The Visceral \u3cem\u3eRetia Mirabilia\u3c/em\u3e of Tuna and Sharks: An Annotated Translation and Discussion of the Eschricht and Müller 1835 Paper and Related Papers

The focus of this volume is an annotated translation of the classic work by J. Müller and D.F. Eschricht on the visceral anatomy of the bluefin tuna, Thunnus thynnus, published in 1835. This text, with its outstanding figures, is to this day the definitive work on the anatomy of the bluefin viscera and especially on the circulation to and from the viscera. In addition, the text is historically important in that it represents the first comprehensive description of visceral relia mirabilia in a fish. In this work, Eschricht & Müller meticulously elucidate the pattern of blood flow to, within, and from the viscera. In addition they describe and speculate about the function of such peculiar anatomical structures such as: the visceral relia mirabilia, the radiating liver vessels and the unusually large visceral nerves seen in this species. We have annotated the translation in order to connect the findings of Eschricht & Müller with our current understanding of warm fishes. Eschricht & Müller published a supplement to the tuna article in which they describe the visceral anatomy of the common thresher shark, Alopias vulpinus. We provide an annotated translation of this text as well. The main point of the supplement is that the vascular arrangement of the thresher viscera is completely analogous to that in T. thynnus, and distinct from that found in the other warm sharks, such as Lamna nasus, implying that endothermy has evolved independently at least twice within elasmobranchs. Finally, to round out the historical aspect of this volume, we include two papers and their abstracts by John Davy, who is credited with the first body temperature measurements of warm fishes. Eschricht & Müller were aware of Davy\u27s measurements and discuss them briefly in their paper on tuna visceral anatomy. We also include plates from the 1923 paper by Kishinouye and sorne color photographs of the visceral relia from our dissections. The last two sections of this volume are facsimiles of the two texts by Eschricht & Müller as they appeared in their original form

A Test of Biochemical Symmorphosis in a Heterothermic Tissue: Bluefin Tuna White Muscle

To test predictions of biochemical symmorphosis, we measured the activity of seven consecutive glycolytic enzymes at three positions along the heterothermic white muscle of the bluefin tuna. Biochemical symmorphosis predicts that adjustments in sequential enzyme concentrations along a thermal gradient should occur as a function of the thermal sensitivity of the enzymes to ensure that no one enzyme in the pathway is in excess at any point along the gradient. We found no evidence for adjustments in enzyme quantity or quality along the thermal gradient, as well as no evidence for the prediction that the more temperature-sensitive enzymes would exhibit more dramatic compensation. Conservation of glycolytic flux in the cold exterior and warm interior muscle may be achieved by the near insensitivity of glyceraldehyde- 3-phosphate dehydrogenase to temperature in this tissue. This may have the added benefit of moderating flux during seasonal or transient changes in the thermal gradient. According to the strictest application of biochemical symmorphosis, such a mechanism represents adequate, yet suboptimal desig

Particle Motion and Scalar Field Propagation in Myers-Perry Black Hole Spacetimes in All Dimensions

We study separability of the Hamilton-Jacobi and massive Klein-Gordon equations in the general Myers-Perry black hole background in all dimensions. Complete separation of both equations is carried out in cases when there are two sets of equal black hole rotation parameters, which significantly enlarges the rotational symmetry group. We explicitly construct a nontrivial irreducible Killing tensor associated with the enlarged symmetry group which permits separation. We also derive first-order equations of motion for particles in these backgrounds and examine some of their properties.Comment: 16 pages, LaTeX2

A novel behavioral fish model of nociception for testing analgesics

Pain is a major symptom in many medical conditions, and often interferes significantly with a person's quality of life. Although a priority topic in medical research for many years, there are still few analgesic drugs approved for clinical use. One reason is the lack of appropriate animal models that faithfully represent relevant hallmarks associated with human pain. Here we propose zebrafish (Danio rerio) as a novel short-term behavioral model of nociception, and analyse its sensitivity and robustness. Firstly, we injected two different doses of acetic acid as the noxious stimulus. We studied individual locomotor responses of fish to a threshold level of nociception using two recording systems: a video tracking system and an electric biosensor (the MOBS system). We showed that an injection dose of 10% acetic acid resulted in a change in behavior that could be used to study nociception. Secondly, we validated our behavioral model by investigating the effect of the analgesic morphine. In time-course studies, first we looked at the dose-response relationship of morphine and then tested whether the effect of morphine could be modulated by naloxone, an opioid antagonist. Our results suggest that a change in behavioral responses of zebrafish to acetic acid is a reasonable model to test analgesics. The response scales with stimulus intensity, is attenuated by morphine, and the analgesic effect of morphine is blocked with naloxone. The change in behavior of zebrafish associated with the noxious stimulus can be monitored with an electric biosensor that measures changes in water impedance. © 2011 by the authors; licensee MDPI, Basel, Switzerland

A modeling and analysis study reveals that CaMKII in synaptic plasticity Is a dominant affecter in CaM systems in a T286 phosphorylation-dependent manner

NMDAR-dependent synaptic plasticity in the hippocampus consists of two opposing forces: long-term potentiation (LTP), which strengthens synapses and long-term depression (LTD), which weakens synapses. LTP and LTD are associated with memory formation and loss, respectively. Synaptic plasticity is controlled at a molecular level by Ca²⁺-mediated protein signaling. Here, Ca²⁺ binds the protein, calmodulin (CaM), which modulates synaptic plasticity in both directions. This is because Ca²⁺-bound CaM activates both LTD-and LTP-inducing proteins. Understanding how CaM responds to Ca²⁺ signaling and how this translates into synaptic plasticity is therefore important to understanding synaptic plasticity induction. In this paper, CaM activation by Ca²⁺ and calmodulin binding to downstream proteins was mathematically modeled using differential equations. Simulations were monitored with and without theoretical knockouts and, global sensitivity analyses were performed to determine how Ca²⁺/CaM signaling occurred at various Ca²⁺ signals when CaM levels were limiting. At elevated stimulations, the total CaM pool rapidly bound to its protein binding targets which regulate both LTP and LTD. This was followed by CaM becoming redistributed from low-affinity to high-affinity binding targets. Specifically, CaM was redistributed away from LTD-inducing proteins to bind the high-affinity LTP-inducing protein, calmodulin-dependent kinase II (CaMKII). In this way, CaMKII acted as a dominant affecter and repressed activation of opposing CaM-binding protein targets. The model thereby showed a novel form of CaM signaling by which the two opposing pathways crosstalk indirectly. The model also found that CaMKII can repress cAMP production by repressing CaM-regulated proteins, which catalyze cAMP production. The model also found that at low Ca²⁺ stimulation levels, typical of LTD induction, CaM signaling was unstable and is therefore unlikely to alone be enough to induce synaptic depression. Overall, this paper demonstrates how limiting levels of CaM may be a fundamental aspect of Ca²⁺ regulated signaling which allows crosstalk among proteins without requiring directly interaction

Real-time X-ray Diffraction Measurements of Shocked Polycrystalline Tin and Aluminum

A new, fast, single-pulse x-ray diffraction (XRD) diagnostic for determining phase transitions in shocked polycrystalline materials has been developed. The diagnostic consists of a 37-stage Marx bank high-voltage pulse generator coupled to a needle-and-washer electron beam diode via coaxial cable, producing line and bremsstrahlung x-ray emission in a 35-ns pulse. The characteristic Kα lines from the selected anodes of silver and molybdenum are used to produce the diffraction patterns, with thin foil filters employed to remove the characteristic Kβ line emission. The x-ray beam passes through a pinhole collimator and is incident on the sample with an approximately 3-mm by 6-mm spot and 1° full-width-half-maximum (FWHM) angular divergence in a Bragg-reflecting geometry. For the experiments described in this report, the angle between the incident beam and the sample surface was 8.5°. A Debye-Scherrer diffraction image was produced on a phosphor located 76 mm from the polycrystalline sample surface. The phosphor image was coupled to a charge-coupled device (CCD) camera through a coherent fiberoptic bundle. Dynamic single-pulse XRD experiments were conducted with thin foil samples of tin, shock loaded with a 1-mm vitreous carbon back window. Detasheet high explosive with a 2-mm-thick aluminum buffer was used to shock the sample. Analysis of the dynamic shock-loaded tin XRD images revealed a phase transformation of the tin beta phase into an amorphous or liquid state. Identical experiments with shock-loaded aluminum indicated compression of the face-centered-cubic (fcc) aluminum lattice with no phase transformation