The use of multibeam sonar mapping techniques to refine population estimates of the endangered white abalone (Haliotis sorenseni)

Multibeam sonar mapping techniques provide detailed benthic habitat information that can be combined with the data on species-specific habitat preferences to provide highly accurate calculations of populations in a particular area. The amount of suitable habitat available for the endangered white abalone (Haliotis sorenseni) was quantified to aid in obtaining an accurate estimate of the number of remaining individuals at two offshore banks and one island site off the coast of southern California. Habitat was mapped by using multibeam sonar survey techniques and categorized by using rugosity and topographic position analysis. Abalone densities were evaluated by using a remotely operated vehicle and video transect methods. The total amount of suitable habitat at these three sites was far greater than that previously estimated. Therefore, although present estimates of white abalone densities are several orders of magnitude lower than historic estimates, the total population is likely larger than previously reported because of the additional amount of habitat surveyed in this study

An aspect of tragedy: inaugural lecture delivered at Rhodes University

Inaugural lecture delivered at Rhodes UniversityRhodes University Libraries (Digitisation

Insurance loss coverage under restricted risk classification: The case of iso-elastic demand

This paper investigates equilibrium in an insurance market where risk classification is restricted. Insurance demand is characterised by an iso-elastic function with a single elasticity parameter. We characterise the equilibrium by three quantities: equilibrium premium; level of adverse selection (in the economist’s sense); and “loss coverage”, defined as the expected population losses compensated by insurance. We consider both equal elasticities for high and low risk-groups, and then different elasticities. In the equal elasticities case, adverse selection is always higher under pooling than under risk-differentiated premiums, while loss coverage first increases and then decreases with demand elasticity. We argue that loss coverage represents the efficacy of insurance for the whole population; and therefore that if demand elasticity is sufficiently low, adverse selection is not always a bad thing

12/17/1947 Letter from the State of Maine Publicity Bureau

Letter from Guy P. Butler, Executive Manager of the State of Maine Publicity Bureau, to Louis-Philippe Gagné.https://digitalcommons.usm.maine.edu/fac-lpg-1947-10-12/1046/thumbnail.jp

Scaling of Traction Forces with Size of Cohesive Cell Colonies

To understand how the mechanical properties of tissues emerge from interactions of multiple cells, we measure traction stresses of cohesive colonies of 1-27 cells adherent to soft substrates. We find that traction stresses are generally localized at the periphery of the colony and the total traction force scales with the colony radius. For large colony sizes, the scaling appears to approach linear, suggesting the emergence of an apparent surface tension of order 1E-3 N/m. A simple model of the cell colony as a contractile elastic medium coupled to the substrate captures the spatial distribution of traction forces and the scaling of traction forces with the colony size.Comment: 5 pages, 3 figure

Two-Photon Accessed Excited State Absorption in bis(terpyridyl Osmium)-(Porphinato)Zinc

Two-photon absorption properties of a (terpyridyl)osmium-(porphinato)zinc (OsPZnOs) are studied in bulk and waveguides. Integration of OsPZnOs (d\u3e1300GM) in waveguides showed enhanced nonlinear performance and potential for photonic applications

Near IR Nonlinear Optics of an Organic Supermolecule

Two-photon accessed excited state absorption is shown to be an important mechanism in the near-IR nonlinear response of an organic supermolecule. This mechanism also provides an enhanced nonlinear absorption in an optical waveguide configuration

Platinum(IV)-azido monocarboxylato complexes are photocytotoxic under irradiation with visible light

Complexes trans,trans,trans-[Pt(N-3)(2)(OH)(OCOR)(py)(2)] where py = pyridine and where OCOR = succinate (1); 4-oxo-4-propoxybutanoate (2) and N-methylisatoate (3) have been synthesized by derivation of trans, trans,trans-[Pt(OH)(2)(N-3)(2)(py)(2)] (4) and characterised by NMR and EPR spectroscopy, ESI-MS and X-ray crystallography. Irradiation of 1-3 with green (517 nm) light initiated photoreduction to Pt(II) and release of the axial ligands at a 3-fold faster rate than for 4. TD-DFT calculations showed dissociative transitions at longer wavelengths for 1 compared to 4. Complexes 1 and 2 showed greater photocytotoxicity than 4 when irradiated with 420 nm light (A2780 cell line IC50 values: 2.7 and 3.7 mu M) and complex 2 was particularly active towards the cisplatin-resistant cell line A2780cis (IC50 3.7 mu M). Unlike 4, complexes 1-3 were phototoxic under green light irradiation (517 nm), with minimal toxicity in the dark. A pK(a)(H2O) of 5.13 for the free carboxylate group was determined for 1, corresponding to an overall negative charge during biological experiments, which crucially, did not appear to impede cellular accumulation and photocytotoxicity.NF thanks the Wellcome Trust (201406/Z/16/Z); Cancer Research UK (CR-UK) grant number C5255/A18085 through the Cancer Research UK Oxford Centre and the John Fell Fund for funding. NF thanks Profs. Stephen Faulkner for support. PJS and NF thank the EPSRC (for grant EP/P030572/1 and studentship for ES), PJS also thanks the ERC (grant 247450). L. S. performed this work under the Severo Ochoa Centres of Excellence Programme run by the Spanish State Research Agency, grant no. CEX2018-000867-S (DIPC). L. S. also thanks the Spanish Multi-MetDrugs network (RED2018-102471-T) for fruitful discussio

Modelling primary blast lung injury: current capability and future direction

Primary blast lung injury frequently complicates military conflict and terrorist attacks on civilian populations. The fact that it occurs in areas of conflict or unpredictable mass casualty events makes clinical study in human casualties implausible. Research in this field is therefore reliant on the use of some form of biological or non-biological surrogate model. This article briefly reviews the modelling work undertaken in this field until now and describes the rationale behind the generation of an in silico physiological model

Alzheimer's disease-associated R47H TREM2 increases, but wild-type TREM2 decreases, microglial phagocytosis of synaptosomes and neuronal loss

Triggering receptor on myeloid cells 2 (TREM2) is an innate immune receptor, upregulated on the surface of microglia associated with amyloid plaques in Alzheimer's disease (AD). Individuals heterozygous for the R47H variant of TREM2 have greatly increased risk of developing AD. We examined the effects of wild-type (WT), R47H and knock-out (KO) of human TREM2 expression in three microglial cell systems. Addition of mouse BV-2 microglia expressing R47H TREM2 to primary mouse neuronal cultures caused neuronal loss, not observed with WT TREM2. Neuronal loss was prevented by using annexin V to block exposed phosphatidylserine, an eat-me signal and ligand of TREM2, suggesting loss was mediated by microglial phagocytosis of neurons exposing phosphatidylserine. Addition of human CHME-3 microglia expressing R47H TREM2 to LUHMES neuronal-like cells also caused loss compared to WT TREM2. Expression of R47H TREM2 in BV-2 and CHME-3 microglia increased their uptake of phosphatidylserine-beads and synaptosomes versus WT TREM2. Human iPSC-derived microglia with heterozygous R47H TREM2 had increased phagocytosis of synaptosomes vs common-variant TREM2. Additionally, phosphatidylserine liposomes increased activation of human iPSC-derived microglia expressing homozygous R47H TREM2 versus common-variant TREM2. Finally, overexpression of TREM2 in CHME-3 microglia caused increased expression of cystatin F, a cysteine protease inhibitor, and knock-down of cystatin F increased CHME-3 uptake of phosphatidylserine-beads. Together, these data suggest that R47H TREM2 may increase AD risk by increasing phagocytosis of synapses and neurons via greater activation by phosphatidylserine and that WT TREM2 may decrease microglial phagocytosis of synapses and neurons via cystatin F