When Does Less Equal More? Assessing The Mechanisms Driving Compensatory Mortality And The Hydra Effect

Many populations across taxa are regulated by negative density-dependence, wherein increased population sizes lead to decreased birth rates and/or increased mortality. By releasing such populations from some level of these density-dependent effects, extrinsic mortality can lead to counter-intuitive results, such as no change in population size (compensation), or an increase in population size (overcompensation). These results have been documented experimentally, but there currently exists a dearth of empirical studies exploring the mechanisms behind the phenomenon. We tested the relationship between extrinsic mortality level and (over)compensation in four mosquito species – Aedes aegypti, A. albopictus, A. triseriatus, and Culex pipiens – by exposing larvae to a range of mortality by artificial harvest and predation and analyzing the numbers of adults produced. Additionally, we examined the ability of three functionally diverse predators – Mesocyclops longisetus, Anopheles barberi, and Corethrella appendiculata – to induce (over)compensation in A. aegypti by exposing larvae to predation by either single or multiple predator species treatments. We found overcompensation across all ranges of mortality in A. triseriatus and C. pipiens and at intermediate levels of mortality in A. aegypti. Low-to-intermediate levels of mortality was compensatory in A. albopictus, followed by a decrease in adult production at the highest mortality level. Predation induced compensation in the second experiment and an increase in population equilibrium, a phenomenon known as the ‘hydra effect.’ These results provide a better understanding of the conditions under which mortality may increase adult production or population equilibrium. Because overcompensation and the hydra effect are predicted to affect a wide range of taxa and food webs, our findings present implications for developing proper population management and pest reduction strategies

AXONAL TRANSPORT AND TURNOVER OF PROLINE- AND LEUCINE-LABELED PROTEIN IN THE GOLDFISH VISUAL SYSTEM

The suitability of radioactively labeled proline as a marker of axonally transported protein in the goldfish visual system is further investigated and compared with another amino acid, leucine, in double-label experiments. Intraocularly injected proline is incorporated into protein in the eye S times more efficiently than is leucine, while local labeling of brain protein from precursor which has left the eye and entered the blood, (observed in the ipsilateral optic tectum) is five- to eight-fold less from proline than from leucine. The difference is attributed to the superior transport of leucine, an essential amino acid, into the brain from the blood. Once in the brain, the apparent rates of incorporation of the two amino acids are similar. Proline- or leucine-labeled, axonally transported proteins have a longer apparent half-life in the brain than do proteins labeled from intracranial injection of the precursors. By either route, proline-labeled proteins have a longer apparent half-life than leucine-labeled proteins. It is proposed that proline, released from protein breakdown is reutilized to a greater extent than is leucine.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65647/1/j.1471-4159.1974.tb10757.x.pd

Intracerebroventricular administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in inflammatory pain

<p>Abstract</p> <p>Background</p> <p>The peptide neurotransmitter <it>N</it>-Acetylaspartylglutamate (NAAG) is the third most prevalent transmitter in the mammalian central nervous system. Local, intrathecal and systemic administration of inhibitors of enzymes that inactivate NAAG decrease responses to inflammatory pain in rat models. Consistent with NAAG's activation of group II metabotropic glutamate receptors, this analgesia is blocked by a group II antagonist.</p> <p>Results</p> <p>This research aimed at determining if analgesia obtained following systemic administration of NAAG peptidase inhibitors is due to NAAG activation of group II mGluRs in brain circuits that mediate perception of inflammatory pain. NAAG and NAAG peptidase inhibitors, ZJ43 and 2-PMPA, were microinjected into a lateral ventricle prior to injection of formalin in the rat footpad. Each treatment reduced the early and late phases of the formalin-induced inflammatory pain response in a dose-dependent manner. The group II mGluR antagonist reversed these analgesic effects consistent with the conclusion that analgesia was mediated by increasing NAAG levels and the peptide's activation of group II receptors.</p> <p>Conclusion</p> <p>These data contribute to proof of the concept that NAAG peptidase inhibition is a novel therapeutic approach to inflammatory pain and that these inhibitors achieve analgesia by elevating synaptic levels of NAAG within pain processing circuits in brain.</p

The effect of head and neck per-cooling on neuromuscular fatigue following exercise in the heat

The effect of localised head and neck per-cooling on central and peripheral fatigue during high thermal strain was investigated. Fourteen participants cycled for 60 min at 50% peak oxygen uptake on 3 occasions: thermoneutral control (CON; 18 °C), hot (HOT; 35 °C), and HOT with head and neck cooling (HOTcooling). Maximal voluntary force (MVF) and central activation ratio (CAR) of the knee extensors were measured every 30 s during a sustained maximal voluntary contraction (MVC). Triplet peak force was measured following cycling, before and after the MVC. Rectal temperatures were higher in HOTcooling (39.2 ± 0.6 °C) and HOT (39.3 ± 0.5 °C) than CON (38.1 ± 0.3 °C; P &lt; 0.05). Head and neck thermal sensation was similar in HOTcooling (4.2 ± 1.4) and CON (4.4 ± 0.9; P &gt; 0.05) but lower than HOT (5.9 ± 1.5; P &lt; 0.05). MVF and CAR were lower in HOT than CON throughout the MVC (P &lt; 0.05). MVF and CAR were also lower in HOTcooling than CON at 5, 60, and 120 s, but similar at 30 and 90 s into the MVC (P &gt; 0.05). Furthermore, they were greater in HOTcooling than HOT at 30 s, whilst triplet peak force was preserved in HOT after MVC. These results provide evidence that central fatigue following exercise in the heat is partially attenuated with head and neck cooling, which may be at the expense of greater peripheral fatigue

Conjugated Imine Polymer Synthesized via Step-Growth Metathesis for Highly Stable Silicon Nanoparticle Anodes in Lithium-Ion Batteries

This work reports a new method to synthesize polyphenylmethanimine (polyPMI) as a linear or a hyperbranched, conjugated polymer using an aldehyde-imine metathesis reaction. This work details the reaction mechanisms of this polymerization by characterizing a red-shift in its absorption spectrum as polymer conjugation length increases and verifies that this optical shift results from extended π-condensation using density functional theory. This new synthetic approach provides a polymer that can potentially be depolymerized for facile recyclability and is compatible with air- and water-sensitive chemistries. As an example of the utility of this new approach, this work demonstrates that this polymer can be directly grown on silicon nanoparticles to create silicon anodes for lithium-ion batteries with a high degree of electrochemical interfacial passivation. These silicon anodes exhibit Coulombic efficiencies above 99.9% and can accommodate silicon nanoparticle expansion and contraction during lithiation and delithiation as demonstrated by stable reversible capacities for 500 cycles. Finally, this work demonstrates that polyPMI facilitates the formation of a lithium fluoride rich solid electrolyte interphase that remains chemically and mechanically stable after long term cycling

Temperature-dependent consolidation of puromycin-susceptible memory in the goldfish

Memory of a shock-avoidance task in goldfish (Carassius auratus) maintained at 20[deg]C shows a temporal gradient of insusceptibility to post-trial injection of puromycin upon testing 7 days later. Treatment with the antimetabolite 24 hr after training has no effect on retention. There is a significant decrease in the puromycin-induced memory loss if fish are warmed to 30[deg]C for a 90-minute interval between conditioning and injection of puromycin. If fish are cooled to 4.5[deg]C for 24 hr between learning and puromycin injection, a significant block of memory results. There are in addition time-independent effects of the cold treatment on performance. Although temperature increase from 20 to 30[deg]C does not in itself affect retention, it does cause a 3-fold stimulation of incorporation of 3H-leucine into brain protein. Decrease in temperature from 20 to 4.5[deg]C reduces protein labeling by 86-97 percent.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/33819/1/0000076.pd

Lack of Association of Rare Functional Variants in TSC1/TSC2 Genes with Autism Spectrum Disorder

Background: Autism spectrum disorder (ASD) is reported in 30 to 60% of patients with tuberous sclerosis complex (TSC) but shared genetic mechanisms that exist between TSC-associated ASD and idiopathic ASD have yet to be determined. Through the small G-protein Rheb, the TSC proteins, hamartin and tuberin, negatively regulate mammalian target of rapamycin complex 1 (mTORC1) signaling. It is well established that mTORC1 plays a pivotal role in neuronal translation and connectivity, so dysregulation of mTORC1 signaling could be a common feature in many ASDs. Pam, an E3 ubiquitin ligase, binds to TSC proteins and regulates mTORC1 signaling in the CNS, and the FBXO45-Pam ubiquitin ligase complex plays an essential role in neurodevelopment by regulating synapse formation and growth. Since mounting evidence has established autism as a disorder of the synapses, we tested whether rare genetic variants in TSC1, TSC2, MYCBP2, RHEB and FBXO45, genes that regulate mTORC1 signaling and/or play a role in synapse development and function, contribute to the pathogenesis of idiopathic ASD. Methods: Exons and splice junctions of TSC1, TSC2, MYCBP2, RHEB and FBXO45 were resequenced for 300 ASD trios from the Simons Simplex Collection (SSC) using a pooled PCR amplification and next-generation sequencing strategy, targeted to the discovery of deleterious coding variation. These detected, potentially functional, variants were confirmed by Sanger sequencing of the individual samples comprising the pools in which they were identified. Results: We identified a total of 23 missense variants in MYCBP2, TSC1 and TSC2. These variants exhibited a near equal distribution between the proband and parental pools, with no statistical excess in ASD cases (P > 0.05). All proband variants were inherited. No putative deleterious variants were confirmed in RHEB and FBXO45. Three intronic variants, identified as potential splice defects in MYCBP2 did not show aberrant splicing upon RNA assay. Overall, we did not find an over-representation of ASD causal variants in the genes studied to support them as contributors to autism susceptibility. Conclusions: We did not observe an enrichment of rare functional variants in TSC1 and TSC2 genes in our sample set of 300 trios