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                <text>Subclinical hypothyroidism and low T3 syndrome are commonly associated with an increased risk of cardiovascular disease (CVD) and mortality. We examined effects of T3 on T-tubule (TT) structures, Ca2+ mobilization and contractility, and clustering of dyadic proteins. Thyroid hormone (TH) deficiency was induced in adult female rats by propyl-thiouracil (PTU; 0.025%) treatment for 8 weeks. Rats were then randomized to continued PTU or triiodo-L-thyronine (T3; 10 μg/kg/d) treatment for 2 weeks (PTU + T3). After in vivo echocardiographic and hemodynamic recordings, cardiomyocytes (CM) were isolated to record Ca2+ transients and contractility. TT organization was assessed by confocal microscopy, and STORM images were captured to measure ryanodine receptor (RyR2) cluster number and size, and L-type Ca2+ channel (LTCC, Cav1.2) co-localization. Expressed genes including two integral TT proteins, junctophilin-2 (Jph-2) and bridging integrator-1 (BIN1), were analyzed in left ventricular (LV) tissues and cultured CM using qPCR and RNA sequencing. The T3 dosage used normalized serum T3, and reversed adverse effects of TH deficiency on in vivo measures of cardiac function. Recordings of isolated CM indicated that T3 increased rates of Ca2+ release and re-uptake, resulting in increased velocities of sarcomere shortening and re-lengthening. TT periodicity was significantly decreased, with reduced transverse tubules but increased longitudinal tubules in TH-deficient CMs and LV tissue, and these structures were normalized by T3 treatment. Analysis of STORM data of PTU myocytes showed decreased RyR2 cluster numbers and RyR localizations within each cluster without significant changes in Cav1.2 localizations within RyR clusters. T3 treatment normalized RyR2 cluster size and number. qPCR and RNAseq analyses of LV and cultured CM showed that Jph2 expression was T3-responsive, and its increase with treatment may explain improved TT organization and RyR-LTCC coupling.</text>
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                <text>A Miocene cetacean vertebra showing a partially healed longitudinal shear-compression fracture, possibly the result of domoic acid toxicity or failed predation</text>
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                <text>Calvert Cliffs&#13;
Cetacean vertebrae&#13;
Failed predation&#13;
Harmful algal bloom&#13;
Miocene&#13;
Otodus megalodon&#13;
Seizure&#13;
Shear-compression fracture&#13;
Acid&#13;
Algal bloom&#13;
Cetacean&#13;
Compression&#13;
Fracture&#13;
Miocene&#13;
Pathology&#13;
Predation&#13;
Shark&#13;
Shear&#13;
Tooth&#13;
Toxicity</text>
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                <text>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.</text>
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                <text>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.&#13;
&#13;
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.&#13;
&#13;
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.</text>
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                <text>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</text>
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