träning av djurparksdjur – inverkan på human-animal relationship, kontroll och motivation : fallstudie av träning av röd panda (Ailurus fulgens) för hantering

Zoo animals are trained for a lot of different reasons including facilitating husbandry procedures, physical exercise and mental stimulation. Training has also been shown to reduce stereotypies in captive wild animals. Among other factors, two of the most important for zoo animal welfare are the Human-Animal Relationship (HAR) between animal and zookeepers, and an environment that allows behavioural choices. These factors are important for the animal´s perceived level of control of its environment. This study is divided into two parts. First, it aims to investigate trainings implications for the HAR, control and motivation. Second, it also includes a case study of training Red Panda (Ailurus fulgens) for weighing and transporting. The method used in the study was literature search in databases. The case study aimed to evaluate a training plan for two Red Pandas and also to assess behavioural change throughout the training period. The results show that training can have positive implications for both the HAR and for the perceived control. The training plan proved functional as a template but may have to be adjusted depending on the individual animal and trainer. The behavioural changes throughout the training period could possibly be due to enhanced HAR, increased control or motivation but which factor, if any of the three, had the most implication could not be concluded

Ympäristöhallintajärjestelmät ympäristöpoliittisina ohjauskeinoina : EMAS hallinnon ja yritysten näkökulmasta

Only abstract. Paper copies of master’s theses are listed in the Helka database (http://www.helsinki.fi/helka). Electronic copies of master’s theses are either available as open access or only on thesis terminals in the Helsinki University Library.Vain tiivistelmä. Sidottujen gradujen saatavuuden voit tarkistaa Helka-tietokannasta (http://www.helsinki.fi/helka). Digitaaliset gradut voivat olla luettavissa avoimesti verkossa tai rajoitetusti kirjaston opinnäytekioskeilla.Endast sammandrag. Inbundna avhandlingar kan sökas i Helka-databasen (http://www.helsinki.fi/helka). Elektroniska kopior av avhandlingar finns antingen öppet på nätet eller endast tillgängliga i bibliotekets avhandlingsterminaler.Tutkielmassa tarkastellaan Euroopan Unionin EMAS-asetuksen (1836/93) mukaisen ympäristöjärjestelmän toimivuutta Suomessa. Tutkielmassa etsitään vastausta siihen, miten EMASin avulla on pystytty ehkäisemään ympäristöongelmia ja parantamaan ympäristön tilaa. Koska EMASissa hallinnolla on keskeinen rooli sen toteuttamisessa ja valvonnassa, on muut ympäristöjärjestelmät jätetty tutkielman tarkastelun ulkopuolelle, ja tarkastellaan EMASin toimivuutta ja tarpeellisuutta erityisesti hallinnon näkökulmasta. Lisäksi tarkastellaan sitä, miten uusiin, vapaaehtoisiin ympäristöpoliittisiin ohjauskeinoihin suhtaudutaan muiden ohjauskeinojen rinnalla. Tutkielman metateoria on Joseph Huberin ja Martin Jänicken alunperin kehittelemä ekologisen modernisaation teoria, jonka avulla kuvataan ympäristöpolitiikan kehitystä sekä sitä, miten ympäristöpolitiikka ja ohjauskeinot ovat muuttuneet. Tutkimusteoriana on Stephen Linderin ja Guy Petersin kehittelemä ohjauskeinojen valinnan teoria. Tämän avulla tarkastellaan sitä, mitkä tekijät vaikuttavat ohjauskeinojen valintaan. Keskeisenä empiirisenä aineistona käytettiin eri hallinnon alojen ja yritysten EMAS-asiantuntijoiden haastatteluja. Empiirisen analyysin tukena käytettiin myös EMAS-ympäristöjärjestelmästä ja ympäristöpoliittisista ohjauskeinoista kertovaa kirjallisuutta. Haastattelut analysoitiin kvalitatiivisen tutkimuksen menetelmin. Litteroidut haastattelut analysoitiin Grounded theoryn ja sisällönanalyysin perusperiaatteita seuraamalla ja soveltamalla näiden kahden metodiperinteen ominaisuuksia tutkielmaan sopiviksi. Tutkimustulosten mukaan EMAS-ympäristöjärjestelmän avulla pystytään vähentämään jätteitä ja energian kulutusta sekä lisäämään kierrätystä. Pääsääntöisesti järjestelmään ollaan tyytyväisiä, erityisesti sen systemaattisuuteen, itsenäiseen tavoitteiden asettamiseen sekä ulkopuolisen verifioijan tarkastamaan selontekoon. Ongelmina nähtiin sen heikko tunnettuus, vähäinen rekisteröityjen yritysten määrä, sen soveltuminen lähinnä suurille yrityksille sekä suuret kustannukset suhteessa hyötyihin. Pidettiin tärkeänä EMAS-järjestelmän tunnettuuden lisäämistä informaation ja markkinoinnin avulla, jotta rekisteröityjä yrityksiä saataisiin enemmän. Tässä korostettiin erityisesti hallinnon roolia informaation jakajana. Tärkeimpiä lähteitä olivat Rauno Sairisen ympäristöpolitiikan ja ohjauskeinojen kehitystä kuvaava väitöskirja, Antero Honkasalon EMAS-ympäristöjärjestelmää koskeva teos ja artikkelit sekä Maarten Haajerin ja Gert Spaargarenin ekologisen modernisaation teoriaa koskevat teokset

RhoD regulates cytoskeletal dynamics via the actin nucleation-promoting factor WASp homologue associated with actin Golgi membranes and microtubules

The Rho GTPases have mainly been studied in association with their roles in the regulation of actin filament organization. These studies have shown that the Rho GTPases are essential for basic cellular processes, such as cell migration, contraction, and division. In this paper, we report that RhoD has a role in the organization of actin dynamics that is distinct from the roles of the better-studied Rho members Cdc42, RhoA, and Rac1. We found that RhoD binds the actin nucleation–promoting factor WASp homologue associated with actin Golgi membranes and microtubules (WHAMM), as well as the related filamin A–binding protein FILIP1. Of these two RhoD-binding proteins, WHAMM was found to bind to the Arp2/3 complex, while FILIP1 bound filamin A. WHAMM was found to act downstream of RhoD in regulating cytoskeletal dynamics. In addition, cells treated with small interfering RNAs for RhoD and WHAMM showed increased cell attachment and decreased cell migration. These major effects on cytoskeletal dynamics indicate that RhoD and its effectors control vital cytoskeleton-driven cellular processes. In agreement with this notion, our data suggest that RhoD coordinates Arp2/3-dependent and FLNa-dependent mechanisms to control the actin filament system, cell adhesion, and cell migration

Nanoscale localization of proteins within focal adhesions indicates discrete functional assemblies with selective force‐dependence

Focal adhesions (FAs) are subcellular regions at the micrometer scale that link the cell to the surrounding microenvironment and control vital cell functions. However, the spatial architecture of FAs remains unclear at the nanometer scale. We used two‐color and three‐color super‐resolution stimulated emission depletion microscopy to determine the spatial distributions and co‐localization of endogenous FA components in fibroblasts. Our data indicate that adhesion proteins inside, but not outside, FAs are organized into nanometer size units of multi‐protein assemblies. The loss of contractile force reduced the nanoscale co‐localization between different types of proteins, while it increased this co‐localization between markers of the same type. This suggests that actomyosin‐dependent force exerts a nonrandom, specific, control of the localization of adhesion proteins within cell–matrix adhesions. These observations are consistent with the possibility that proteins in cell–matrix adhesions are assembled in nanoscale particles, and that force regulates the localization of the proteins therein in a protein‐specific manner. This detailed knowledge of how the organization of FA components at the nanometer scale is linked to the capacity of the cells to generate contractile forces expands our understanding of cell adhesion in health and disease

SCAR knockouts in Dictyostelium: WASP assumes SCAR's position and upstream regulators in pseudopods

Under normal conditions, the Arp2/3 complex activator SCAR/WAVE controls actin polymerization in pseudopods, whereas Wiskott–Aldrich syndrome protein (WASP) assembles actin at clathrin-coated pits. We show that, unexpectedly, Dictyostelium discoideum SCAR knockouts could still spread, migrate, and chemotax using pseudopods driven by the Arp2/3 complex. In the absence of SCAR, some WASP relocated from the coated pits to the leading edge, where it behaved with similar dynamics to normal SCAR, forming split pseudopods and traveling waves. Pseudopods colocalized with active Rac, whether driven by WASP or SCAR, though Rac was activated to a higher level in SCAR mutants. Members of the SCAR regulatory complex, in particular PIR121, were not required for WASP regulation. We thus show that WASP is able to respond to all core upstream signals and that regulators coupled through the other members of SCAR’s regulatory complex are not essential for pseudopod formation. We conclude that WASP and SCAR can regulate pseudopod actin using similar mechanisms

The Formin-Homology Protein SmDia Interacts with the Src Kinase SmTK and the GTPase SmRho1 in the Gonads of Schistosoma mansoni

BACKGROUND:Schistosomiasis (bilharzia) is a parasitic disease of worldwide significance affecting human and animals. As schistosome eggs are responsible for pathogenesis, the understanding of processes controlling gonad development might open new perspectives for intervention. The Src-like tyrosine-kinase SmTK3 of Schistosoma mansoni is expressed in the gonads, and its pharmacological inhibition reduces mitogenic activity and egg production in paired females in vitro. Since Src kinases are important signal transduction proteins it is of interest to unravel the signaling cascades SmTK3 is involved in to understand its cellular role in the gonads. METHODOLOGY AND RESULTS:Towards this end we established and screened a yeast two-hybrid (Y2H) cDNA library of adult S. mansoni with a bait construct encoding the SH3 (src homology) domain and unique site of SmTK3. Among the binding partners found was a diaphanous homolog (SmDia), which was characterized further. SmDia is a single-copy gene transcribed throughout development with a bias towards male transcription. Its deduced amino acid sequence reveals all diaphanous-characteristic functional domains. Binding studies with truncated SmDia clones identified SmTK3 interaction sites demonstrating that maximal binding efficiency depends on the N-terminal part of the FH1 (formin homology) domain and the inter-domain region of SmDia located upstream of FH1 in combination with the unique site and the SH3 domain of SmTK3, respectively. SmDia also directly interacted with the GTPase SmRho1 of S. mansoni. In situ hybridization experiments finally demonstrated that SmDia, SmRho1, and SmTK3 are transcribed in the gonads of both genders. CONCLUSION:These data provide first evidence for the existence of two cooperating pathways involving Rho and Src that bridge at SmDia probably organizing cytoskeletal events in the reproductive organs of a parasite, and beyond that in gonads of eukaryotes. Furthermore, the FH1 and inter domain region of SmDia have been discovered as binding sites for the SH3 and unique site domains of SmTK3, respectively

The F-BAR domain of SRGP-1 facilitates cell–cell adhesion during C. elegans morphogenesis

SRGP-1 activity leads to outward bending and projections of membranes at cell–cell junctions, promoting robust adhesion between cells during embryonic closure events

Antigen Receptor–Induced Activation and Cytoskeletal Rearrangement Are Impaired in Wiskott-Aldrich Syndrome Protein–Deficient Lymphocytes

The Wiskott-Aldrich syndrome protein (WASp) has been implicated in modulation of lymphocyte activation and cytoskeletal reorganization. To address the mechanisms whereby WASp subserves such functions, we have examined WASp roles in lymphocyte development and activation using mice carrying a WAS null allele (WAS−/−). Enumeration of hemopoietic cells in these animals revealed total numbers of thymocytes, peripheral B and T lymphocytes, and platelets to be significantly diminished relative to wild-type mice. In the thymus, this abnormality was associated with impaired progression from the CD44−CD25+ to the CD44−CD25− stage of differentiation. WASp-deficient thymocytes and T cells also exhibited impaired proliferation and interleukin (IL)-2 production in response to T cell antigen receptor (TCR) stimulation, but proliferated normally in response to phorbol ester/ionomycin. This defect in TCR signaling was associated with a reduction in TCR-evoked upregulation of the early activation marker CD69 and in TCR-triggered apoptosis. While induction of TCR-ζ, ZAP70, and total protein tyrosine phosphorylation as well as mitogen-activated protein kinase (MAPK) and stress-activated protein/c-Jun NH2-terminal kinase (SAPK/JNK) activation appeared normal in TCR-stimulated WAS−/− cells, TCR-evoked increases in intracellular calcium concentration were decreased in WASp-deficient relative to wild-type cells. WAS−/− lymphocytes also manifested a marked reduction in actin polymerization and both antigen receptor capping and endocytosis after TCR stimulation, whereas WAS−/− neutrophils exhibited reduced phagocytic activity. Together, these results provide evidence of roles for WASp in driving lymphocyte development, as well as in the translation of antigen receptor stimulation to proliferative or apoptotic responses, cytokine production, and cytoskeletal rearrangement. The data also reveal a role for WASp in modulating endocytosis and phagocytosis and, accordingly, suggest that the immune deficit conferred by WASp deficiency reflects the disruption of a broad range of cellular behaviors

Pincher-generated Nogo-A endosomes mediate growth cone collapse and retrograde signaling

RhoA is activated from internalized Nogo-A to promote growth cone collapse and inhibit neurite outgrowth

Kank attenuates actin remodeling by preventing interaction between IRSp53 and Rac1

In this study, insulin receptor substrate (IRS) p53 is identified as a binding partner for Kank, a kidney ankyrin repeat–containing protein that functions to suppress cell proliferation and regulate the actin cytoskeleton. Kank specifically inhibits the binding of IRSp53 with active Rac1 (Rac1G12V) but not Cdc42 (cdc42G12V) and thus inhibits the IRSp53-dependent development of lamellipodia without affecting the formation of filopodia. Knockdown (KD) of Kank by RNA interference results in increased lamellipodial development, whereas KD of both Kank and IRSp53 has little effect. Moreover, insulin-induced membrane ruffling is inhibited by overexpression of Kank. Kank also suppresses integrin-dependent cell spreading and IRSp53-induced neurite outgrowth. Our results demonstrate that Kank negatively regulates the formation of lamellipodia by inhibiting the interaction between Rac1 and IRSp53