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Herbivory is a common ecological function among extant lepidosaurs, but little is known about the origin of this feeding strategy within Lepidosauria. Here we describe a sphenodontian (Lepidosauria) from the Late Triassic of western North America, Trullidens purgatorii n. gen. n. sp., that reveals new aspects of the earliest radiation of herbivorous lepidosaurs. This taxon is represented by an isolated lower jaw with robust structure bearing transversely widened dentition and extensive wear facets, suggesting a masticatory apparatus specialized for herbivory. An unusual 'incisor-like' tooth is present at the anterior end of the jaw; a unique feature among lepidosaurs, this tooth is convergent with the incisors of extant rodents and lagomorphs. Phylogenetic analyses support the placement of this taxon within opisthodontian sphenodontians, a group sharing derived cranio-dental morphologies specialized for herbivory. The new taxon was recovered in a recently discovered and unnamed series of Upper Triassic strata in southeastern Colorado, USA, exposed in Canyons incised by the Purgatoire River and its tributaries. These strata comprise a dominantly red-bed sequence of conglomerates, sandstones, and siltstones deposited in a fluvio-lacustrine setting, preserving a Late Triassic biota of invertebrate and vertebrate ichnofossils, plant macrofossils, bony fish, temnospondyl amphibians, and reptiles. We use aetosaur osteoderms as biostratigraphic links to the nearby Chinle Formation of Arizona, USA, establishing a middle Norian age for these strata. The presence of an opisthodontian from western equatorial Pangaea in the Norian Stage reveals a near-global radiation of this clade across the Pangaean supercontinent during the Late Triassic. UUID: http://zoobank.org/A737c03f-863a-488e-a860-5cc914548774. Virginia Tech Paleobiology Group Published version M.R. Stocker and S.J. Nesbitt of the Virginia Tech Paleobiology Group provided funding for and conducted mu CT scanning, which was conducted at the Duke Shared Instrumentation Facility and facilitated by J. Gladman. J. Autry, the Southeast Colorado Project Director at The Nature Conservancy, facilitated access to the J.E. Canyon Ranch and provided logistical support, supplies, and housing for the authors. B. Preston, S. Korbitz, B. Small, and Y. Huang assisted in field work. The Virginia Tech Paleobiology Research Group provided useful critiques and suggestions for figures in the manuscript. M. R. Stocker provided useful critiques and discussions on the manuscript. W.G. Parker of Petrified Forest National Park provided assistance in identifying aetosaur osteoderms. K. MacKenzie and J. Sertich of the DMNH facilitated curation of specimens used in this study. B. Creisler provided valuable etymological assistance. D. Whiteside and an anonymous reviewer provided valuable reviews of the manuscript. Public domain – authored by a U.S. government employee

Therapeutic options for Duchenne muscular dystrophy (DMD), the most common and lethal neuromuscular disorder in children, remain elusive. Oxidative damage is implicated as a pertinent factor involved in its pathogenesis. Protandim((R)) is an over-the-counter supplement with the ability to induce antioxidant enzymes. In this study we investigated whether Protandim((R)) provided benefit using surrogate markers and functional measures in the dystrophin-deficient (mdx)mouse model of DMD. Male 3-week-old mdx mice were randomized into two treatment groups: control (receiving standard rodent chow) and Protandim((R))-supplemented standard rodent chow. The diets were continued for 6-week and 6-month studies. The endpoints included the oxidative stress marker thiobarbituric acid-reactive substances (TBARS), plasma osteopontin (OPN), plasma paraoxonase (PON1) activity, HE histology, gadolinium-enhanced magnetic resonance imaging (MRI) of leg muscle and motor functional measurements. The Protandim((R)) chow diet in mdx mice for 6 months was safe and well tolerated. After 6 months of Protandim((R)), a 48% average decrease in plasma TBARS was seen; 0.92 nmol/mg protein in controls versus 0.48 nmol/mg protein in the Protandim((R)) group (p = .006). At 6 months, plasma OPN was decreased by 57% (p = .001) in the Protandim((R))-treated mice. Protandim((R)) increased the plasma antioxidant enzyme PON1 activity by 35% (p = .018). After 6 months, the mdx mice with Protandim((R)) showed 38% less MRI signal abnormality (p = .07) than mice on control diet. In this 6-month mdx mouse study, Protandim((R)) did not significantly alter motor function nor histological criteria.

Duchenne muscular dystrophy (DMD) is a fatal neuromuscular human disease caused by dystrophin deficiency. The mdx mouse lacks dystrophin protein, yet does not exhibit the debilitating DMD phenotype. Investigating compensatory mechanisms in the mdx mouse may shed new insights into modifying DMD pathogenesis. This study targets two metabolic genes, guanidinoacetate methyltransferase (GAMT) and arginine:glycine amidinotransferase (AGAT) which are required for creatine synthesis. We show that GAMT and AGAT mRNA are up-regulated 5.4- and 1.9-fold respectively in adult mdx muscle compared to C57. In addition, GAMT protein expression is up-regulated at least 2.5-fold in five different muscles of mdx vs. control. Furthermore, we find GAMT immunoreactivity in up to 80% of mature mdx muscle fibers in addition to small regenerating fibers and rare revertants; while GAMT immunoreactivity is equal to background levels in all muscle fibers of mature C57 mice. The up-regulation of the creatine synthetic pathway may help maintain muscle creatine levels and limit cellular energy failure in leaky mdx skeletal muscles. These results may help better understand the mild phenotype of the mdx mouse and may offer new treatment horizons for DMD.

The purpose of this study was to determine the influence of local contractile activity on lipoprotein lipase (LPL) regulation in skeletal muscle. Short-term voluntary run training increased LPL mRNA concentration and LPL immunoreactive mass about threefold in white skeletal muscles of the rat hindlimb (all P < 0.01). Training also increased total and heparin-releasable LPL enzyme activity in white hindlimb muscles and in postheparin plasma ( P< 0.05). Training did not enhance LPL regulation in a white muscle that was not recruited during running (masseter). LPL levels were already high in red skeletal muscles of control rats, and training did not result in a further rise. In resting rats, local electrical stimulation of a motor nerve to a predominantly white muscle caused a significant rise in LPL mRNA, immunoreactive mass, and enzyme activity relative to the contralateral control muscle of the same animals (all P < 0.01). Finally, LPL expression was several times greater in a red muscle (soleus) of rats with normal postural activity than rats with immobilized hindlimbs ( P < 0.01). In summary, these studies support the hypothesis that local contractile activity is required for increasing LPL expression during exercise training and for maintaining a high level of LPL expression in postural muscles.