php</b> on line <b>207</b><br />
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3768">
    <dcterms:title><![CDATA[Are endocasts good proxies for brain size and shape in archosaurs throughout ontogeny?]]></dcterms:title>
    <dcterms:subject><![CDATA[Alligator<br />
Gallus<br />
Diffusible iodine-based contrast-enhanced computed tomography<br />
Geometric morphometrics<br />
Micro-computed tomography<br />
Neuroanatomy]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Cranial endocasts, or the internal molds of the braincase, are a crucial correlate for investigating the neuroanatomy of extinct vertebrates and tracking brain evolution through deep time. Nevertheless, the validity of such studies pivots on the reliability of endocasts as a proxy for brain morphology. Here, we employ micro-computed tomography imaging, including diffusible iodine-based contrast-enhanced CT, and a three-dimensional geometric morphometric framework to examine both size and shape differences between brains and endocasts of two exemplar archosaur taxa – the American alligator (Alligator mississippiensis) and the domestic chicken (Gallus gallus). With ontogenetic sampling, we quantitatively evaluate how endocasts differ from brains and whether this deviation changes during development. We find strong size and shape correlations between brains and endocasts, divergent ontogenetic trends in the brain-to-endocast correspondence between alligators and chickens, and a comparable magnitude between brain–endocast shape differences and intraspecific neuroanatomical variation. The results have important implications for paleoneurological studies in archosaurs. Notably, we demonstrate that the pattern of endocranial shape variation closely reflects brain shape variation. Therefore, analyses of endocranial morphology are unlikely to generate spurious conclusions about large-scale trends in brain size and shape. To mitigate any artifacts, however, paleoneurological studies should consider the lower brain–endocast correspondence in the hindbrain relative to the forebrain; higher size and shape correspondences in chickens than alligators throughout postnatal ontogeny; artificially ‘pedomorphic’ shape of endocasts relative to their corresponding brains; and potential biases in both size and shape data due to the lack of control for ontogenetic stages in endocranial sampling.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Watanabe, A., Gignac, P. M., Balanoff, A. M., Green, T. L., Kley, N. J., &amp; Norell, M. A. ]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Journal of Anatomy</em>, Volume 234, Issue 3, December 2018, pages 291-305]]></dcterms:source>
    <dcterms:publisher><![CDATA[Wiley]]></dcterms:publisher>
    <dcterms:date><![CDATA[2019]]></dcterms:date>
    <dcterms:rights><![CDATA[Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/6cf271c0c7cc2bfcfe261ec3fbe66313.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<span class="linkify-target external-link">https://doi.org/10.1111/joa.12918</span>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Watanabe, A., Gignac, P. M., Balanoff, A. M., Green, T. L., Kley, N. J., &amp; Norell, M. A. (2018). Are endocasts good proxies for brain size and shape in archosaurs throughout ontogeny? In Journal of Anatomy (Vol. 234, Issue 3, pp. 291–305). Wiley. <a href="https://doi.org/10.1111/joa.12918">https://doi.org/10.1111/joa.12918</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3728">
    <dcterms:title><![CDATA[Assessment of Abdominal Constrictor’s Forces for Informing Computational Models of Orthostatic Hypotension]]></dcterms:title>
    <dcterms:subject><![CDATA[Abdominal constrictor<br />
Force loads<br />
Orthostatic hypotension<br />
Statistical analysis]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Orthostatic hypotension is defined as a sudden drop in blood pressure upon standing from a sitting or supine position. The prevalence of this condition increases exponentially with age. Nonpharmacological treatments are always the first step in the management of this condition, such as the use of an abdominal constriction belt to optimize the blood volume in the abdomen. A multitude of clinical trials have shown the efficacy of elastic abdominal compression as well as compression using an inflatable bladder; however, there are currently few accessible consumer products that can provide abdominal compression by using an inflatable bladder that ensures the correct amount of pressure is being exerted on the subject. This study serves to quantitatively analyze forces exerted in inflatable abdominal binders, a novel treatment that fits the criterion for a first-line intervention for orthostatic hypotension. Quantitative values aim to indicate both the anatomic regions of the body subjected to the highest pressure by abdominal binding. Quantitative values will also create a model that can correlate the amount of compression on the subject with varying levels of pressure in the inflatable bladder. Inflatable binders of varying levels of inflation are used and localized pressure values are recorded at 5 different vertical points along the abdomen in the midsternal line and midclavicular line, at the locations of the splanchnic veins. These findings indicate both the differences in the compressive force applied through elastic and inflatable binding, as well the regions on the abdomen subject to the highest force load during compression by an abdominal binder. A medical manikin called the iStan Manikin was used to collect data. The pressure values on a manikin were sensed by the JUZO pressure monitor, a special device created for the purpose of measuring the force under compressive garments. The pressure inside the inflatable bladder was extrapolated from a pressure gauge and the pressure was recorded at different degrees of inflation of the belt (mmHG) along two different areas of the abdomen, the midsternal line and the midclavicular line, to discern differences in force exerted on the patient (mmHG). Computational studies on the data from the JUZO pressure monitor as well as the data from the pressure gauge on the inflatable bladder allow us to create a model that can correlate the amount of pressure in the inflatable bladder to the amount of pressure exerted on the belt, thus making sure that the patient is not being harmed by the compressive force. The results of our study indicate that there is no significant difference between the pressures exerted on the midsternal and midclavicular lines of the body by the abdominal binder and that no significant difference exists between the external pressure measured by the inflatable belt and the pressure sensed on the human body by the JUZO sensor; however, we were able to extrapolate an equation that can tell the user the amount of pressure that is actually being exerted on them based on the pressure in the inflatable bladder as recorded by the gauge.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Syed, F., Jose, R., Devine, T., Coletti, C., &amp; Toma, M.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Materials</em>, Volume 15, Issue 9, April 2022, page 3116]]></dcterms:source>
    <dcterms:publisher><![CDATA[MDPI AG]]></dcterms:publisher>
    <dcterms:date><![CDATA[2022]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (</span><a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noreferrer noopener">https://creativecommons.org/licenses/by/4.0/</a><span>).</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/351c173ce5a4f2c097d23991543348db.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3390/ma15093116">https://doi.org/10.3390/ma15093116</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Syed, F., Jose, R., Devine, T., Coletti, C., &amp; Toma, M. (2022). Assessment of Abdominal Constrictor’s Forces for Informing Computational Models of Orthostatic Hypotension. In Materials (Vol. 15, Issue 9, p. 3116). MDPI AG. <a href="https://doi.org/10.3390/ma15093116">https://doi.org/10.3390/ma15093116</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3757">
    <dcterms:title><![CDATA[Attenuated evolution of mammals through the Cenozoic]]></dcterms:title>
    <dcterms:subject><![CDATA[Animals<br />
Biological Evolution<br />
Eutheria anatomy &amp; histology<br />
Female<br />
Fossils<br />
Index Medicus<br />
Phylogeny<br />
Rodentia<br />
Skull anatomy &amp; histology]]></dcterms:subject>
    <dcterms:abstract><![CDATA[The Cenozoic diversification of placental mammals is the archetypal adaptive radiation. Yet, discrepancies between molecular divergence estimates and the fossil record fuel ongoing debate around the timing, tempo, and drivers of this radiation. Analysis of a three-dimensional skull dataset for living and extinct placental mammals demonstrates that evolutionary rates peak early and attenuate quickly. This long-term decline in tempo is punctuated by bursts of innovation that decreased in amplitude over the past 66 million years. Social, precocial, aquatic, and herbivorous species evolve fastest, especially whales, elephants, sirenians, and extinct ungulates. Slow rates in rodents and bats indicate dissociation of taxonomic and morphological diversification. Frustratingly, highly similar ancestral shape estimates for placental mammal superorders suggest that their earliest representatives may continue to elude unequivocal identification.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Goswami, A., Noirault, E., Coombs, E. J., Clavel, J., Fabre, A.-C., Halliday, T. J. D., Churchill, M., Curtis, A., Watanabe, A., Simmons, N. B., Beatty, B. L., Geisler, J. H., Fox, D. L., &amp; Felice, R. N.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Science</em>, Volume 378, Issue 6618, October 2022, pages 377-383]]></dcterms:source>
    <dcterms:publisher><![CDATA[American Association for the Advancement of Science (AAAS)]]></dcterms:publisher>
    <dcterms:date><![CDATA[2022]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>Copyright © 2022 the authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original US government works. </span><a href="https://www.science.org/content/page/science-licenses-journal-article-reuse?adobe_mc=MCMID%3D20966568074372452772299603847900596611%7CMCORGID%3D242B6472541199F70A4C98A6%2540AdobeOrg%7CTS%3D1700174153">https://www.science.org/about/science-licenses-journal-article-reuse</a>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/e9b15442736432b2304a1d23eaac5f32.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<br /><a href="https://doi.org/10.1126/science.abm7525">https://doi.org/10.1126/science.abm7525</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Goswami, A., Noirault, E., Coombs, E. J., Clavel, J., Fabre, A.-C., Halliday, T. J. D., Churchill, M., Curtis, A., Watanabe, A., Simmons, N. B., Beatty, B. L., Geisler, J. H., Fox, D. L., &amp; Felice, R. N. (2022). Attenuated evolution of mammals through the Cenozoic. In Science (Vol. 378, Issue 6618, pp. 377–383). American Association for the Advancement of Science (AAAS). <a href="https://doi.org/10.1126/science.abm7525">https://doi.org/10.1126/science.abm7525</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3718">
    <dcterms:title><![CDATA[BNP as a New Biomarker of Cardiac Thyroid Hormone Function]]></dcterms:title>
    <dcterms:subject><![CDATA[BNP<br />
Physiology<br />
Experimental pharmacology<br />
T3<br />
Gene expression<br />
Heart failure<br />
Hypothyroidism<br />
Thyroid hormones]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<p class="mb15"><b>Background:</b><span> </span>Cardiac re-expression of fetal genes in patients with heart failure (HF) suggests the presence of low cardiac tissue thyroid hormone (TH) function. However, serum concentrations of T3 and T4 are often normal or subclinically low, necessitating an alternative serum biomarker for low cardiac TH function to guide treatment of these patients. The clinical literature suggests that serum Brain Natriuretic Peptide (BNP) levels are inversely associated with serum triiodo-L-thyronine (T3) levels. The objective of this study was to investigate BNP as a potential serum biomarker for TH function in the heart.</p>
<p class="mb15"><b>Methods:</b><span> </span>Two animal models of thyroid hormone deficiency: (1) 8-weeks of propyl thiouracil-induced hypothyroidism (Hypo) in adult female rats were subsequently treated with oral T3 (10 μg/kg/d) for 3, 6, or 14 days; (2) HF induced by coronary artery ligation (myocardial infarction, MI) in adult female rats was treated daily with low dose oral T3 (5 μg/kg/d) for 8 or 16 wks.</p>
<p class="mb15"><b>Results:</b><span> </span>Six days of T3 treatment of Hypo rats normalized most cardiac functional parameters. Serum levels of BNP increased 5-fold in Hypo rats, while T3 treatment normalized BNP by day 14, showing a significant inverse relationship between serum BNP and free or total T3 concentrations. Myocardial BNP mRNA was increased 2.5-fold in Hypo rats and its expression was decreased to normal values by 14 days of T3 treatment. Measurements of hemodynamic function showed significant dysfunction in MI rats after 16 weeks, with serum BNP increased by 4.5-fold and serum free and total T3 decreased significantly. Treatment with T3 decreased serum BNP while increasing total T3 indicating an inverse correlation between these two biologic factors (<i>r</i><sup>2</sup><span> </span>= 0.676,<span> </span><i>p</i><span> </span>&lt; 0.001). Myocardial BNP mRNA was increased 5-fold in MI rats which was significantly decreased by T3 over 8 to 16 week treatment periods.</p>
<p class="mb0"><b>Conclusions:</b><span> </span>Results from the two models of TH dysfunction confirmed an inverse relationship between tissue and serum T3 and BNP, such that the reduction in serum BNP could potentially be utilized to monitor efficacy and dosing of T3 treatment. Thus, serum BNP may serve as a reliable biomarker for cardiac TH function.</p>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Wang, K., Ojamaa, K., Samuels, A., Gilani, N., Zhang, K., An, S., Zhang, Y., Tang, Y.-D., Askari, B., &amp; Gerdes, A. M.]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Frontiers in Physiology</em>, Volume 11, July 2020]]></dcterms:source>
    <dcterms:publisher><![CDATA[Frontiers Media SA]]></dcterms:publisher>
    <dcterms:date><![CDATA[2020]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>Copyright</span><span> © 2020 Wang, Ojamaa, Samuels, Gilani, Zhang, An, Zhang, Tang, Askari and Gerdes. This is an open-access article distributed under the terms of the </span><a href="http://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noreferrer noopener">Creative Commons Attribution License (CC BY)</a><span>. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/6aa336bf64feefd5da01a6f4a4b4382a.pdf">https://repository.nyitlibrary.org/files/original/6aa336bf64feefd5da01a6f4a4b4382a.pdf<br /><br /></a>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3389/fphys.2020.00729">https://doi.org/10.3389/fphys.2020.00729</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Wang, K., Ojamaa, K., Samuels, A., Gilani, N., Zhang, K., An, S., Zhang, Y., Tang, Y.-D., Askari, B., &amp; Gerdes, A. M. (2020). BNP as a New Biomarker of Cardiac Thyroid Hormone Function. In Frontiers in Physiology (Vol. 11). Frontiers Media SA. <a href="https://doi.org/10.3389/fphys.2020.00729">https://doi.org/10.3389/fphys.2020.00729</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3673">
    <dcterms:title><![CDATA[Breaking up prolonged sitting with a 6 min walk improves executive function in women and men esports players: a randomised trial]]></dcterms:title>
    <dcterms:subject><![CDATA[Original research<br />
Randomised controlled trial<br />
Sitting time<br />
Walking]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<div class="subsection">
<p><strong>Objective</strong><span> </span>The effect of prolonged sitting on executive function and performance in competitive esports players are unknown. This study aimed to evaluate executive function following a 6 min bout of walking or rest during prolonged gaming in competitive esports players.</p>
</div>
<div class="subsection">
<p><strong>Methods</strong><span> </span>12 men and 9 women completed three separate 2-hour gaming session days assigned in randomised order consisting of a 6 min walk break, 6 min rest break and continuous before and after each session. Postintervention participant exit survey data were also collected.</p>
</div>
<div class="subsection">
<p><strong>Results</strong><span> </span>The walk condition produced a significantly faster mean solution time (7613.6±3060.5 min, p=0.02) and planning time (5369.0±2802.09, p=0.04) compared with the resting condition (9477±3547.4; 6924±3247.7) and continuous play (8200.0±3031.6; 5862.7±2860.7). The rest condition resulted in the slowest mean solution time (9477.0±3547.4) and planning time (6924.0±3247.7), with the continuous play resulting in a faster mean solution time (8200.1±3031.6) and planning time (5862.7±2860.7) than the rest condition. There was no impact on game performance in any of the conditions. However, over 70% of participants felt that the walk break improved esports performance.</p>
</div>
<div class="subsection">
<p><strong>Conclusions</strong><span> </span>Reducing sit time and breaking up prolonged sitting have acute and chronic health benefits. This study provides evidence that a 6 min walking break in the middle of 2 hours of gameplay allows gamers to have these health benefits while improving processing speed and executive function.</p>
</div>
<div class="subsection">
<p><strong>Trial registration number</strong><span> </span><a class="external-ref external-ref-type-clintrialgov" href="https://bmjopensem.bmj.com/lookup/external-ref?link_type=CLINTRIALGOV&amp;access_num=NCT04674436&amp;atom=%2Fbmjosem%2F7%2F3%2Fe001118.atom">NCT04674436</a>.</p>
</div>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Difrancisco-Donoghue J., Jenny S.E., Douris P.C., Ahmad S., Yuen K., Hassan T., Gan H., Abraham K., Sousa A.<br />
]]></dcterms:creator>
    <dcterms:source><![CDATA[<i>BMJ Open Sport &amp; Exercise Medicine</i><span>, Volume 7, Issue 3, August 2021</span>]]></dcterms:source>
    <dcterms:publisher><![CDATA[BMJ]]></dcterms:publisher>
    <dcterms:date><![CDATA[2021]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: </span><a href="http://creativecommons.org/licenses/by-nc/4.0/">http://creativecommons.org/licenses/by-nc/4.0/</a><span>.</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<a href="https://repository.nyitlibrary.org/files/original/383d15ee26866f0c85c7d085dca55d13.pdf">https://repository.nyitlibrary.org/files/original/383d15ee26866f0c85c7d085dca55d13.pdf</a>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.1136/bmjsem-2021-001118">https://doi.org/10.1136/bmjsem-2021-001118</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>DiFrancisco-Donoghue, J., Jenny, S. E., Douris, P. C., Ahmad, S., Yuen, K., Hassan, T., Gan, H., Abraham, K., &amp; Sousa, A. (2021). Breaking up prolonged sitting with a 6 min walk improves executive function in women and men esports players: a randomised trial. In BMJ Open Sport &amp;amp; Exercise Medicine (Vol. 7, Issue 3, p. e001118). BMJ. <a href="https://doi.org/10.1136/bmjsem-2021-001118">https://doi.org/10.1136/bmjsem-2021-001118</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><br />
<b>Warning</b>:  Undefined array key "path" in <b>/home/nyitlibr/repository.nyitlibrary.org/plugins/ClickableLinksPlus/ClickableLinksPlusPlugin.php</b> on line <b>207</b><br />
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3770">
    <dcterms:title><![CDATA[Caffeine and Dobutamine Challenge Induces Bidirectional Ventricular Tachycardia in Normal Rats]]></dcterms:title>
    <dcterms:subject><![CDATA[Bidirectional ventricular tachycardia<br />
Caffeine<br />
Dantrolene<br />
Dobutamine<br />
Ventricular arrhythmia]]></dcterms:subject>
    <dcterms:abstract><![CDATA[<div>
<h4 class="u-h4 u-margin-m-top u-margin-xs-bottom">Background</h4>
<p>Bidirectional<span> </span><a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/ventricular-tachycardia" title="Learn more about ventricular tachycardia from ScienceDirect's AI-generated Topic Pages" class="topic-link">ventricular tachycardia</a><span> </span>(BD-VT) is an intriguing arrhythmia, characterized by a beat-to-beat alternation of the QRS polarity on electrocardiogram. Currently there is no simple BD-VT animal model.</p>
</div>
<div>
<h4 class="u-h4 u-margin-m-top u-margin-xs-bottom">Objective</h4>
<p><span>We report a simple animal model of BD-VT induced by caffeine and <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/dobutamine" title="Learn more about dobutamine from ScienceDirect's AI-generated Topic Pages" class="topic-link">dobutamine</a> (C+D) challenge in normal rats in which the arrhythmia can be attenuated by </span><a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/dantrolene" title="Learn more about dantrolene from ScienceDirect's AI-generated Topic Pages" class="topic-link">dantrolene</a><span> (a <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/ryanodine-receptor" title="Learn more about ryanodine receptor from ScienceDirect's AI-generated Topic Pages" class="topic-link">ryanodine receptor</a> stabilizer) <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/therapeutic-procedure" title="Learn more about treatment from ScienceDirect's AI-generated Topic Pages" class="topic-link">treatment</a>, but not by the pacemaker <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/channel-blocker" title="Learn more about channel blocker from ScienceDirect's AI-generated Topic Pages" class="topic-link">channel blocker</a> <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/ivabradine" title="Learn more about ivabradine from ScienceDirect's AI-generated Topic Pages" class="topic-link">ivabradine</a> treatment.</span></p>
</div>
<div>
<h4 class="u-h4 u-margin-m-top u-margin-xs-bottom">Methods</h4>
<p>Adult (4–5 months old) Sprague-Dawley rats (both sexes) were randomized into C+D (n = 8, received caffeine 120 mg/kg intraperitoneally [IP] and dobutamine 60 μg/kg IP, sequentially) and control (n = 8) groups. In addition, a group of 7 rats were pretreated with dantrolene (10 mg/kg, IP) 30 minutes before the C+D challenge and another group of 8 rats were pretreated with ivabradine (5 mg/kg, IP) 30 minutes before the C+D challenge.</p>
</div>
<div>
<h4 class="u-h4 u-margin-m-top u-margin-xs-bottom">Results</h4>
<p><span>C+D challenge induced spontaneous <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/premature-ventricular-contraction" title="Learn more about premature ventricular contractions from ScienceDirect's AI-generated Topic Pages" class="topic-link">premature ventricular contractions</a> (PVCs) in 7 of 8 rats and BD-VT (lasted 4.3 ± 2.9 minutes, terminated spontaneously) in 6 of 8 (75%) rats. No <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/heart-ventricle-arrhythmia" title="Learn more about ventricular arrhythmia from ScienceDirect's AI-generated Topic Pages" class="topic-link">ventricular arrhythmia</a> was induced in the control group (</span><em>P</em><span> </span>&lt; .05 vs C+D group). Dantrolene treatment significantly decreased BD-VT (1 of 7 rats in the Dantrolene+C+D group vs 6 of 8 rats in C+D group,<span> </span><em>P</em><span> </span>&lt; .05). Ivabradine treatment did not affect C+D-induced BD-VT (7 of 8 rats in the Ivabradine+C+D group vs 6 of 8 in the C+D group,<span> </span><em>P</em><span> </span>&gt; .05).</p>
</div>
<div>
<h4 class="u-h4 u-margin-m-top u-margin-xs-bottom">Conclusion</h4>
<p>Caffeine and dobutamine challenge induces BD-VT in a majority of normal rats. Stabilizing<span> </span><a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/ryanodine-receptor-2" title="Learn more about cardiac ryanodine receptors from ScienceDirect's AI-generated Topic Pages" class="topic-link">cardiac ryanodine receptors</a><span> </span>with dantrolene treatment can significantly decrease the occurrence of BD-VT, but pacemaker channel blocker ivabradine treatment does not have effect in this animal model.</p>
</div>]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Zhang, C., &amp; Zhang, Y. ]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Heart Rhythm O2</em>, Volume 1, Issue 5, December 2020, pages 359-367]]></dcterms:source>
    <dcterms:publisher><![CDATA[Elsevier BV]]></dcterms:publisher>
    <dcterms:date><![CDATA[2020]]></dcterms:date>
    <dcterms:rights><![CDATA[<h3>Copyright</h3>
<div class="copyright">© 2020 Heart Rhythm Society. Published by Elsevier Inc.</div>
<h3>User license</h3>
<a href="http://creativecommons.org/licenses/by-nc-nd/4.0/" class="userLicLnk">Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0)</a><span> </span>|<span> </span>
<div class="dropBlock reference-citations"><a href="https://www.heartrhythmopen.com/article/S2666-5018(20)30114-8/fulltext#" class="reference-citations__ctrl">How you can reuse</a><span> </span></div>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/667c55996f468c6e5304c4e1655510f0.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<span class="linkify-target external-link">https://doi.org/10.1016/j.hroo.2020.08.005</span>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Zhang, C., &amp; Zhang, Y. (2020). Caffeine and dobutamine challenge induces bidirectional ventricular tachycardia in normal rats. In Heart Rhythm O2 (Vol. 1, Issue 5, pp. 359–367). Elsevier BV. <a href="https://doi.org/10.1016/j.hroo.2020.08.005">https://doi.org/10.1016/j.hroo.2020.08.005</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3762">
    <dcterms:title><![CDATA[Cannabidiol (CBD) as a Promising Anti-Cancer Drug]]></dcterms:title>
    <dcterms:subject><![CDATA[CBD<br />
Cannabidiol<br />
Cannbinoids<br />
Anti-cancer drug]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Recently, cannabinoids, such as cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), have been the subject of intensive research and heavy scrutiny. Cannabinoids encompass a wide array of organic molecules, including those that are physiologically produced in humans, synthesized in laboratories, and extracted primarily from the Cannabis sativa plant. These organic molecules share similarities in their chemical structures as well as in their protein binding profiles. However, pronounced differences do exist in their mechanisms of action and clinical applications, which will be briefly compared and contrasted in this review. The mechanism of action of CBD and its potential applications in cancer therapy will be the major focus of this review article.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Seltzer, E. S., Watters, A. K., MacKenzie, D., Jr., Granat, L. M., &amp; Zhang, D. ]]></dcterms:creator>
    <dcterms:source><![CDATA[<em>Cancers</em>, Volume 12, Issue 11, October 2020, page 3203]]></dcterms:source>
    <dcterms:publisher><![CDATA[MDPI AG]]></dcterms:publisher>
    <dcterms:date><![CDATA[2020]]></dcterms:date>
    <dcterms:rights><![CDATA[<span>© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (</span><a href="http://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noreferrer noopener">http://creativecommons.org/licenses/by/4.0/</a><span>).</span>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/247fa735fc0f1dbe794c4196fae1a8d1.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<a href="https://doi.org/10.3390/cancers12113203">https://doi.org/10.3390/cancers12113203</a>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[<span>Seltzer, E. S., Watters, A. K., MacKenzie, D., Jr., Granat, L. M., &amp; Zhang, D. (2020). Cannabidiol (CBD) as a Promising Anti-Cancer Drug. In Cancers (Vol. 12, Issue 11, p. 3203). MDPI AG. <a href="https://doi.org/10.3390/cancers12113203">https://doi.org/10.3390/cancers12113203</a></span>]]></dcterms:bibliographicCitation>
</rdf:Description><br />
<b>Warning</b>:  Undefined array key "path" in <b>/home/nyitlibr/repository.nyitlibrary.org/plugins/ClickableLinksPlus/ClickableLinksPlusPlugin.php</b> on line <b>207</b><br />
<rdf:Description rdf:about="https://repository.nyitlibrary.org/items/show/3664">
    <dcterms:title><![CDATA[Cardioprotection by triiodothyronine following caloric restriction via long noncoding RNAs]]></dcterms:title>
    <dcterms:subject><![CDATA[Animals<br />
Arrhythmias, Cardiac etiology metabolism prevention &amp; control<br />
Body Weight physiology<br />
Caloric Restriction adverse effects methods trends<br />
Calorie restriction<br />
Cardiotonic Agents administration &amp; dosage<br />
Fasting<br />
Female<br />
Heart<br />
Index Medicus<br />
Long noncoding RNA<br />
Male<br />
Mice<br />
Mice, Inbred C57BL<br />
RNA, Long Noncoding biosynthesis<br />
Starvation<br />
Thyroid hormones<br />
Triiodothyronine administration &amp; dosage]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Severe caloric-restriction compromises thyroid hormone (TH) status, apparently to save energy and proteins for enduring stress stimulus. However, a persistent decrease in TH levels may compromise heart function. We hypothesized that supplementation of low dose active TH or targeting hypoxia-inducible factor-1-alpha, HIF-1α (a strong activator of deiodinase enzyme that degrades peripheral active THs) will prevent deterioration of cardiac performance. Adult mice were subjected to acute fasting based on institutional animal protocols with ad libitum access to water. The following groups were studied: Control mice with free access to food; severe caloric restriction fasting only group; Fasting with Triiodo- l -Thyronine (T3); Fasting with HIF-1α inhibitor (BAY). Cardiac hemodynamic and electrophysiological studies were performed and role of long noncoding RNAs were explored. Following severe caloric-restriction, we found that body weights, and heart weights to a partial extent, were decreased. Low-dose T3 treatment attenuated left ventricular hemodynamic impairment in indices of cardiac contractility and relaxation. In electrophysiology studies, fasting mice developed atrial tachyarrhythmias upon induction. This reverted to control levels following T3 treatment. There was a significant increase in atrioventricular conduction time and significant decrease in heart rate following fasting. Both these changes were attenuated following T3 treatment. Furthermore, BAY partially improved hemodynamics. Compared to the severe caloric-restriction group, both T3 and BAY reduced MALAT1 and GAS5 long noncoding RNA expression. These new findings indicate that T3 and BAY protect from cardiac decompensation secondary to acute severe caloric-restriction partly mediated by long noncoding RNAs.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[Rajagopalan V., Gorecki M., Costello C., Schultz E., Zhang Y., Gerdes A.M.]]></dcterms:creator>
    <dcterms:source><![CDATA[Biomedicine &amp; Pharmacotherapy, Volume 131, Article 110657, November 2020]]></dcterms:source>
    <dcterms:publisher><![CDATA[Elsevier BV]]></dcterms:publisher>
    <dcterms:date><![CDATA[2020]]></dcterms:date>
    <dcterms:rights><![CDATA[Copyright © 2020 The Authors]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[English]]></dcterms:language>
    <dcterms:type><![CDATA[Text]]></dcterms:type>
    <dcterms:identifier><![CDATA[<span class="linkify-target internal-link">https://repository.nyitlibrary.org/files/original/4063dd6e7acab4eec26bce686d3667a4.pdf</span>]]></dcterms:identifier>
    <dcterms:identifier><![CDATA[<span class="linkify-target external-link">https://doi.org/10.1016/j.biopha.2020.110657</span>]]></dcterms:identifier>
    <dcterms:bibliographicCitation><![CDATA[Rajagopalan, V., Gorecki, M., Costello, C., Schultz, E., Zhang, Y., &amp; Gerdes, A. M. (2020). Cardioprotection by triiodothyronine following caloric restriction via long noncoding RNAs. In Biomedicine &amp; Pharmacotherapy (Vol. 131, p. 110657). Elsevier BV. https://doi.org/10.1016/j.biopha.2020.110657<br />
]]></dcterms:bibliographicCitation>
</rdf:Description></rdf:RDF>
