Foraging ecology of common dolphins (Delphinus sp.) in the Hauraki Gulf, New Zealand : a thesis presented in fulfilment of the requirements for the degree of Master of Science (Zoology), Massey University, Albany, New Zealand

This study investigated the foraging ecology of common dolphins (Delphinus sp.) in the Hauraki Gulf Marine Park, off the east coast of Auckland. New Zealand. Like most species of small cetacea in the Southern Hemisphere, its foraging habits are poorly described. A total of 59 focal group follows of common dolphins were conducted between January and April 2006. Observations were conducted at the surface, recording the predominant behavioural state of the group, foraging phase, foraging strategy, group dispersion, group formation, swimming style, group heading, calf presence and associated species. All occurrences of fission-fusion events and surface behaviours were recorded. This study tested the hypothesis that foraging behaviour of common dolphins would be influenced by environmental and physical parameters, group size, calf presence and associations with other species. In the Hauraki Gulf, foraging behaviour was recorded during all common dolphin follows, with 14% ± 1.7 (mean ± s.e.) of time spent feeding. Larger groups of dolphins spent more time foraging than smaller groups. Herding accounted for a large part of the foraging behaviour of common dolphins (mean ± s.e. = 28% ± 2.3. n = 54). Larger groups were found to spend significantly more time herding than smaller groups. Herding was generally directed towards the nearest landmass. Common dolphins use a variety of foraging strategies, both individual and group coordinated strategies. High-speed pursuits (n = 29) and kerplunkmg (n= 15) were the only individual foraging strategies recorded. Coordinated feeding strategies employed were synchronous diving (n = 50), Ime-abreast (n = 28), carouselling (n = 26) and wall-formation (n = 4). Synchronous diving and carouselling were the most enduring strategies, accounting for a significant proportion of foraging behaviour (mean ± s.e. - 32% ± 0.05 and 24% ± 0.08 of instantaneous samples, respectively). Foraging strategies were typified by vanous group formations, dispersion between group members, swimming styles and breathing intervals. Foraging strategies were also observed to have different roles in dolphin foraging. Line-abreast and wall- formation were associated with herding. However, high-speed pursuit, kerplunking and carouselling were strategies synonymous with feeding. Foraging strategies were shown to be dynamic, with dolphin groups changing strategies within a foraging bout (mean ± s.e. = 3 ± 0.4). Larger groups spent more time engaged in coordinated foraging strategies than smaller groups. Noisy surface behaviours and fission-fusion events were frequently seen in synchrony with foraging behaviour. Calves present in a foraging group, typically assumed a central position in the group during herding, but remained on the periphery during feeding. When feeding, common dolphins frequently were associated with Australasian gannets (Morus senator), shearwaters (Puffinus spp.) and Bryde's whales (Balaenoptera brydei) Observations on the predatory behaviour of each species suggested a temporary close association between birds, whales and dolphins. This study showed an association of Australasian gannet flocks (n =46) and Bryde's whales (n = 27) with common dolphins, and described the nature of the joint aggregations of mixed-species feeding in the Hauraki Gulf. The behaviour of gannots and whales strongly coincided with that of the foraging dolphin group. Whales were recorded tracking behind foraging dolphins for up to one and a half hours (mean ± s.e. = 23 min ± 2.3). Observations suggest that the relationship between gannets and whales with common dolphins was deliberate, and that these species take advantage of the superior ability of dolphins to locate and concentrate prey. The associations with gannets and whales had a significant impact on common dolphin foraging behaviour. Duration of the phenomenon was predicted to be a direct function of the quantity of prey fish available. The presence of a whale had a sizable impact on the diffusion of feeding aggregations. Results from this study indicate that the benefits of coordinated team hunts implemented by common dolphins in the Hauraki Gulf are a key factor in their foraging ecology. Their cooperative foraging skills appear to not only benefit the common dolphin individual, but other species as well. Ultimately, their role as a social hunter and an abundant, apex predator in the ocean, suggests that the common dolphin is a strongly interacting species which may facilitate population viability of other species in the Hauraki Gulf ecosystem

Fecal glucocorticoids and anthropogenic injury and mortality in North Atlantic right whales Eubalaena glacialis

© The Author(s), 2017. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Endangered Species Research 34 (2017): 417-429, doi:10.3354/esr00866.As human impacts on marine ecosystems escalate, there is increasing interest in quantifying sub-lethal physiological and pathological responses of marine mammals. Glucocorticoid hormones are commonly used to assess stress responses to anthropogenic factors in wildlife. While obtaining blood samples to measure circulating hormones is not currently feasible for free-swimming large whales, immunoassay of fecal glucocorticoid metabolites (fGCs) has been validated for North Atlantic right whales Eubalaena glacialis (NARW). Using a general linear model, we compared fGC concentrations in right whales chronically entangled in fishing gear (n = 6) or live-stranded (n = 1), with right whales quickly killed by vessels (n = 5) and healthy right whales (n = 113) to characterize fGC responses to acute vs. chronic stressors. fGCs in entangled whales (mean ± SE: 1856.4 ± 1644.9 ng g-1) and the stranded whale (5740.7 ng g-1) were significantly higher than in whales killed by vessels (46.2 ± 19.2 ng g-1) and healthy whales (51.7 ± 8.7 ng g-1). Paired feces and serum collected from the live-stranded right whale provided comparison of fGCs in 2 matrices in a chronically stressed whale. Serum cortisol and corticosterone in this whale (50.0 and 29.0 ng ml-1, respectively) were much higher than values reported in other cetaceans, in concordance with extremely elevated fGCs. Meaningful patterns in fGC concentration related to acute vs. chronic impacts persisted despite potential for bacterial degradation of hormone metabolites in dead whales. These results provide biological validation for using fGCs as a biomarker of chronic stress in NARWs.This research was funded by the NOAA/NMFS, Office of Naval Research Marine Mammals and Biology Program, Northeast Consortium, Island Foundation, Irving Oil, NEAq Internal Research Fund, Prescott Grant NA08NMF4390590, and NOAA CINAR Cooperative Agreement NA09OAR4320129

Deficits of knowledge versus executive control in semantic cognition: Insights from cued naming

Deficits of semantic cognition in semantic dementia and in aphasia consequent on CVA (stroke) are qualitatively different. Patients with semantic dementia are characterised by progressive degradation of central semantic representations, whereas multimodal semantic deficits in stroke aphasia reflect impairment of executive processes that help to direct and control semantic activation in a task-appropriate fashion [Jefferies, E., & Lambon Ralph, M. A. (2006). Semantic impairment in stroke aphasia vs. semantic dementia: A case-series comparison. Brain 129, 2132-2147]. We explored interactions between these two aspects of semantic cognition by examining the effects of cumulative phonemic cueing on picture naming in case series of these two types of patient. The stroke aphasic patients with multimodal semantic deficits cued very readily and demonstrated near-perfect name retrieval when cumulative phonemic cues reached or exceeded the target name's uniqueness point. Therefore, knowledge of the picture names was largely intact for the aphasic patients, but they were unable to retrieve this information without cues that helped to direct activation towards the target response. Equivalent phonemic cues engendered significant but much more limited benefit to the semantic dementia patients: their naming was still severely impaired even when most of the word had been provided. In contrast to the pattern in the stroke aphasia group, successful cueing was mainly confined to the more familiar un-named pictures. We propose that this limited cueing effect in semantic dementia follows from the fact that concepts deteriorate in a graded fashion [Rogers, T. T., Lambon Ralph, M. A., Garrard, P., Bozeat, S., McClelland, J. L., & Hodges, J. R., et al. (2004). The structure and deterioration of semantic memory: A neuropsychological and computational investigation. Psychological Review 111, 205-235]. For partially degraded items, the residual conceptual knowledge may be insufficient to drive speech production to completion but these items might reach threshold when they are bolstered by cues. (C) 2007 Elsevier Ltd. All rights reserved

Cardiomyocyte Deletion of \u3ci\u3eBmal1\u3c/i\u3e Exacerbates QT- and RR-Interval Prolongation in \u3ci\u3eScn5a\u3c/i\u3e\u3csup\u3e+/ΔKPQ\u3c/sup\u3e Mice

Circadian rhythms are generated by cell autonomous circadian clocks that perform a ubiquitous cellular time-keeping function and cell type-specific functions important for normal physiology. Studies show inducing the deletion of the core circadian clock transcription factor Bmal1 in adult mouse cardiomyocytes disrupts cardiac circadian clock function, cardiac ion channel expression, slows heart rate, and prolongs the QT-interval at slow heart rates. This study determined how inducing the deletion of Bmal1 in adult cardiomyocytes impacted the in vivo electrophysiological phenotype of a knock-in mouse model for the arrhythmogenic long QT syndrome (Scn5a+/ΔKPQ). Electrocardiographic telemetry showed inducing the deletion of Bmal1 in the cardiomyocytes of mice with or without the ΔKPQ-Scn5a mutation increased the QT-interval at RR-intervals that were ≥130 ms. Inducing the deletion of Bmal1 in the cardiomyocytes of mice with or without the ΔKPQ-Scn5a mutation also increased the day/night rhythm-adjusted mean in the RR-interval, but it did not change the period, phase or amplitude. Compared to mice without the ΔKPQ-Scn5a mutation, mice with the ΔKPQ-Scn5a mutation had reduced heart rate variability (HRV) during the peak of the day/night rhythm in the RR-interval. Inducing the deletion of Bmal1 in cardiomyocytes did not affect HRV in mice without the ΔKPQ-Scn5a mutation, but it did increase HRV in mice with the ΔKPQ-Scn5a mutation. The data demonstrate that deleting Bmal1 in cardiomyocytes exacerbates QT- and RR-interval prolongation in mice with the ΔKPQ-Scn5a mutation

Platform-directed allostery and quaternary structure dynamics of SAMHD1 catalysis

SAMHD1 regulates cellular nucleotide homeostasis, controlling dNTP levels by catalysing their hydrolysis into 2’-deoxynucleosides and triphosphate. In differentiated CD4+ macrophage and resting T-cells SAMHD1 activity results in the inhibition of HIV-1 infection through a dNTP blockade. In cancer, SAMHD1 desensitizes cells to nucleoside-analogue chemotherapies. Here we employ time-resolved cryogenic-EM imaging and single-particle analysis to visualise assembly, allostery and catalysis by this multi-subunit enzyme. Our observations reveal how dynamic conformational changes in the SAMHD1 quaternary structure drive the catalytic cycle. We capture five states at high-resolution in a live catalytic reaction, revealing how allosteric activators support assembly of a stable SAMHD1 tetrameric core and how catalysis is driven by the opening and closing of active sites through pairwise coupling of active sites and order-disorder transitions in regulatory domains. This direct visualisation of enzyme catalysis dynamics within an allostery-stabilised platform sets a precedent for mechanistic studies into the regulation of multi-subunit enzymes

Long QT Syndrome Type 2: Emerging Strategies for Correcting Class 2 \u3cem\u3eKCNH2 (hERG)\u3c/em\u3e Mutations and Identifying New Patients

Significant advances in our understanding of the molecular mechanisms that cause congenital long QT syndrome (LQTS) have been made. A wide variety of experimental approaches, including heterologous expression of mutant ion channel proteins and the use of inducible pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from LQTS patients offer insights into etiology and new therapeutic strategies. This review briefly discusses the major molecular mechanisms underlying LQTS type 2 (LQT2), which is caused by loss-of-function (LOF) mutations in the KCNH2 gene (also known as the human ether-à-go-go-related gene or hERG). Almost half of suspected LQT2-causing mutations are missense mutations, and functional studies suggest that about 90% of these mutations disrupt the intracellular transport, or trafficking, of the KCNH2-encoded Kv11.1 channel protein to the cell surface membrane. In this review, we discuss emerging strategies that improve the trafficking and functional expression of trafficking-deficient LQT2 Kv11.1 channel proteins to the cell surface membrane and how new insights into the structure of the Kv11.1 channel protein will lead to computational approaches that identify which KCNH2 missense variants confer a high-risk for LQT2

Weak-Singlet Fermions: Models and Constraints

We employ data from precision electroweak tests and collider searches to derive constraints on the possibility that weak-singlet fermions mix with the ordinary Standard Model fermions. Our findings are presented within the context of a theory with weak-singlet partners for all ordinary fermions and theories in which only third-generation fermions mix with weak singlets. In addition, we indicate how certain results can be applied more widely in theories containing exotic fermions.Comment: 29 pages, 12 figures; added 1 reference, expanded introductio

Explaining semantic short-term memory deficits:evidence for the critical role of semantic control

Patients with apparently selective short-term memory (STM) deficits for semantic information have played an important role in developing multi-store theories of STM and challenge the idea that verbal STM is supported by maintaining activation in the language system. We propose that semantic STM deficits are not as selective as previously thought and can occur as a result of mild disruption to semantic control processes, i.e., mechanisms that bias semantic processing towards task-relevant aspects of knowledge and away from irrelevant information. We tested three semantic STM patients with tasks that tapped four aspects of semantic control: (i) resolving ambiguity between word meanings, (ii) sensitivity to cues, (iii) ignoring irrelevant information and (iv) detecting weak semantic associations. All were impaired in conditions requiring more semantic control, irrespective of the STM demands of the task, suggesting a mild, but task-general, deficit in regulating semantic knowledge. This mild deficit has a disproportionate effect on STM tasks because they have high intrinsic control demands: in STM tasks, control is required to keep information active when it is no longer available in the environment and to manage competition between items held in memory simultaneously. By re-interpreting the core deficit in semantic STM patients in this way, we are able to explain their apparently selective impairment without the need for a specialised STM store. Instead, we argue that semantic STM patients occupy the mildest end of spectrum of semantic control disorders

Association between a longer duration of illness, age and lower frontal lobe grey matter volume in schizophrenia

The frontal lobe has an extended maturation period and may be vulnerable to the long-term effects of schizophrenia. We tested this hypothesis by studying the relationship between duration of illness (DoI), grey matter (GM) and cerebro-spinal fluid (CSF) volume across the whole brain. Sixty-four patients with schizophrenia and 25 healthy controls underwent structural MRI scanning and neuropsychological assessment. We performed regression analyses in patients to examine the relationship between DoI and GM and CSF volumes across the whole brain, and correlations in controls between age and GM or CSF volume of the regions where GM or CSF volumes were associated with DoI in patients. Correlations were also performed between GM volume in the regions associated with DoI and neuropsychological performance. A longer DoI was associated with lower GM volume in the left dorsomedial prefrontal cortex (PFC), right middle frontal cortex, left fusiform gyrus (FG) and left cerebellum (lobule III). Additionally, age was inversely associated with GM volume in the left dorsomedial PFC in patients, and in the left FG and CSF excess near the left cerebellum in healthy controls. Greater GM volume in the left dorsomedial PFC was associated with better working memory, attention and psychomotor speed in patients. Our findings suggest that the right middle frontal cortex is particularly vulnerable to the long-term effect of schizophrenia illness whereas the dorsomedial PFC, FG and cerebellum are affected by both a long DoI and aging. The effect of illness chronicity on GM volume in the left dorsomedial PFC may be extended to brain structure–neuropsychological function relationships